Neutral Citation Number [2004] EWHC 780 (QB)
Case No: U 20040156

IN THE HIGH COURT OF JUSTICE
QUEENS BENCH DIVISION

Royal Courts of Justice
Strand, London, WC2A 2LL

Date: 22 April 2004

Before :

THE HONOURABLE MR JUSTICE GROSS
- - - - - - - - - - - - - - - - - - - - -
Between :

	Roy Mellor and as Administrator of the Estate of Susan Mellor deceased	Claimant	
	- and -		
	(1) Sheffield Teaching Hospitals NHS Trust
and  (6) Dr E.L. Groves
and(7) Dr J.E. Richards	Defendants	

- - - - - - - - - - - - - - - - - - - - -
- - - - - - - - - - - - - - - - - - - - -

Christopher Gardner QC and Richard Ough (instructed by Keeble Hawson) for the Claimant
Jonathan Holl-Allen (instructed by Eversheds) for the 1st Defendant
George Hugh-Jones (instructed by Radcliffes Le Brasseur) for the 6th & 7th Defendants

Hearing dates : 24 February 2004 – 5 March 2004
- - - - - - - - - - - - - - - - - - - - -
Judgment
Mr Justice  Gross:
INTRODUCTION
1.	On the 1st January, 1998, Mrs. Susan Mellor (“Mrs. Mellor”) died following a a cardiac arrest in an ambulance on her way to Rotherham District General Hospital.  She was born on the 2nd February, 1954 and was, accordingly, aged only 43 at the time of her death. 
2.	An autopsy was carried out on the 2nd January, 1998.   The post mortem report (“the PM”) of Dr. Slater, a Consultant Histopathologist, included the following: 
“ Thoracic Cavity & Neck:  There is symmetrical hypertrophy of the left ventricle to 19 mm. There are scattered areas of fribrosis up to 2 mm in diameter.  There is no evidence of infarction…. The right coronary artery displays 20% luminal occlusion by atheroma. There is no thrombotic occlusion. The left common coronary artery displays 30% luminal occlusion by atheroma but no thrombotic occlusion. The left circumflex coronary artery displays 60% luminal occlusion by atheroma but no thrombotic occlusion. The left anterior descending coronary artery displays focal 95% luminal occlusion by atheroma but no thrombotic occlusion….
CONCLUSIONS
In my opinion immediate death was due to gross congestion of the lungs (pulmonary oedema) secondary to the presence of a combination of severe hypertensive and ischaemic heart disease…. I have been informed that Mrs. MELLOR’s essential hypertension was known during life. I have also been informed that there may have been a family history of some type of heart disease. In view of the severity of hardening of Mrs. MELLOR’s blood vessels, I have recommended to HM Coroner’s Officer that the immediate family… are screened for possible lipid (fat) abnormalities….
In my opinion the cause of death was … (a) Pulmonary oedema due to or as a consequence of Hypertensive and ischaemic heart disease…”
3.	Given the debate at the trial as to the cause of death and the significance of the pathologist’s observations, it will be necessary to return to the PM later. For the moment, it suffices to underline the following matters of importance arising from the PM:
i)	The pathologist found significant left ventricular hypertrophy (“LVH”).  In simple terms, LVH means a thickening of the muscle in the area of the left ventricle;  the effect of the muscle thickening is that the left ventricle has to work harder than would normally be the case to pump or supply sufficient blood to the body’s organs for which it is responsible. In neutral terms, LVH may be caused by hypertension (i.e. raised or high blood pressure, “BP”) and/or coronary artery disease (“CAD”), also known as ischaemic or coronary heart disease (“IHD” or “CHD”).  LVH is itself a known cause of sudden death, even if no IHD is present.
ii)	 IHD results in the narrowing (“stenosis”) of the coronary arteries; on the material before me, it is the leading cause of death in the United Kingdom. In the case of Mrs. Mellor, it is of note that the important left anterior descending (“LAD”) coronary artery showed 95% narrowing.
iii)	The heart muscle (“myocardium”) showed scattered areas of fibrosis (scarring).  Again in simple terms, such fibroses or scarring occur when or because the muscle outgrows its blood supply; the muscle dies and is replaced by scarring.  Fibroses may be attributable or secondary to LVH and /or CAD.
iv)	At least in the vast majority of cases, a heart attack, to use the colloquial expression, has two components: a coronary thrombosis (i.e. a blood clot in a coronary artery) resulting in the death of a part of the heart muscle (myocardium) by reason of lack of blood supply – in more technical language, a myocardial infarction (“MI”).   The pathologist found no evidence of infarction or thromboses.
v)	The PM does not state whether the focal 95% stenosis of the LAD was found in the proximal (i.e. early), mid- or distal (end) segment of the LAD.
vi)	The pathologist’s use of the word “focal” may be taken as meaning that there was one discrete or localised lesion.
vii)	The pathologist was sufficiently concerned to recommend the screening of Mrs. Mellor’s immediate family.
4.	The Claimant (“Mr. Mellor”) is the widower and administrator of the estate of the deceased Mrs. Mellor (“the estate”). He brings this action on his own behalf, on behalf of his son Kirk Mellor (“Kirk”), a child of the marriage, aged 11 as at the date of Mrs. Mellor’s death and now aged 17 and for the benefit of the estate.  Claims are brought under the Fatal Accidents Act 1976 as amended and under the Law Reform (Miscellaneous Provisions) Act 1934. In addition, Mr. Mellor brings a claim for nervous shock.
5.	The action has been discontinued against the Second to Fifth and Eighth to Tenth Defendants. The Defendants against whom the action continues are the First, Sixth and Seventh Defendants.
6.	The Sixth and Seventh Defendants (“Dr. Groves” and “Dr. Richards”, respectively) are General Practitioners (“GPs”). Essentially, the case against the GPs is that, over the period 1992 to 1996, they were negligent in failing, timeously, to diagnose that Mrs. Mellor may have been suffering from IHD and to refer her to a cardiologist.  Specific criticism is made of Dr. Groves in respect of a consultation on the 9th January, 1992 and of Dr. Richards in respect of consultations on the 22nd and 28th April, 1994, the 3rd November, 1995 and the 29th March, 1996.   It may be noted that Dr. Richards in fact referred Mrs. Mellor to Dr. West (“Dr. West”), a Consultant Cardiologist at the Royal Hallamshire Hospital, Sheffield, on the 29th April, 1996.  Had a timely referral been made, it is alleged that Mrs. Mellor’s IHD would have been diagnosed in sufficient time for it to be effectively treated within the routine timetable for such treatment.
7.	The First Defendant is the body now responsible for the acts and omissions of clinical staff at the Royal Hallamshire Hospital in 1996 and 1997.  The case against the First Defendant turns on the allegation that Dr. West negligently discharged Mrs. Mellor on the 13th January, 1997.  In coming to his decision to discharge Mrs. Mellor it is, in particular, alleged that Dr. West negligently interpreted the result of an Exercise Tolerance Test (“ETT”) conducted on the 14th August, 1996.  Furthermore, it is alleged that Dr. West negligently gave Dr. Richards and Mrs. Mellor reassurance as to Mrs. Mellor’s chest pain not being cardiac in nature.  The Claimant’s case is that Dr. West should instead have conducted further investigations into Mrs. Mellor’s condition, which investigations would, as a matter of probability, have led to urgent surgical intervention saving Mrs. Mellor’s life.
8.	It has to be said that, at the start of the trial and as Mr. Holl-Allen for the First Defendant submitted, the Claimant’s case on causation as against the First Defendant was anything but clear.  I therefore invited Mr. Gardner QC, leading counsel for the Claimant, to pin his colours to the mast. He did so, in writing, as follows:
“ It is C’s case that W was negligent in:
(1) describing the result of the exercise test as negative
(2) diagnosing the chest pain as not cardiac in nature and discharging Mrs. M without further investigation
(3) assuring her and her GP that the chest pain was not cardiac in nature, rather than advising them that the test result was inconclusive, that CHD [coronary heart disease] could not be excluded, and that persisting symptoms should be monitored
(4) in view of her symptoms, young age, inconclusive exercise test, low exercise tolerance and multiple risk factors, including significant family history, failing to arrange within 3 months (or at least offer) an angiogram to determine whether she had CHD. This, on the balance of probabilities, would have demonstrated stenosis in the proximal segment of the LAD coronary artery requiring a PCI [i.e. an angioplasty] as a matter of urgency, either during the same admission or at least within 3 months.”
9.	Had Mrs. Mellor survived, the Claimant’s case is that her life expectancy  would have been some 19 years – a significant prolongation of life obviously desirable to her and her family.
10.	Dr. Groves, Dr. Richards and the First Defendant (in practical terms, Dr. West) all deny negligence.  Even if negligence is established, there are significant disputes as to causation.  As regards Drs. Groves and Richards, the nature of these disputes will become apparent in due course. So far as Dr. West is concerned, the question arises, notably, of whether the Claimant can show, on a balance of probability, that had he followed a pathway which cannot be criticised as unreasonable, the timescale was such that Mrs. Mellor’s life would have been saved. Furthermore, there is an issue as to whether angioplasty – even if reached “in time” – would, on the balance of probability, have been effective to save Mrs. Mellor’s life.
11.	In a nutshell, the issue as to liability is whether the deceased’s death was not only tragic (which is of course common ground) but also avoidable by the exercise of due diligence on the part of the Defendants, or any of them.
12.	If the Claimant does make good his case on liability then, as to quantum, there has been a significant measure of agreement between the parties.  Issues however remain as to claims for emotional support, care and attention, pain and suffering, nervous shock and a remoteness argument advanced on behalf of Drs. Groves and Richards.  
THE FACTUAL HISTORY
13.	I come to the evidence of fact. In general, it will be convenient to record the evidence and to defer conclusions on disputed topics until later.
14.	(1) Background: Before turning to the detail, it should be recorded that Mrs. Mellor had a longstanding history of health problems.  There was no or no real dispute that a number of these, together with the other matters in the list which follow, disclose risk factors associated with IHD:
i)	Longstanding high BP;
ii)	Raised cholesterol levels (albeit that these would have given rise to markedly less concern in 1992-1997 than they might now);
iii)	A smoking habit;
iv)	Family history: Mrs. Mellor’s mother and sister had both suffered MIs at the age of 43.  Her father had suffered from angina (i.e. pain felt in the chest when there is reduced oxygen supply to the heart muscle and therefore heart related).
15.	Other health problems, unrelated to IHD included:
i)	A subarachnoid haemorrhage in August, 1993, leading to neurosurgery.  In November 1993, a shunt was inserted. Subsequently, she remained under the observation of neurosurgeons and underwent further surgery to her shunt before it was finally removed in January 1997.
ii)	A variety of what may be termed (loosely) gastric concerns, including hiatus hernia and oesophagitis.
iii)	Recurrent anaemia, a matter which, as it seems to me, was of undoubted significance in November 1995.
16.	(2) Dr. Groves:   From 1988 to 2000, Dr. Groves was a practising GP at the Crystal Peaks practice in Sheffield (“the practice”).  He now works as a medical manager in the Medical Services Department of the Benefits Agency in Leeds.
17.	Dr. Groves’ first contact with Mrs. Mellor was a home visit on the night of the 7th March, 1988 at about 21.00. He referred her to the Northern General Hospital that night with a suspected MI. His notes included the following:
“Chest & arm
 pain … sweating arm
14 fast int[ermittent] pain
1 weeks chest pain
Occasional/ stabbing, clammy…
BP200/120…
Smokes 20 per day Mother
Has IHD (MI x 4)
 NGH? MI”
18.	As he explained in his evidence, he was concerned by the need for a home visit, her BP was abnormal, she was sweaty and clammy (which might be significant) and he recorded the risk factors (associated with IHD) as set out in the notes.  In the event, Mrs. Mellor was discharged the next day by the hospital, on the ground that her symptoms were atypical and there was no sign of MI;   a letter from the hospital to Dr. Groves, dated 23rd March, 1988, records the diagnosis as “Nonspecific chest pain”. 
19.	Subsequently, Dr. Groves saw Mrs. Mellor on a number of occasions.  There were recurrent BP problems and difficulties counteracting it, given that Mrs. Mellor had significant problems with Beta Blockers. On the 5th October, 1989, Dr. Groves noted that he had impressed on Mrs. Mellor the need to avoid MI and strokes.    Later notes are to like effect and record “poor compliance” by Mrs. Mellor in taking the prescribed medication.  I should make it clear that Mrs. Mellor was plainly concerned about side effects; there was no suggestion that “poor compliance” was wilful or casual.   
20.	Dr. Groves’ notes for the 13th September, 1991 gave rise to controversy.   The note for that day records that Mrs. Mellor had stopped taking her BP tablets. A side note, which then “loops” around and under an entry for the 25th September – which simply recorded that Mrs. Mellor “DNA” (did not attend) a consultation for that day – states “discussed high risk BP including stroke and heart …”.  The next note recorded that a letter was sent by the practice to Mrs. Mellor on the 30th September, 1991 concerning her DNA and her high BP.   
21.	Mr. Gardner explored this topic in cross-examination.  He put to Dr. Groves that he had felt vulnerable at a later stage and therefore felt the need to add the note.  Mr. Gardner indicated that he could not say when the note was added and drew back from suggesting that it was added after Mrs. Mellor’s death, accepting (rightly) that he would need a proper basis before advancing any such allegation.  It emerged in Dr. Groves’ evidence that he did not know of any allegation against him until 2001, after he had ceased practising as a GP. Moreover, as Dr. Richards explained, after Mrs. Mellor’s death, her records had been transferred to the health authority.  For the avoidance of any doubt, I should make it plain that I regard any suggestion that Dr. Groves altered the notes after Mrs. Mellor’s death as wholly unfounded.   As to some later alteration but before Mrs. Mellor’s death, I regard this as implausible; no good reason appears as to why, between 1993 and 1998, Dr. Groves should have thought more of his involvement with Mrs. Mellor; certainly Mr. Gardner had no persuasive suggestion to offer in this regard. While the non-contemporaneous alteration of these notes inevitably gives rise to curiosity, I regard Dr. Groves’ explanation as the most likely; there was nothing sinister about the alteration and he made it in the context of the sending of the letter of the 30th September, 1991, while the discussion with Mrs. Mellor remained fresh in his memory.   
22.	So far as the case against Dr. Groves is concerned, the key consultation was that held on the 9th January, 1992.  It is, indeed, the only consultation in respect of which a complaint is pursued against Dr. Groves.  His notes of that consultation read as follows:
“ Not sleeping
Flu 6-7 weeks  [= no] cough chest pain
And arm pain
SOB (short of breath) chest 
BP 184/102
Atenelol 50 mg
Migraleve duo
Amoxycillin 250 mg tds
REQ sleeping tabs temazepam 10 mg 1/12”
23.	Unsurprisingly, at this distance in time, Dr. Groves does not remember the 9th January, 1992 consultation.  Working from his notes, the consultation appears to have been complicated. Note taking was difficult.  For instance, there was no note as to headaches but migraleve (for headaches) was prescribed. The primary presenting symptoms were not sleeping and flu.  Dr. Groves remains puzzled and unsure about the entry “ cough chest pain and arm pain”. He is not sure whether that meant (1) no cough but chest pain and arm pain; or (2) no cough and no chest pain and arm pain. In his first witness statement he tended to think that (1) was the right interpretation. However, his doubts even led him to produce a second witness statement in which he canvassed the interpretation in (2).  In his oral evidence, he said that he remained unsure but on balance he preferred interpretation (1). 
24.	Dr. Groves did not think that Mrs. Mellor was or might be suffering from angina.  This was very different from 1988.  Then she had been clammy; here the chest complaint appeared secondary.  If he had thought there was a real risk of angina, he would have thought of trying a GTN spray (i.e., a Glyceryl Trinitrate spray used to ease the pain of angina) and discussing a referral. 
25.	At the outset in cross-examination, Dr. Groves agreed to a number of principles or parameters applicable to his approach as a GP:
i)	The duty of the GP was to find out what is or maybe wrong with the patient and, if potentially serious, to refer. The GP’s task  was to recognise the small percentage of cases where the patient may be seriously ill;  in performing that task, the GP should consider symptoms described by the patient and information given by the patient as to history and lifestyle.
ii)	The most common killer in the United Kingdom was CHD.
iii)	Often, CHD was present but without physical symptoms.
iv)	The history could mean an increased risk of CHD; where even one of the patient’s mother, father or sister had suffered from IHD, that was significant; here, where all three had suffered, the history was as significant as a history could get.
v)	Long-standing high BP and smoking would involve an increased risk of IHD; raised cholesterol levels were not to be ignored – though less was known in 1992 than now as to cholesterol as a risk factor.
vi)	All these risk factors could be present in young women – though the risk of IHD was lower in young women.
vii)	A combination of the presence of these risk factors and chest pain (“CP”) means that CHD should be considered as a differential diagnosis, because it could evidence angina and stenosis with the risk of  heart attack and sudden death.
viii)	A GP would try and spot if a chest pain was angina – in order to treat it the earliest opportunity.
ix)	All the above risks of IHD were to be kept in mind even if the patient presented prioritising other matters; it was also to be kept in mind that some patients were more or less intelligent than others and might be poor historians.  The patient cannot be relied on to volunteer everything.   
x)	The GP should record the answers given by the patient to the GP’s questions so as to build up the information available on the patient’s history.
26.	Susan Mellor, said Dr. Groves, was astute and knew her own mind. They had discussed and she was aware of BP and heart disease.
27.	As to the 9th January 1992 consultation, Dr. Groves was convinced that he must have asked about the chest pain; but he made no record of any such queries. He was aware of the risks affecting Mrs. Mellor and so was she. He was convinced they would not have gone through the consultation without excluding IHD and angina (though CHD cannot be excluded by excluding angina). He cannot believe he would not have asked questions designed to exclude these.   Mr. Gardner put it this way: three of the four classic symptoms of angina were present;  chest pain, radiating to the arm and shortage of breath (“SOB”);  if considering CHD and seeking to exclude angina, it was, he suggested “essential” to know how the pain felt, its duration and its relationship with exertion. While maintaining that SOB was not typical, Dr. Groves accepted that he should have asked such questions (to exclude IHD and angina) but believes that he did ask; the difficulty, which he further accepted, was that there was no note or record to that effect. If he did not ask, he accepts that it was a failure on his part which should not have occurred.  It was not, however, always possible to write everything down. Nor could he help on what Mrs. Mellor had said to rule out IHD. He agreed that there were, accordingly, no notes on a vital decision, on what questions had been asked and as to what answers were given.
28.	Asked about his referral (in fact, a hospital admission) in 1988, he agreed that his decision had a “low threshold”.  A number of GPs would not have admitted. He took no chances on that occasion.  He was influenced by the need for a home visit and her being sweaty.
29.	Dr. Groves denied that his second witness statement was a “sign of desperation”.  His conscience is and always has been clear. It was some ten years after the relevant consultation before he was told of the allegations against him.
30.	Re-examined by Mr. Hugh-Jones (representing both Dr. Groves and Dr. Richards), Dr. Groves underlined that in his notes of the 9th January, 1992 consultation, he did not write that Mrs. Mellor’s pain had radiated to her arms.  Had Mrs. Mellor then been suffering from angina, it was more likely that the pain would have radiated.
31.	As to why he had reacted differently in 1988 and 1992, essentially Dr. Groves said that in 1988 he suspected a possible MI (heart attack); by contrast, in 1992, he did not think that Mrs. Mellor was or might be suffering from angina. This was a patient who often had flu (or flu like ailments). The symptoms in 1992 were not typically suggestive of angina; instead, they were suggestive of a viral illness. Had he been concerned, however, he would have referred in 1992 as he had done in 1988.  
32.	On the assumption that he had referred in 1992 and on the basis of his understanding of the practice at the hospital, he was in any event unsure whether an ETT would have been given to Mrs. Mellor, by reason of her presenting with atypical features for angina.
33.	(3) Dr. Richards: Dr. Richards qualified in medicine in 1986; she became a GP at the (Crystal Peaks) practice in 1992 and remained there until 2001 when she moved away from the area.   She saw Mrs. Mellor between 1993 and her death on more than 90 occasions.  She had not “taken over” the care of Mrs. Mellor; it had been Mrs. Mellor’s choice to come to her, perhaps because they got on well.  Before turning to the detail of the consultations, it is convenient to record Dr. Richards’ evidence as to her general approach.
34.	General approach: In general terms, Dr. Richards indicated that relevant inquiries as to the risk of angina would include these.  First the location of the pain; central chest pain could be indicative of angina, the more so if it radiated to the shoulders, the left shoulder being more likely than the right. Secondly, the character of the pain; burning pain would not be associated with angina; pressure would be more suggestive of angina.  Thirdly, the duration of the pain; a few seconds meant that angina was unlikely; a few minutes was a different matter.  Fourthly, was the pain exacerbated by exertion (exercise) or emotion? Was it relieved by rest (stopping what the patient had been doing) or by the use of a GTN spray under the tongue?  If the answers to these questions were yes, then they were or could be suggestive of angina.
35.	In response to Mr. Gardner, Dr. Richards agreed with the following:  (1) It was the GP’s task to find out what was wrong or maybe wrong with a patient; (2)  If the matter was serious or potentially serious, a GP could and did refer;   (3) The GP would try and spot the few patients with serious conditions; (4) IHD was something to look out for, not least having regard to the patient’s history; (5) Patients could suffer from concurrent complaints; it was important to guard against some of those complaints masking others;  (6) Women more often presented atypically;  (7) Given the grave results which may occur if angina was not treated, it was right to rule it out rather than in; (8) A risk/benefit analysis was an essential consideration;  the benefit of a referral might be the saving of life; the risks of a referral were nil.  In re-examination, Dr. Richards underlined that, most of the time, a GP did not reach a concluded diagnosis.
36.	Explaining her criteria for referral, Dr. Richards put it this way: she would refer if she thought that there was a possibility that notwithstanding atypical symptoms, the patient may have angina.   With regard to Mrs. Mellor she took into account that (1) women may have atypical symptoms  (2) Mrs. Mellor had a tendency to tell Dr. Richards what she wanted Dr. Richards to know; (3) the risk factors, including family history and smoking.  Dr. Richards would not refer on the basis of risk factors alone; she would refer when suspicious of symptoms, taking into account the risk factors.  With reference to a chart, “Risk of Coronary Heart Disease”, used by GPs in the 1990s and introduced into evidence by Dr. West (“the chart”, of which more later),  Dr. Richards said that, in percentage terms, Mrs. Mellor was throughout in the low or mild category of CHD risk. 
37.	Lastly in this immediate context, Dr. Richards explained that time could be used as a factor in making a differential diagnosis.  It would be helpful to monitor a patient over a period of time, in order to form a view as to the possible true nature of the patient’s complaint.
38.	The consultations: Dr. Richards first saw Mrs. Mellor on the 8th February, 1993.  Clearly, a detailed examination was undertaken.  Her notes record Mrs. Mellor telling her that she had had flu for some two weeks and was feeling tired and run down. She spoke of chest pain, front and back. It lasted a few seconds, several times a day but there was no tightness.  Dr. Richards’ assessment was that Mrs. Mellor was suffering from a viral illness. She excluded angina, because of the duration of the chest pain (a few seconds) and the fact that there was not tightness.
39.	On the 16th February, 1993, Dr. Richards saw Mrs. Mellor again.  On this occasion, Mrs. Mellor spoke of a pain in the back which felt “like a foot in back of chest”.  It was worse on “inspiration”.  The notes go on to record that Mrs. Mellor felt “SOBOE [i.e. short of breath on exertion] + hot + cold”.   On the basis of all the material available to her, Dr. Richards was satisfied that here the chest complaint was attributable to chest infection – and no criticism is advanced in respect of this consultation.
40.	Over a series of many consultations in 1993, a picture emerges of the unfortunate Mrs. Mellor’s non-cardiac related complaints.  These included: 
i)	Viral (flu like) problems; indeed for much of 1993, if on an intermittent basis, Mrs. Mellor was suffering from what she described as “flu”;
ii)	Neurological problems;
iii)	Stomach or gastric concerns, covering indigestion, reflux and the like; reflux, it may be noted, was capable of giving rise to chest pains;
iv)	Anaemia.
In short and in answer to Mr. Holl-Allen, Dr. Richards said that Mrs. Mellor’s attended her GP considerably more frequently than was to be expected from a person of her age and sex.  Mrs. Mellor suffered from a number of separate pathologies – several of which were significant.
41.	Pausing there, when Dr. Richards began to treat Mrs. Mellor, she had read Dr. Groves’ notes. She picked up that Mrs. Mellor was a smoker and that her family history was significant.  In dealing with Mrs. Mellor, IHD was always in the back of her mind but from explanations given by Mrs. Mellor she was satisfied that Mrs. Mellor’s problems did not include IHD.
42.	April 1994:  I come now to the first time period, in respect of which criticism is made of Dr. Richards, namely, April 1994.   I start with the 19th April, 1994, though no criticism is made of this particular consultation. On this occasion, Mrs. Mellor was complaining of feeling “flu-like” with  tenderness in the front of the chest.  Dr. Richards did not suspect angina.  She was in any event seeing Mrs. Mellor regularly with regard to BP problems after her subarachnoid haemorrhage operation.
43.	The first consultation of which specific criticism is made was that on the 22nd April, 1994.  This was a home visit by Dr. Richards.  Her notes include the following:
“ Felt a lot better yesterday 
Today feels unwell
burning pain  across chest and pressure on
chest comes and goes 
There a few min 
Also intermittent pain
at different points along 
arms  º cough º sputum
Been hot. Nausea. Vomited 
yesterday not today Headaches
OK today …
Tender across chest anteriorly 
on pressing ….
Abdo[men] soft some mild epigastric
discomfort …
Shunt not inflamed …
Chest pain not ischaemic
Not on exertion but describes 
as pressure for GTN trial …”
44.	Dr. Richards’ view was that a number of symptoms here were not suggestive of angina, or were atypical of it; these were the burning nature of the pain, the fact that it was intermittent or came and went and the fact that pain was felt at different points along the arms.  Moreover, the tenderness on the chest was inconsistent with angina and the discomfort in the abdomen region made her think of indigestion rather than a cardiac related pain. Still further, it was not suggested that the chest pressure was related to exercise or exertion; if anything, the notes suggest the contrary. Conversely, Dr. Richards thought it right to stop and think given the reference by Mrs. Mellor to “pressure”.  Bearing in mind the risk of women presenting with atypical angina pains, Dr. Richards took the view that a GTN trial should be undertaken;  if the GTN spray “worked” in the sense of relieving the pain, that would point to angina; if it did not, then angina would be negatived or unlikely.  
45.	Cross-examined by Mr. Gardner, Dr. Richards accepted that relief from the GTN spray could be highly significant.    However, any such information should not be considered in isolation, all the more so when the GTN spray was used as a trial.  Dr. Richards wanted more information before making a referral.   She was uneasy because of the reference to pressure and arranged to see her the next day. Dr. Richards thought that the symptoms were atypical of angina and she did not think Mrs. Mellor did have angina or that the problem was IHD; but Dr. Richards was trying to see whether it could possibly have been angina – hence she had given Mrs. Mellor the spray as a trial. While there was no risk in a referral, she would not refer every patient simply on the basis of having prescribed a chest spray. In not referring Mrs. Mellor at this stage, Dr. Richards did not think she was taking unnecessary risks.
46.	On the next day, the 23rd April, 1994, Dr. Richards made another home visit.  Mrs. Mellor felt a lot better. The chest pain had settled; she had not needed the spray.  Dr. Richards recognised that these were early days but she felt reassured.  Mrs. Mellor was in any event to see her in the surgery the next week. 
47.	On the 28th April, 1994, the next consultation of which specific criticism is made, Mrs. Mellor attended at the surgery.  Dr. Richards’ notes include the following:
“ Still under weather
Better than ….23rd…
Headache today started lunchtime …
shunt not tender …
chest ok used GTN spray 1 x 
Monday 25th Not since ”
The notes did not record whether the spray had “worked”;  In her evidence, Dr. Richards said that she presumed it had not worked; had the spray worked she would not have ignored it. Asked whether Mrs. Mellor had mentioned using her mother’s spray, Dr. Richards was strongly of the view that Mrs. Mellor had not said so; Dr. Richards would “definitely” have recorded that if Mrs. Mellor had said anything of the sort.
48.	Cross-examined by Mr. Gardner, Dr. Richards said that a single use of the spray did not mean that Mrs. Mellor was suffering from angina. She did not think that Mrs. Mellor did have angina. One episode of using the GTN spray had not provided sufficient information to refer.  Dr. Richards was convinced that she had told Mrs. Mellor to monitor whether the spray worked for pain – even though this was not recorded. 
49.	November 1995: Coming next to the 3rd November, 1995, another consultation in respect of which specific criticism is advanced, Mrs. Mellor was again feeling run down; she had various complaints; she was to see the neurosurgeons; she had cold sores; Dr. Richards suspected anaemia. Dr. Richards took the opportunity to arrange for blood tests to be done.   Of direct relevance here, the notes record the following:
“ … used GTN Sat night for pain
Chest settled”
Dr. Richards took the view that nothing much could be deduced from one use of the spray; it had to have been the same spray as Dr. Richards had prescribed back in April 1994, some 18 months previously.   If the spray had not been used over that 18 month period, then this was a new presentation.
50.	Dr. Richards accepted in cross-examination that she had not recorded the location, nature and duration of the pain; she presumed that she had not done so because she did not think it was significant.  She did not act on the fact of the use of the GTN spray, because she did not regard one use of the spray over an 18 month period as significant.  There was not enough there to refer;  thousands of patients have chest pain; doctors cannot refer them all. 
51.	Dr. Richards was firmly of the view that if the spray had been used over this 18 month period, Mrs. Mellor would have reported it and she would have recorded it.  She said that she asked Mrs. Mellor to tell her (Dr. Richards) if she had used the spray. She could not say, however, that she asked on every occasion.   A “negative” (i.e. non-use of the spray) did not necessitate recording. Dr. Richards regarded it as very unlikely that Mrs. Mellor had simply continued to use the spray over 18 months.  With regard to 1994/ 1995, she would have been surprised if Mrs. Mellor had used the spray without telling her, albeit that she accepted that such may have been the case in 1997, after the reassurance given by Dr. West (see below).  In her mind, the outcome of the trial was that the GTN spray had not been used.  If Mrs. Mellor had suffered from angina, the fact that she had used the spray once over 18 months was very surprising. Therefore the absence of reported use was reassuring. 
52.	In re-examination by Mr. Hugh-Jones, Dr. Richards emphasised Mrs. Mellor’s haemoglobin reading of 8.5 in November 1995.  That reading, suggestive of an iron deficiency and anaemia, was “pretty worrying”.  It could not be left and was, at the time, of more concern than possible angina.  A referral was indeed made to an appropriate specialist for this matter to be attended to. 
53.	March 1996: On the 15th March, 1996, Dr. Richards saw Mrs. Mellor again.  She reported chest pains but these appeared atypical. 
54.	On the 29th March, 1996, the last of the consultations forming the subject of criticism, Mrs. Mellor again had a number of other complaints; it was noted that she was due to have a hospital appointment for gastric matters in a few weeks and she had suffered from diarrhoea and vomiting.   Importantly, however, the notes also record this:
“Used spray 2 x
Took discomfort away
Lasted few secs to min only
Therefore use spray PRN + monitor
only gets discomfort on exertion not at rest…
See 3/52 [i.e. in 3 weeks]”
On the one hand, the fact that the pain lasted only for a few seconds was atypical of stable angina.  Conversely, the reference to discomfort on exertion and the fact that the spray had been used twice, were of concern.  The spray had, however, only been used twice. Dr. Richards decided not to refer. She wanted more information. She was due to see Mrs. Mellor in three weeks anyway.
55.	Cross-examined by Mr. Gardner, Dr. Richards said that she did not refer because the spray had simply been used twice and the pain had lasted a few seconds only.  In any event, she had made arrangements for Mrs. Mellor to return within 3 weeks.  Although this was the first time that the word “monitor” appeared in her notes, it was her practice to say that to a patient such as Mrs. Mellor.
56.	Mr. Gardner made it plain that the 29th March, 1996 was being investigated not because of any causative impact of a failure to refer on that occasion (it was rightly not suggested that there was) but to explore the threshold applied by Dr. Richards before making a referral; it was suggested that Dr. Richards was applying the wrong test and had only referred Mrs. Mellor when satisfied that she had angina. Dr. Richards insisted that she would refer when suspicious rather than when satisfied of angina;  in this regard, she relied on the terms of her letter of referral to Dr. West (see below).
57.	April 1996 and the referral letter: On the 19th April, 1996, Mrs. Mellor cancelled the appointment which had been arranged.
58.	On the 23rd April, 1996, Dr. Richards saw Mrs. Mellor.  On this occasion, she decided that it was appropriate to refer Mrs. Mellor to see Dr. West.  The notes read as follows:
“ Using spray  - 10 x since last seen but for sharp pain in chest
Not ischaemic in nature 
Suggest refer Dr West for assessment 
? exercise ECG”
Dr. Richards felt that the threshold for a referral had been crossed. The spray had been used on a significant number of occasions.  She was suspicious that this may be an atypical presentation of angina.  
59.	By letter dated the 29th April, 1996 (“the referral letter”), Dr. Richards made a referral to Dr. West, Consultant Cardiologist at the Royal Hallamshire Hospital, Sheffield.  The referral letter included the following:
“ I would be grateful if you would see this 42 year old lady who I am finding difficult to assess. She has been hypertensive following her first pregnancy in 1976 and she had a subarachnoid haemorrhage ….in 1993.
She has a strong family history of ischaemic heart disease and I suspect that Susan herself may have angina.  She was initially given a GTN spray in April 1994 for chest pain which did not sound like typical angina. She said she had a burning pain across the chest but she also described it as a pressure which came and went, she said it was there for a few minutes at a time and was not related to anything…. She was given a trial of a GTN and on looking through her notes she has used it occasionally since then for chest pain but never on a regular basis. However, when I saw her recently she said she had pain again in her chest and again it was only a short lasting pain for a few seconds to a few minutes, but she had used her spray and she said it took the discomfort away. On questioning she said she only got the discomfort on exertion…..”
60.	Subsequent to the referral letter: In answer to Mr. Holl-Allen, Dr. Richards said that as of September 1996, Mrs. Mellor’s predominant complaint was of headaches.  As already foreshadowed, she underwent a neurosurgical procedure for shunt revision.  There was no record of chest pain in 1997; had it been mentioned, it would have been recorded.  That said, Mrs. Mellor was reticent in reporting problems, in that she knew that Dr. Richards would be likely to act on those she reported.
61.	Asked by Mr. Gardner, what she would have done had she received an equivocal letter from Dr. West, she said that cardiologists did not send equivocal letters; their letters said “yes” or “no”.  Dr. West’s letter of 13th January, 1997, discharging Mrs. Mellor, had been conclusive at that stage and reassuring. 
62.	When she heard of Mrs. Mellor’s death, she was concerned that Mrs. Mellor might have died from colonic cancer.   She did not think then that CHD might have been the cause.
63.	(4) Dr. West:   He is a consultant cardiologist at the Royal Hallamshire Hospital, Sheffield. He was appointed a consultant in 1994 and was seen in that capacity by Mrs. Mellor in 1996.   There were, at the time, two consultant cardiologists at that hospital.   
64.	As to the referral letter, Dr. West knew the (Crystal Peaks) practice well. He read the symptoms as being fairly long-standing and stable. Had the practice wanted urgency, they would have said so.  
65.	On the 4th July, 1996, Mrs. Mellor was seen at the hospital by Dr. Yellop, the SHO, then undertaking six months full-time cardiology. Although Dr. West did not recall any consultations with Mrs. Mellor, he described his practice at the time as follows. New patients would be seen by the SHO, who would take a full history and examine the patient. Thereafter, the SHO would go into his (adjoining) consulting room and discuss the case with him.  He would then go back with the SHO, introduce himself to the patient and discuss the planned treatment.
66.	Dr. Yellop’s notes record the following.  Mrs. Mellor was complaining of chest pain. She spoke of 6 months of intermittent chest pain, currently some three times per week. The duration of the pain was a number of seconds. It was unpredictable. It occurred mainly in bed at night and also with exertion when going up stairs. As to the location of the pain, there was central chest discomfort and it radiated into the back and right shoulder.  The notes listed the various drugs Mrs. Mellor was taking. The risk factors associated with IHD (already set out) were recorded, as was a discussion with Dr. West, leading to a decision to conduct an ETT.  A diagram was drawn showing “epigastric discomfort” in an abdominal area contiguous with the chest. The notes remarked that the risk factors were “++” but that the history was “atypical”. Cholesterol levels were to be checked.
67.	As to Dr. Yellop’s notes, Dr. West made a number of observations:
i)	The notation “risk factors ++” recognised Mrs. Mellor’s high blood pressure, heavy lifelong cigarette smoking and family history. Against that, basing himself on the chart, there was a low absolute risk of MI, even allowing for these risk factors.  
ii)	The reference to “atypical history” reflects the fact that a diagnosis of angina is essentially a clinical diagnosis based on information supplied by the patient.  Typically, the pain in the chest will radiate to the back and arms, it will be related to exertion and it will be relieved in minutes. That which Mrs. Mellor described and which is recorded in Dr. Yellop’s notes was atypical of angina; this was not a clinical history of angina.   The duration of the pain was in seconds and it was unpredictable. 
iii)	On this occasion, the ECG was normal; there was no electronic evidence of thickening (i.e., LVH). With a normal ECG and atypical history, the best way of clarifying the position was by way of an ETT.  Hence the decision to undertake an ETT.
iv)	As to the “epigastric discomfort”, this was an important sign. The site of the pain was contiguous with the chest; palpation of the stomach resulted in pain.  This was neutral with regard to angina but raised other concerns. Indeed Mrs. Mellor had a long history of non-cardiac pathology. 
v)	As recorded in the notes, Mrs. Mellor was, at the time, taking a “battery” of drugs, intended to combat high BP, heavy periods and acid reflux; she was also taking night-time tranquilisers. 
68.	On the 4th July, 1996, Dr. Yellop wrote to Dr. Richards.  The letter summarised her notes (set out above) and concluded in the following terms:
“ I have discussed her case with Dr. West. She obviously has strong factors for ischaemic heart disease in that she is a smoker, she has a strong family history of heart disease and she is hypertensive [high blood pressure]. However, we thought her history was atypical. We have ordered her an exercise tolerance test and checked some routine bloods including a lipid screen [cholesterol]. She will be reviewed with the results of these tests.”
69.	On the 2nd August 1996, Dr. Yellop wrote again to Dr. Richards.  Blood tests had, inter alia, revealed that cholesterol was raised at 6.4
“…and may require treatment if we find she has a positive exercise test. We have also found her to be anaemic with an iron deficiency picture. Her Hb is 10.2…”
 
70.	In simple terms, the ETT involves the patient working “against” a treadmill. At the lowest stage, the treadmill is set at a speed of 1.7 mph, with an elevation of 5.  The speeds and elevation are then increased, up to a maximum, at the highest stage, of 6 mph, at an elevation of 22. Again simply put, the test is designed to produce enough exercise to bring the heart rate up to the maximum predicted rate for the patient in question and then to see what changes there are to the ECG. 
71.	Turning to the ETT, it was carried out by a trained cardiac technician on the 14th August, 1996.  Dr. West was not personally present at the time but would have seen the report either on the next day or within a few days. Mrs. Mellor, at the age of 42, barely completed the lowest stage, having to stop no more than 4 seconds into stage 2. In other words, she could not effectively accomplish more than 1.7 miles in an hour on a 5 slope.  The maximum predicted heart rate for a woman of Mrs. Mellor’s age was 178 but Mrs. Mellor’s heart rate rose only from 95 to 118.  As recorded by the test report dated 14th August, the test had to be terminated after 3.04 minutes because of “Chest pains S.O.B. [shortness of breath]”.   Symptoms during the exercise were recorded as chest pains, S.O.B. and leg pains. No ECG changes were recorded.  On the test report, Dr. West gave the “Conclusion” as “Negative”. 
72.	Dr. West’s evidence was that he drew some comfort from the ETT. An ECG reading was taken before (“resting”), during and after the test. The “resting” ECG was normal; there was no trace of any thickening of the heart muscle  (i.e., LVH).    The ECG during the test showed no significant abnormalities. On the basis of a concern as to IHD, the focus would have been upon the ECG pattern, heart rate (“HR”) and BP.  The rise during the test of  BP (from 146/99 to 165/104) and the rise in HR, suggested good health rather than the reverse; a drop in BP or HR suggests the most risk of coronary heart disease.   Moreover, there was no pattern of ST depression.  Although Mrs. Mellor’s usual symptoms had been reproduced (SOB and chest pains), there was no evidence of IHD.   He was therefore confident she was not suffering from angina.
73.	An appointment was booked for the 30th December, 1996 which Mrs. Mellor did not attend. She was then seen on a routine basis on the 13th January, 1997.  Dr. West’s note of that consultation are, to say the least, exiguous. They say simply this:
“ [ETT] neg[ative] sub-maximal
Imp[ression]: atypical CP [chest pain]”
He said though that his practice was to summarise his thoughts in a contemporaneous letter to the GP (see below).  Dr. West explained why he had recorded the observation “negative sub-maximal”. The reason was that, taken overall, though Mrs. Mellor had reproduced her usual symptoms in the test, she had shown no signs of IHD. Therefore he characterised the test as negative.  There were no ECG changes and neither the BP nor the HR changes were worrying.
74.	He did not think there was any urgency in the matter. Mrs. Mellor’s low exercise tolerance – as shown by the ETT – was explained by co-morbidity, probably anaemia or cigarette smoking.  
75.	This had been an obvious tragedy, involving “sub-clinical” coronary heart disease; all cardiologists live in fear of that.   Other features of the history had included a life threatening cerebral haemorrhage, indigestion and pathological anaemia.  Moreover, there were concerns about cancer of the stomach or the gastric tract – these (as his letter to the GP made clear) were to be investigated by others.  “Taken in its entirety”, on death there was material which led to a suspicion that she had been suffering from sub-clinical coronary artery disease all along. 
76.	With regard to the consultation of the 13th January, 1997, it was conducted by him alone.  He did not now recall it but his usual practice was to re-take the history. If anything featured in the history was different from that recorded by Dr. Yellop, he would have recorded it.  In the event, on the 13th January, 1997, Dr. West wrote to Dr. Richards in the following terms (“the 13th January letter”):
“ …[Mrs. Mellor] gave a history of rather atypical chest pain. I think she can be reassured that this is not cardiac in nature. 
She does, however, have a collection of cardiovascular risk factors and I have reiterated the importance of stopping smoking.
I think her …[shortness of breath] … can be attributed to the recurrent iron deficiency anaemia which is being separately investigated…
Her recent treadmill exercise test was negative and there were no significant ST segment changes during her normal symptoms.”
77.	Dr. West did not accept that he had said at the consultation on the 13th January (or in his letter to the GP) that there was nothing to worry about. The second paragraph of the 13th January letter had dealt expressly with risk factors. 
78.	Staying with the 13th January letter, the statement that Mrs. Mellor’s chest pain was “not cardiac in nature” reflected the fact that Dr. West thought it appropriate to give reassurance.   In his judgment, the pain did not fit the clinical picture of angina.   He disagreed that it would be appropriate to make the jump from a negative (or even equivocal) ETT to angiography.  Certainly at the time, it was wrong to portray angiography as having all gain and no risk.  The statistics showed the risk of a fatal heart attack or stroke to be 1/1000 and the risk of very distressing vascular complication to be 1/100.  Every year, Dr. West and his colleagues see something like 1000 patients; over 10 years, if they had carried out angiography on each one, statistically they would have been likely to have caused 10 unnecessary deaths and 100 vascular complications.   In his opinion, coronary angiography was not justified here, given the risks.
79.	Had he thought it necessary to undertake further investigations, he would have conducted a thallium scan, involving the insertion of a radioactive tracer in a vein (not in an artery).  This was a non-invasive way of obtaining more specific information than could be obtained from an ETT.  If the findings of such a scan showed multiple defects throughout the heart muscle, that would have shown a patient most at risk – and therefore a situation likely to lead him to proceed to angiography.   If he decided on angiography, he would have done it – but at the Northern General hospital rather than the Royal Hallamshire.  For urgent angiography, he would have needed to see characteristic angina symptoms, profound BP/HR/ECG changes on the ETT and large deficits on the thallium scan.  As to then proceeding to angioplasty, he would not have been in favour of treatment on the same day; such an approach would negate informed consent.  The degree of stenosis would in any event have to be such as to justify proceeding to angioplasty, despite the risks in that procedure.  Something like 90% stenosis would have been needed; if less, he would favour secondary intervention aimed at stopping smoking and reducing cholesterol.  For urgent angioplasty, the patient would have had to be an in-patient on a cardiac ward, in severe pain not settled by intra-venous medication and facing a threatened heart attack.  There was in any event no evidence of which Dr. West was aware that angioplasty improved the patient’s prognosis. 
80.	Cross-examined by Mr. Hugh-Jones,  Dr. West said that the referral letter was, qualitatively, “well above average”.   Dr. West thought that reflux was very important – it causes pain in the chest and is difficult to distinguish from coronary related chest pains.  Dr. Yellop in her 4th July notes had made no mention of the GTN spray; this was because the spray was too non-specific to be useful in the exercise of diagnosis. Further, Mrs. Mellor had not exhibited classical angina.
81.	Reverting to various features of Dr. Richards’ notes of April 1994, the “burning”, the pressure coming and going and the intermittent nature of the pain were all atypical. Throughout, the shunt problems were important. Overall, the symptoms in 1994 were even more atypical of angina than those manifesting themselves in 1996;  that said, Dr. West was adamant that the symptoms in 1996 were not typical.   Dr. West could not say what would have happened had he received a referral letter couched in the language of Dr. Richards’ notes of April 1994.   Had Mrs. Mellor been referred following a consultation with Dr. Richards on the 29th March, 1996 (i.e., about one month earlier than she was referred) he very much doubted that it would have made any difference. 
82.	Cross-examined by Mr. Gardner, Dr. West clarified that if angiography had been decided upon, he would himself have performed it but at the Northern General hospital, rather than the Royal Hallamshire; if an angioplasty had been called for, he would not have undertaken it but would instead have referred it to an appropriate specialist at the Northern General hospital. 
83.	In 1997, he had done some 150 angiograms; of that number, about 30% had led on to angioplasty.  As to thallium scans, some 5 per week were undertaken throughout the year at the Royal Hallamshire.
84.	Dr. West was cross-examined on some medical literature available in 1997. First, “Effective Health Care” of October 1997, an NHS Bulletin. Secondly, “Management of stable angina pectoris”, recommendations of the Task Force of the European Society of Cardiology, European Heart Journal (1997). In summary:
i)	Dr. West accepted that coronary heart disease (“CHD”), i.e. narrowing of the coronary arteries, is the leading cause of death in the United Kingdom.  Accordingly, those with angina were an important group to target. However, as he pointed out, the same literature, while noting that angioplasty can improve relief in some patients, contained the observation that “it has not been shown to improve survival”.
ii)	Dr. West accepted that angina may be under-diagnosed in young women and symptoms of chest pain in this category were “often atypical”.  That he appreciated in 1996; he would nonetheless have expected to find one or two major characteristics.
iii)	Against this background, Dr. West accepted that atypical chest pains might be angina based, though ultimately the patient might or might not suffer from angina. 
iv)	 Dr. West further accepted that with proper management the symptoms of angina could usually be controlled and the prognosis substantially improved.  He pointed however to the same literature observing that an “initial non-invasive strategy …[was] .. appropriate for most patients.”
v)	Dr. West agreed that “suspected” angina patients should receive prompt and appropriate cardiological investigation, within the constraints of the NHS.  It may be noted that the recommendation in question calls for “As a minimum, each patient should have a carefully taken history and physical examination, an assessment of risk factors and a resting electrocardiogram”. 
vi)	When the “diagnosis remains uncertain or functional assessment is inadequate, especially when there are electrocardiographic features which are difficult or impossible to interpret”, Dr. West agreed that alternative investigations were needed; but that was not this case; there was no difficulty here in interpreting the ECG.
vii)	He accepted that an invasive strategy could be justified if angina was suspected, even though it was ultimately established that the patient did not suffer from angina; Dr. West, however, underlined throughout the risks involved in angiography. 
85.	Returning to the referral letter, Dr. West knew well that there would have been no reference from that practice unless the GP needed assistance and that Mrs. Mellor had been referred to him because the practice had suspected angina. He underlined the atypical features described in the referral letter; the burning pain, the fact that it came and went and that the pain was unrelated to exercise. He could not, however, exclude angina on the symptoms described in the letter.   The GTN spray did not assist one way or another. The reference to exertion was very suspicious but that was not the history he had been given when Mrs. Mellor attended at the hospital (see Dr. Yellop’s notes).  The referral letter would be taken into account and would be the prompt; the history upon which he would ultimately rely would be that taken by the SHO from the patient.  In effect, his judgment was based on the patient in front of him.
86.	As to the 4th July consultation, there would have been no examination by him. It was a matter of interpreting the patient’s history. He accepted that the only noted record of his involvement was the discussion referred to by Dr. Yellop.  He accepted that the history as taken by Dr. Yellop, though atypical, could not exclude angina. Family history gave rise to a significant risk factor – though Dr. West was adamant that it was no more or less of a risk factor than cigarette smoking.  The notation “++” indicated the presence of significant risk factors. Therefore, the decision was taken to conduct an ETT and a cholesterol check.  The letter written by Dr. Yellop to Dr. Richards, on the 4th July, 1996, had been written by her on his behalf.
87.	The letter writtten by Dr. Yellop to Dr. Richards on the 2nd August, 1996, confirmed the discovery of raised cholesterol levels; that was to be taken into account though it did not necessarily increase the risk. He later remarked that this was not far above the average.  He regarded the figure of 10.2 for Hb, however, as “pathological” and an abnormality, albeit within the normal range.
88.	Cross-examined at some length on the ETT, Dr. West’s answers can be shortly summarised:
i)	He accepted that the HR had not gone up to the maximum required when seeking to carry out the test.
ii)	However, the symptoms of Mrs. Mellor’s chest pains had been reproduced at less than the maximum heart rate with no objective evidence of ischaemia.  Moreover, although the fact of no ECG changes could be attributed to the test not being effective, the fact that there were no changes within the 3 minutes and 4 seconds for which the test lasted “excluded ischaemia of the type which benefits from revascularisation”. 
iii)	The test had been stopped at the lowest level (or 4 seconds thereafter) because Mrs. Mellor had been unable to keep up. A lot of patients, especially women, found the mechanics of the treadmill difficult.  But the essence of the matter was that the stopping of the test did not surprise him in the light of Mrs. Mellor’s “clinical condition”.
iv)	The explanation for Mrs. Mellor’s chest pains was reflux; cigarettes and anaemia explained the SOB.
v)	The characterisation of the test was best expressed, as in his note but not in the 13th January letter, as “negative sub-maximal”, not simply “negative”.   With hindsight and with the classifications now in use, he would characterise the test as “equivocal”. 
89.	Turning to the 13th January letter, it was put to him that there was nothing to alert the GP to the fact that the test had to be stopped. He disputed this, pointing to the second paragraph of the letter as listing the risk factors and also to the referral of the anaemia and abdominal pain to others.   He was convinced that the cause of nausea and ongoing sickness was a hiatus hernia.   He accepted that the letter did not alert the GP to the equivocal nature of the test and Mrs. Mellor’s exercise intolerance.  He accepted that of course angina could co-exist with other health difficulties but stressed the nightmare of “sub-clinical” coronary disease.    He emphasised that Mrs. Mellor had not given a clinical history of angina. Indeed, he remains of the view (I think) that she never did have angina; certainly at the time, he was more concerned about possible abdominal disease.  He could not be certain that Mrs. Mellor did not have CHD – but he was of the opinion that she did not have CHD which could benefit from revascularisation.
90.	He accepted that in 1996 an angiogram could determine whether or not Mrs. Mellor had CHD.  He had not proceeded to undertake angiography as he was satisfied that her problems were not cardiac; he also took into account the risks in angiography.  A jump to angiography could not be justified simply on the basis of a negative ETT.  He accepted that the assessment of risk and the decision to be taken in the light of that had not been put to Mrs. Mellor.  But he was adamant that had his diagnosis been different, he would have opted for a thallium scan not angiography, applying the principle that the physician should do no harm.   He had reassured the GP and Mrs. Mellor because he had concluded that her problems were not cardiac though CHD could not be excluded.   Asked why he did not say instead that he could not be sure and therefore that Mrs. Mellor should be monitored, he said that paragraph 2 of the 13th January letter set out the risks.  It should not be assumed that the GP and other medical practitioners whom Mrs. Mellor was in any event seeing would not re-refer and would not continue to monitor the patient. Allowing for all the risk factors, the chart – as he underlined, in GP use in 1996-1997 - showed that Mrs. Mellor had a 5-10% risk of a coronary event over 10 years, equivalent to a 1% risk per annum; even doubling that risk would produce a risk of no more than 2% per annum.
91.	Dr. West was challenged as to whether in fact he had re-taken Mrs. Mellor’s history on the 13th January and, if so, why it had not been noted. Dr. West maintained the account given in his evidence in chief; namely, that his practice was to re-take the patient’s history but that he probably did not note it because it was not different from that recorded by Dr. Yellop (in the previous July).
92.	In re-examination by Mr. Holl-Allen, Dr. West said that had he proceeded to undertake a thallium scan, he would not have classified it as urgent; Mrs. Mellor’s symptoms suggested a relatively low absolute risk of a coronary event; within its limitations, the outcome of the ETT excluded the need for urgent investigation.
93.	(5) Ms. Woodcock:  Ms. Woodcock was in 1997 the Cardiology Services Manager at the Northern General Hospital.  Her evidence was straightforward and reassuring. Had angiography or angioplasty been urgently required, such treatment would have been promptly accommodated by the hospital.  Interposing, I am bound to say that had Ms. Woodcock’s evidence in this regard been different, then other issues would necessarily have arisen; fortunately, however, that is not this case.
94.	 (6) Mr. Mellor: Mr. Mellor married Mrs. Mellor in 1971; they had a good relationship; she had been a good mother and a “brilliant” wife; he could not have wished for anything more. They were always together. He had been in trouble with the law some years ago; Mrs. Mellor’s influence and strength of character had much to do with him thereafter keeping “straight”.   Neither Mr. nor Mrs. Mellor had worked;  she did the most with regard to running the house and household, arranging holidays, spending money and the like;  he helped when he could.  As to her hospital or medical appointments, with one exception (to which I shall come), he would drive her to the appointments but would not himself come in.
95.	Although, as became apparent, he could not be precise as to dates, he thought he remembered that from about 1994, Mrs. Mellor had used a spray to alleviate pains and tightness in her chest.  It used to help a lot.  She had difficulty walking any distances; what she could do, could be measured in yards.  It was hard for her, as she was very short of breath. She frequently complained of pains in the chest – but nothing seemed to be done; she was given pain killers and anti-biotics.
96.	With regard to the ETT, he took her to the hospital and waited for her; when he saw her, she was very red and out of breath;  she had not completed the test. 
97.	On the occasion when Dr. West discharged Mrs. Mellor (the 13th January, 1997), Mr. Mellor had attended.  He and Mrs. Mellor spent some 5-10 minutes with Dr. West, who had given Mrs. Mellor a clean bill of health.  The ETT had been negative; he did not think that she had a heart problem;  the pain and SOB she encountered had more to do with the tablets she was prescribed by her GP for other matters, her high BP and anaemia. Mr. Mellor had his doubts but Dr. West had convinced him. Mrs. Mellor thought she had been given an “all clear”.  Any pain – and she continued to have pain – was not to do with her heart. 
98.	On the 1st January, 1998, he had been watching television; Mrs. Mellor had gone upstairs to have a bath. Their son Kirk, then aged 11, came running down to say that she was “poorly”.    Her face was red;  she could not breathe; she had been sick;  an ambulance was called; He did not think the problem was related to her heart; he thought it was a problem to do with her head or the tablets she had been taking.  At all events, Mr. Mellor followed the ambulance to hospital.  His expectation was that he would later bring her home.
99.	Shortly after his arrival at the hospital he was seen by medical personnel. They told him that Mrs. Mellor was dead.  He was disbelieving and shocked. He let out a scream.  They asked him if he wanted to see her. He said yes. This proved very distressing. She was in a theatre of sorts.  Her tongue had been out of her mouth and was tied down near her chin. It was not right. A nurse cut the string at his insistence.  He constantly thinks back to that; he cannot get it out of his mind.
100.	He was devastated. He would visit her grave every day, perhaps 2-3 times a day. He wanted to be near to her. He took flowers regularly.  He felt very alone.   His daughter, Kerry Mellor (“Kerry”) came every day and provided “tremendous input”, for both him and Kirk.  She did the cleaning and the cooking.  These were very difficult times for him.  On two occasions he contemplated suicide.  He has had mood swings. He has not looked at the future.  Even now, after six years, his distress has only eased a little.
101.	Cross-examined by Mr. Holl-Allen, he was asked whether, given his perception of Mrs. Mellor’s very bad headaches and other (heart unrelated) medical problems, her ability to carry out domestic tasks had been reduced after the operation for the shunt. Mr. Mellor did not think so; none of this had stopped her trying to do things around the home.  She was a strong person. Mr. Mellor did however accept that she had bad headaches throughout.  Likewise she had had bad periods and anaemia.  He was not sure about tiredness but he accepted that she had suffered from SOB.   Roy Mellor was “not sure” whether Mrs. Mellor had complained of chest pain in the last year of her life.  He accepted that in her last year of life, she had complained of headaches. 
102.	Asked as to his overall impression of Mrs. Mellor’s health towards the end of her life, he had not noticed that she had been putting on weight; she seemed the same but did suffer from SOB.
103.	Mr. Mellor said that he remained on anti-depressants, which he takes regularly together with tablets for his back.
104.	Cross-examined by Mr. Hugh-Jones, it became clear that Mr. Mellor was uncertain as to dates. He was not sure why he had taken April 1994 as the start date for her chest pains.  He could not distinguish between chest pains due to her suffering from flu, or heartburn or acids, or cardiac problems.  He thought she had used her mother’s GTN spray from 1994 and even before it had been prescribed but he might be wrong. He could not assist as to why Mrs. Mellor had apparently told Dr. Yellop, the SHO, in July 1996 (set out above) that she had suffered from 6 months (rather than years) of chest pains.  When asked whether the start date for her chest pains was 1996, rather than 1994 as suggested in his statement, he answered that he did not think so.  Mr. Mellor could not assist with regard to an entry in the medical notes for September 1994 (relating to the shunt) which said that she had no problems with breathing and smoked some 10-20 cigarettes a day.  He agreed that she had probably used the spray more towards the end.
105.	Re-examined, Mr. Mellor said that he had found giving evidence an upsetting experience.  He does now have a memory problem; but did not have one prior to Mrs. Mellor’s death.
106.	(7) Kerry Mellor (“Kerry”):   Kerry spoke of Mrs. Mellor as having been a “brilliant mother” who took good care of the family. She was chatty, funny and very much liked.  To her, Mrs. Mellor had been both a mother and a very good friend.  Mrs. Mellor had looked after the house well; she was also a good cook; Kerry Mellor missed that “a hell of a lot”. Mrs. Mellor had spent a lot of time with Kirk, who had no learning difficulties before her death but had not fared well since. 
107.	Kerry remembered her mother’s chest pains.  She remembered her mother saying it felt tight; some times she had to sit down. Kerry dated the start of these pains as 1994;  she was then pregnant with her first son, Jordan and she spent a lot of time with her mother.  She had no doubt that her mother very much wanted to go on living; if investigations or operations had been suggested, her mother would have gone through with them.  Her mother’s chest pains had continued until her death.
108.	Mrs. Mellor’s mobility had not been too good for a person her age; she was out of breath easily and would sweat a lot. Kerry remembers that this was the case just after Jordan was born (in April 1995).  Some times her mother was white and clammy; then she would be red from the chest upwards, bright red.  While her mother would try to work around the house, Kerry would help a lot.  Mrs. Mellor’s mobility worsened; she found it tiring to play with Jordan.
109.	Her mother’s death had not been at all expected.  Kerry had, however, moved on. From then and continuing even now, she had become a mother as well as older sister to Kirk. He did not get on at all well at school; she helps him with everything, including filling in forms for applications.  What she is doing now is likely to continue in the future “for as long as it takes”.  There is no one else Kirk can come to.
110.	As to her father, after her mother’s death, her father was sad, on his own and had been crying – something she had never seen him do before.   He needed watching for his suicidal tendencies; when he had mood swings, he had to be left alone.    His demeanour in court was much as he was every day; he does not remember.  She has taken on running the family; she can keep coping; she is strong like her mother.
111.	With regard to emotional support for her father, Kerry Mellor estimated that she devoted about 3 hours per day for a 3 year period, followed by 1.5 hours per day thereafter and continuing.
112.	Cross-examined, Kerry was asked why she had visited her father’s house some 2-3 days per week in 1998 but every day from 1999. She said, frankly, that this was because neither she nor her father wanted to be on their own.  She had enrolled her first son, Jordan, at a school near her father’s house.   She spent her time at her father’s home doing things which she did at her own; cleaning, washing and helping Kirk – though with regard to Kirk, she accepted that on an ordinary day he would then have gone to school before she arrived and would not have returned before she left.  He was, however, bullied a good deal and was not infrequently out of school.  Kerry accepted that, inevitably, a large amount of time was spent looking after her second son, Blaine, born on the 28th October, 1998 and then an infant.  The presence of the grandson(s) helped her father.  Kerry further accepted that her father was not present throughout her visits to his home; he was away at the cemetery visiting Mrs. Mellor’s grave during her visits, perhaps 3-4 times a week.  While she resisted the suggestion that the time claimed for emotional support (in effect listening, talking and bringing the grandchild to her father’s home) was excessive, she accepted that her visits could be described as “mutual support”; she supported her father; he supported her.
113.	Turning to her mother’s symptoms, Kerry’s evidence in cross-examination was that her mother had not complained “that often” of chest pains in 1995; but that she had noticed the problem.  Her mother’s predominant complaint at the time was nausea and not being able to eat. She denied however that the nausea and the chest pains were, so far as she was aware, associated.   Her mother’s chest pains worsened in 1996-7; she could remember dates by reference to Jordan’s age.  Nausea was a recurrent symptom.  With regard to 1997, headaches were significant. Moreover, her mother was tired.   She noticed chest pains a lot more in 1997; not just that – her mother was sweating; she had a red neck and face; she would hold on to things and she was catching her breath.  She disagreed in this regard with her father; her mother’s chest pains were worse in 1997. 
114.	Still further, Kerry accepted that her mother’s subarachnoid haemorrhage in 1993 had altered her lifestyle; she had worked as a cleaner before then but not thereafter.  In 1995 when Kerry was pregnant with Jordan, she had visited her mother daily; she did not notice much about her mother’s mobility then. The medical notes of September 1994 which had recorded her mother as having no problems with her breathing, accorded with her recollection.  Her mother had taken a turn for the worse in 1996-7, when Jordan was one to two years old.
THE EXPERT EVIDENCE - LIABILITY
115.	There were three groups of expert witnesses:  (1) The GPs – Dr. Isaac called by the Claimant, Dr. Crouch called by the Sixth and Seventh Defendants;  (2) The cardiologists – Dr. Dawkins called by the Claimant, Dr. Saltissi called by the First Defendant and Prof. Littler called by the Sixth and Seventh Defendants; (3) The psychiatrists -  Dr. Hayes called by the Claimant, Dr Bradley called by the Defendants jointly.   As the psychiatrists were relevant only to quantum, it is convenient to defer reference to their evidence until quantum comes to be dealt with.   As with the witnesses of fact, it is convenient to begin by recording the evidence of the experts and, in general, to postpone comments and conclusions until later.
116.	(1) The GP experts:  I start with Dr. Isaac.   He has been a partner in a GP practice since 1986; he was an approved GP trainer over the period 1990-1997; he is on the list of approved GP experts for AVMA (Action for Victims of Medical Accidents);  so far as his appearances as an expert are concerned, the approximate division is 65% claimant work and 35% defendant work.
117.	General approach: In Dr. Isaac’s opinion, once a patient’s symptoms give a possible indication of IHD, a GP should make a referral to a cardiologist.  He emphasised that Mrs. Mellor was, for a GP, an extremely unusual patient, both in terms of her family history of cardiac related problems and because it would be very rare to find a young, pre-menopausal woman presenting with the suspicion of cardiac concerns. The context in which to consider her complaint of chest pain included her family history, her age and sex, her history of poorly controlled BP and the fact that she was a smoker.  The purpose of making such a referral would be to eliminate a cardiac cause for her chest pain.  Dr. Isaac did, however, make it plain that he would not have made a referral on the basis of risk factors alone.  While he accepted it was true that cardiac units in hospitals could not cope if every patient with chest pain was referred because of possible angina, in his view this patient was not such a run of the mill case.  There ought in this case to have been a high index of suspicion and no more than a low threshold to be satisfied in order for a referral to be made. The criterion was the need – to take reasonable care, as he accepted in evidence – to rule out a cardiac cause for the chest pain.
118.	Dr. Isaac accepted that a GP was entitled to assess the possible alternative causes of chest pain and, if he/she proceeded carefully, to come to a conclusion.  Reasonably careful GPs could disagree; there was a range of opinion which could properly be held by careful GPs as to the assessment of alternative diagnoses.  Though the patient’s history and symptoms were to be taken into account, he was not advocating diagnosis, so to speak, by ticking a list. 
119.	With regard to angina (at least of the variety relevant to these proceedings), it was necessary to have regard to the location, nature and duration of the pain, together with its relationship with exertion.  The key was the relationship between pain and exertion.  Indeed, if the symptoms were atypical, a connection with exertion was necessary to trigger the suspicion of angina. As to the relationship between the pain and exertion, the reason, he accepted, was physiological.  Bearing in mind that angina is cardiac related pain, once the occlusion passed the 50% level, it would cause pain on exertion. Such pain was reproducible; hence the utility of the (treadmill) ETT. 
120.	Criticism of Dr. Groves:  Criticism of Dr. Groves was, as already foreshadowed, confined to the 9th January, 1992 consultation. The basis for this criticism best appears from the joint responses of Drs. Isaac and Crouch, following their telephone conference held on the 17th December, 2003:
“ We both agree that according to the notes there should have been further specific questions asked about the chest pain, i.e. its duration, radiation, cause of onset, whether exacerbated with exercise and relieved by rest. We cannot say from the notes what was said at this consultation.”
121.	Against this background and as Dr. Isaac’s further answers made clear, the question of whether criticism of Dr. Groves was warranted (apart from criticism of his note-taking as such), turned, upon analysis, on a short question of fact.  While Dr. Isaac was of the view (understandably and as conceded by Dr. Groves) that if the above questions were asked they and the answers to them should have been noted, he agreed that if such questions had been asked and negative answers were given, then he could not say that a referral should have been made. If the questions were not asked, then further investigation ought to have taken place and, if the answers were other than negative, then a referral should have been made.  In this regard, Dr. Isaac further agreed that the questions contemplated by him and Dr. Crouch were questions which would be second nature to a GP – they would be asked, as it were, by rote. 
122.	Criticism of Dr. Richards:  The broad thrust of Dr. Isaac’s criticism of Dr. Richards, in his supplementary report (dated 24th February, 2004) and oral evidence, proceeded as follows. In April 1994, given that Dr. Richards thought it appropriate to consider prescribing the GTN spray (used to relieve pain associated with IHD), then, always bearing in mind Mrs. Mellor’s risk factors and young age, even one use of the spray to positive effect (i.e. serving to relieve chest pain) ought to have triggered referral.  In the light of Dr. Richards’ notes of the 22nd and 28th April consultations, she should then have referred Mrs. Mellor to a cardiologist. The effectiveness of the spray would give rise to a suspicion that Mrs. Mellor’s pain was angina, crossing Dr. Isaac’s threshold for referral.  In his experience, he had never come across a woman in her late thirties or early forties using a GTN spray.
123.	As to the period between April 1994 and November 1995, Dr. Isaac was critical of Dr. Richards for not following up her inquiries.  If Dr. Richards had told Mrs. Mellor to monitor her condition, he would have expected that to have been recorded – as it was in Dr. Richards’ notes of the later 29th March, 1996 consultation.   Likewise, questions put by Dr. Richards as to any recurrence of chest pain or use of the spray, together with the answers given by Mrs. Mellor, whether positive or negative, should have been recorded.  If the GTN spray had been prescribed as a trial in April 1994, the lack of recorded follow-up made it an unsatisfactory trial.
124.	As to the 3rd November, 1995 consultation, given the reference in Dr. Richards’ notes to the use of the GTN spray, Dr. Isaac’s view was that a referral should then have been made. 
125.	As to the 29th March, 1996 consultation, the reference in Dr. Richards’ notes to the use of the GTN spray required a referral without more ado; all the more so, said Dr. Isaac, when regard was had to the entry linking Mrs. Mellor’s discomfort to exertion and therefore indicative of angina. 
126.	Dealing with the absence of recorded complaint as to chest pains by Mrs. Mellor to Dr. Richards after April 1996, in Dr. Isaac’s view it was possible that Mrs. Mellor simply used the spray to relieve pain and, perhaps, restricted exercise so as to manage it.  It was for doctors to ask questions of their patients; if they did not ask, they would not get answers. Moreover, it was to be kept in mind that patients might have “different agendas” from their doctors.
127.	Cross-examination of Dr. Isaac yielded the following answers of significance:
i)	Save that reliance was placed on the reference in Mr. Mellor’s witness statement to Mrs. Mellor having used a GTN spray in 1994 to relieve her chest pain, no criticism was advanced in Dr. Isaac’s first report in respect of the April 1994 consultations.  Dr. Isaac’s explanation was that he had “missed” the 28th April consultation, both in his first report and in his meeting with Dr. Crouch.
ii)	Dr. Isaac accepted that Dr. Richards’ notes were of a high standard, suggestive of attentive care.  On the face of it, Dr. Richards and Mrs. Mellor had enjoyed a good doctor-patient relationship; Dr. Richards had seen Mrs. Mellor on some 93 occasions, far in excess of the average of 4 GP consultations per patient per year.  Further, following Mrs. Mellor’s subarachnoid haemorrhage, Dr. Richards had made a beneficial intervention with regard to bringing Mrs. Mellor’s BP under some degree of control and she had doggedly investigated Mrs. Mellor’s anaemia.  Dr. Richards’ referral letter (of 29th April, 1996) had been a letter “of quality”. 
iii)	Ordinarily, an 18 month gap without a report of chest pain, such as that between April 1994 and November 1995, would be reassuring; such a gap would be unusual if the patient was suffering from angina – though Dr. Isaac maintained that angina should not be discounted on the basis of this gap alone.   Moreover, said Dr. Isaac, much turned on whether in fact Mrs. Mellor had not used the spray over that period.
iv)	No doctor had positively diagnosed angina prior to Mrs. Mellor’s death; this was true even of the anaesthetists who saw Mrs. Mellor in connection with her other non-cardiac problems.
128.	Ultimately, as it appeared to me, the core criticisms which Dr. Isaac maintained against Dr. Richards were these:
i)	One successful use of the GTN spray in April 1994 to relieve pain, following its prescription, was sufficient to require a referral. It was negligent to await a pattern of use or a link between the pain and exertion.
ii)	It was no answer, or at least not one which Dr. Isaac was minded to accept, that Dr. Richards had done no more than prescribe a trial use of the GTN spray in April 1994, out of an abundance of caution.
iii)	In the absence of recorded questions and answers, the gap between April 1994 and November 1995 during which there is no report of chest pain or the use of the spray, did not provide the reassurance for which Dr. Richards was contending.
iv)	In the light of the entries in Dr. Richards’ notes for the dates in questions, a referral should have been made following the consultations on the 3rd November, 1995 and the 29th March, 1996, even if not before.
129.	Dr. Crouch:   Dr. Crouch has been a partner in a GP practice since 1973. He holds various other posts relating to GP training and assessment. He is also a non-executive director (receiving an honorarium as such) and a member of the council of the Medical Protection Society (“MPS”) – a mutual non profit making body and effectively the insurer standing behind Dr. Groves and Dr. Richards in these proceedings.  In the present case he had produced his expert’s report at the request of the MPS, which had much earlier asked him to give an opinion to its claims committee at a stage when the MPS was deciding whether or not to defend the claim. As an expert witness,  some 65% of Dr. Crouch’s work involved instructions from defendants and some 35% involved instructions from claimants;  in short, the inverse of the ratio applicable to Dr. Isaac.  Dr. Crouch had last given evidence in court some four years ago.
130.	General approach: Dr. Crouch’s general approach was broadly to the following effect.  Having regard to the chart, taking account of all Mrs. Mellor’s risk factors while recognising that in the period 1992-1996 cholesterol was not the concern it is today, she was at low absolute risk of a coronary event.  All the more so, given that following her subarachnoid haemorrhage, Dr. Richards had done much to bring her BP under control.   In Dr. Crouch’s view, the most crucial factor was the link between chest pain and exertion;  granted that angina could present atypically, there nonetheless had to be a relationship between the pain complained of and exertion for angina to be suspected and for a referral to be warranted.   
131.	When considering the picture as presented by Mrs. Mellor to the GPs, it was to be kept in mind that viral illnesses (such as flu) do cause muscle pain;  moreover, though the spotlight (with hindsight) was here on Mrs. Mellor's cardiac problems, viral complaints were to be taken seriously and could not be dismissed out of hand.  
132.	Patients could of course have “concurrent symptoms”.  It was important to avoid one symptom masking another. One of the tasks of the GP was to try and pick up what was important and to prioritise appropriately.  It was also very rare that a GP would be given a classical description of any condition. “Bits” of the history would be given over a period of time; it was important to try and build up a picture.  It was not Dr. Crouch’s practice to refer a patient to a cardiologist based on one consultation possibly indicative of angina.
133.	The position of Dr. Groves:  With regard to the criticism made of Dr. Groves, Dr. Crouch stood by the agreed comment made by him and Dr. Isaac in their telephone conference of 17th December, 2003:
“ Any patient [who] .. attends a GP is entitled to have an appropriate history and examination. The GP should note relevant clinical details and management.”
It was important too that negatives were recorded.  All that said, in his oral evidence, Dr. Crouch contrasted the “ideal” and the “real” worlds.  Given the limits on a GP’s time, especially when a patient presented, as Mrs. Mellor did on the 9th January, 1992, with several symptoms, it was understandable that note taking could suffer – notwithstanding that considerations of “good practice” pointed towards the taking of a good note.
134.	The position of Dr. Richards:  On the basis of the available material as to the consultation of the 22nd April, 1994, Dr. Crouch would not have made a referral.   While the reference to “pressure” would have rung alarm bells, Mrs. Mellor was also describing something different in the form of “burning” pain – not typical of angina.  The reference in these “excellent” GP notes to pain “at different points along the arms” was again not typical of angina.  Most importantly, the notes recorded that the pain was “not on exertion”. In all the circumstances, it was reasonable for Dr. Richards to reach the conclusion that the pain was not ischaemic in origin. 
135.	The prescription of a GTN trial (possibly out of an abundance of caution) was not a matter for criticism; reasonable GPs could disagree over whether to have prescribed the spray or not.  A decision either way could not properly be criticised. The fact that Dr. Richards had prescribed the trial did not impact on the question of whether the time had come for a referral to be made.  In Dr. Crouch’s view, it was still appropriate to wait for a link between the pain and exertion. 
136.	On the 23rd April, 1994, Dr. Richards had again seen Mrs. Mellor.  Had the pain in truth been angina, he would have expected Mrs. Mellor to have used the spray immediately; yet the notes recorded that the spray had not been used.
137.	Coming on to the consultation on the 28th April, 1994, Dr. Crouch accepted that the fact of no chest pain coupled with the use of the spray was significant. However, on the available material, again he would not have made a referral. Had the pain in fact been angina, he would have expected the spray to have been used more than once over six days.  Before referring, he would have wished to see some repetition of use associated with a relationship between the pain and exercise. Certainly he would have wanted to know more before referring;  for example,  how often the spray had been used and how quickly it had worked.  He emphasised the history and the difficulty of reaching a diagnosis of angina given the absence of a reported link between the pain and exertion. The instruction to a patient, use the spray (if you feel pain) and report, was a common instruction given by GPs, especially when uncertain as to the diagnosis.
138.	 As to the consultation of the 3rd November, 1995, Dr. Crouch was firmly of the view that he would not have wished to make a referral based on one use of the spray over an 18 month period.  The expectation, in the case of a patient with angina, is that use of the spray would have increased. In a perfect world, there would have been more noted as to the pain and the use of the spray; overall, however, Dr. Richards’ notes were excellent. Further, treating the single use of the GTN spray as a “re-trial” was a reasonable course to adopt. In any event, at the time, Mrs. Mellor’s haemoglobin level of 8.5 was of greater significance; anaemia had to take precedence and there were concerns as to cancer. 
139.	Finally, as to the consultation on the 29th March, 1996, although there was now a reference to the spray having been used twice and a link between pain and exertion, Dr. Crouch would have wished to build up more of a picture before referring.  He emphasised that, according to the chart, Mrs. Mellor remained at low (absolute) risk.  
140.	(2) The cardiology experts:  Dr. Dawkins, the cardiologist expert called by the Claimant, is the senior cardiologist at the Wessex Cardiac Unit, Southampton University Hospital.   Amongst his qualifications, Dr. Dawkins includes a BSc in Pathology; he has an interest in post-mortems, especially those concerning the heart.   He also has a particular interest in angioplasty.  His team carries out some 450 angioplasty procedures per year; the highest in the United Kingdom for an individual team.
141.	It will be convenient to record Dr. Dawkins’ evidence (and in due course that of the other cardiology experts) under the following broad headings:  (i) background and the alleged negligence of Dr. West (“negligence”);  (ii) causation;  (iii) evidence of relevance to the position of Drs. Groves and Richards (“the GPs”).
142.	Negligence:  Dr. Dawkins explained that heart disease has a genetic basis; Mrs. Mellor therefore was at high risk of premature cardiac disease, her mother and sister having had a major cardiac event at the same age.
143.	As to the referral letter, the symptoms were not entirely typical.  However, it was noteworthy that the GTN trial was effective and the discomfort was linked to exertion.  With the caveat that the GTN spray can relax or relieve certain pains of non-cardiac origin, in Dr. Dawkins’ view the GTN spray can be used to identify cardiac pain.
144.	As to Dr. Yellop’s notes, the primary complaint was chest pain.  A number of features remarked on in her notes support the diagnosis of angina, though a few features were not typical.  The references to the pain having existed for some six months and to it occurring three times a week were suggestive of angina; the duration (seconds) and the unpredictable nature were atypical. All cardiologists were, however, aware of the difficulty of assessing chest pain in young women.  Pausing there, the fact that Mrs. Mellor gave a history of six months (rather than several years) for her chest pains, was neither here nor there; as with many patients, a consistent history is not always given. A very important matter in connection with classic angina was linkage between exertion and pain. Also suggestive of classic angina was central chest pain, radiating to the arms and back, well described in Dr. Yellop’s notes.  On all the material in the notes, the balance favoured a diagnosis of angina.   On other matters referred to in the notes, Dr. Dawkins could not agree that the tenderness in the abdominal region, the epigastric discomfort, could be confused with chest pain.
145.	With regard to Dr. Yellop’s letter of 4th July, 1996 to Dr. Richards, it contained only one diagnosis – namely, possible angina. 
146.	As to Mrs. Mellor’s cholesterol level of 6.4 (reported by Dr. Yellop to Dr. Richards) on the 2nd August, 1996, this was elevated, even at the time.   The figure of 10.2 for Hb was indicative of very mild anaemia, the lower limit being 11.   Anaemia would not be confused with chest pain.
147.	Turning to the ETT, even an unfit 43 year old should have reached the 4th stage.  As all three cardiology experts had agreed in the report following their meeting on 8th February, 2004 (“the cardiology meeting”), Mrs. Mellor’s performance disclosed “a very restricted exercise capability indeed”. On the treadmill for only a short time, Mrs. Mellor displayed a number of symptoms; a small amount of exercise had resulted in chest pain.  With reference to the ECG readings, Dr. Dawkins agreed there were no changes and no ST segment changes; however, a modest increase in the heart rate had resulted in chest pain.   Mrs. Mellor’s symptoms prevented her reaching the predicted heart rate for her age and gender. Here, there had been no ECG change when the exercise had been negligible.  The lower the workload, the less likely the test would show an ECG change.  
148.	In summary, the ETT was a simple, non-invasive, reproducible test. It had its limitations but, if the patient could reach the maximum predicted HR without symptoms, the probability of important, occlusive CHD would be low, if not negligible.  The test here had been inadequate to stimulate the heart; the conclusions must therefore reflect the inadequacy of the test.  On the basis of this test, Dr. West could not properly describe the test as negative; it was a non-contributory test.    This was a young person, with severely reduced tolerance and no cause had been found. 
149.	Dr. Dawkins disagreed with Dr. West’s suggested explanations for Mrs. Mellor’s ETT performance.   Mrs. Mellor’s anaemia was mild;  had she been suffering from flu, the ETT would not have taken place;  she did have neurological complaints but these were not the cause of SOB or chest pains. Smoking was not an acceptable explanation of Mrs. Mellor’s exercise intolerance. More than 50% of patients on the treadmill were smokers, the test being one for CHD.   Unless there was evidence of lung disease (absent here), smoking was not an issue  - save that Mrs. Mellor was unfit. But her performance was way below that expected for an unfit person of her age and gender; it showed a “profound” rather than a “subtle” reduction in exercise capability. Likewise, a hiatus hernia was not an explanation.  All these  points were irrelevant.   The absence of ECG or ST changes were likewise not relevant – given that insufficient exercise had been undertaken.  The test was positive for symptoms even without ECG changes.  At all events, the test could not be called negative.
150.	As to the 13th January letter, Dr. West had not been justified in giving the reassurance contained in the first paragraph.   As to the third paragraph, anaemia (at least of the degree suffered by Mrs. Mellor) could not explain breathlessness.
151.	As to the discharge of Mrs. Mellor without further investigation, this was a young patient, with multiple risk factors for CAD. Her chest pain had a number of features suggestive of angina. It was possible that this was atypical angina.  It was important not to dismiss atypical symptoms in young women; a failure to investigate and treat them had been recognised for many years.  Dr. West was wrong to discharge this young patient without any cause having been found and without any follow-up having been arranged; by discharging her, he put the GPs off the scent.
152.	Given the seriousness of the risks should CHD materialise (including death), CHD had to be ruled out.   Dr. West needed to be sure that CHD was not the cause of the symptoms.   The investigations thus far had not done that. 
153.	Instead of discharging Mrs. Mellor, further investigations should have been undertaken. As explained below, these, in the opinion of Dr. Dawkins, would and should have involved proceeding to an angiogram, with or without a prior thallium scan and, thereafter to intervention by way of angioplasty. 
154.	Causation:  As it seems to me, it is helpful here to disentangle a number of separate strands of Dr. Dawkins’ thesis. First, the basis on which an urgent angiogram would have been mandatory. Secondly, the basis on which urgent angioplasty would have been mandatory. Third, the cause of death and its relationship to the question of whether angioplasty would have been effective (on the balance of probability) to prolong Mrs. Mellor’s life.
155.	Before proceeding further, much of the discussion on causation is best understood when considered in the light of agreed evidence as to waiting times in Sheffield in 1997- 98 for the procedures in question.  It is therefore convenient to introduce at this stage the evidence, agreed between the cardiology experts, both as to the waiting times and their reasonableness:
i)	2-3 months for a thallium scan;
ii)	6 weeks for a follow up clinical appointment;
iii)	1 year for non-urgent coronary angiography;
iv)	1 year for non-urgent coronary intervention, whether by way of angioplasty or by-pass surgery.
156.	Reverting to Dr. Dawkins’ evidence, a thallium scan would show areas of the heart muscle getting an inadequate blood supply.   It was relatively non-invasive and  a little more sensitive and specific than an ETT. But it does not show the “plumbing” of the heart in the way an angiogram would do.
157.	An angiogram was a routine procedure; in 1996 more than 100,000 were undertaken, as day cases, under local anaesthetic.  The test involved the taking of x-ray pictures, it lasted some 15-20 minutes and involved a very low level of discomfort.  It was associated with a small risk of fatality, something like 1/1000 in 1993 and less subsequently. On a risk/benefit analysis, this was the only way of obtaining a full picture as to CHD; the matter could be put to the patient as carrying a low risk but that there was no other way of getting such information.  As Dr. Dawkins put it, this “must be one of the most common invasive tests in the United Kingdom”; some 165,000 were now performed per annum.
158.	Although Dr. Dawkins would himself have preferred to proceed directly from the ETT to an angiogram, he recognised that there were two approaches. The first involved proceeding via a thallium scan. Although he was concerned that such a scan might be equivocal, he would not criticise the reasonableness of this approach.  The second (his preferred option) was to go directly from an ETT to an angiogram, accepting the risk that for, say, 15% of patients it would prove to have been unnecessary; at least in such cases reassurance could be given ruling out occlusive CHD.
159.	Here, on the balance of probability, a scan would have shown a large area of heart muscle, in the region of the left ventricle (the main pumping chamber) with inadequate blood supply.  Such a discovery would have made an angiogram mandatory. 
160.	As to the timescale for proceeding to an angiogram, Dr. Dawkins’ first report said nothing. In the report following the cardiology meeting, Dr. Dawkins had said this:
“On the balance of probabilities and taking into account the local waiting times, this test [i.e. angiography] would have been undertaken prior to death.”  [Italicisation added].
161.	In the light of the italicised words, it appeared from that report that Dr. Dawkins envisaged proceeding to an angiogram, not as a matter of urgency but in accordance with non-urgent, routine, waiting times. However, in his subsequent supplementary report (of 24th February, 2004), Dr. Dawkins stated that, following the ETT, Mrs. Mellor should have been offered a thallium scan (if one formed part of the local investigation pathway) and an angiogram as a matter of urgency:  within three months of referral. In answer to questions in cross-examination, Dr. Dawkins said that urgency had come to a head in the cardiology meeting.  Challenged that the need for urgency would not become apparent until the angiogram had been performed (which on the evidence of Dr. Dawkins to which I shall presently come, would have disclosed the proximal occlusion of the LAD), Dr. Dawkins said that a stage by stage approach was to be followed. 
162.	As to why there should have been urgency in proceeding to an angiogram, Dr. Dawkins’ opinion may be summarised as follows:  (1) Mrs. Mellor’s risk factors;  (2) Mrs. Mellor’s age;  (3) the outcome of the ETT; (4) the pattern shown by the thallium scan indicating that a large amount of heart muscle was in jeopardy (a “sizeable defect”).  
163.	Cross-examined as to Mrs. Mellor’s risk level in the light of the chart, Dr. Dawkins said that Mrs. Mellor should have been placed in the moderate or high category, i.e., a 10-20% or 20-40% risk of a coronary event in 10 years – rather than the mild category, a 5-10% risk - by reason of her having CHD at the time.  He accepted, however, that Dr. West did not know that at the time.  In any event, Dr. Dawkins added that the chart dealt with absolute risk whereas in relative terms, Mrs. Mellor’s risk was high – as a 43 year old woman, she should have had a negligible risk of a coronary event.
164.	Challenged as to his statement in the report following the cardiology meeting that, in the light of the ETT:
“ It would have been appropriate .. to suggest to the general practitioner that had her symptoms persisted … further investigation would have been appropriate with a view to reaching a definitive diagnosis…”
he said that he stood by it; however, this statement and his approach to urgency were not mutually exclusive and all his answers in that report were to be read together.
165.	With regard to the commencement of the three month period within which the urgent investigations were to be undertaken, Dr. Dawkins expressed the view that Dr. West had simply conveyed to Mrs. Mellor in the 13th January, 1997 consultation a conclusion he had arrived at in August 1996; accordingly, the three month period for urgent action began to run from August 1996 (a start date different, it may be noted, from the January 1997 date given by Mr. Gardner, when pressed early on in the trial to clarify his case). Dr. Dawkins did accept that if the local investigation pathway had been followed, some 6-7 months would have elapsed from the start date (whatever it was) to the angiogram, taking into account the thallium scan conducted on the way.
166.	As expressed for the first time in Dr. Dawkins’ supplementary report (of the 24th February, 2004, post-dating the cardiology meeting) on the balance of probability, an angiogram would have shown severe stenosis in the proximal segment of the LAD. 
167.	As to the significance of the location of the stenosis, there were two coronary arteries, the left and the right.  Both come from the aorta.  They perfuse different areas with blood, to allow the heart to pump.   The left artery divides into two branches, one down the front (the LAD) and one (the circumflex) down the back.  The LAD was a vital artery;  colloquially, an occlusion in the proximal segment (i.e. close to the origin of the vessel) was known as a “widow maker” – because a blockage here meant that so large an area was compromised. As a result, the heart pump would not prove sufficient to maintain output or an abnormal heart rhythm would ensue. The LAD tapers further downstream.
168.	Dr. Dawkins recognised that there were two problems with the PM. First, it contained no histology. Secondly, it did not say where in the LAD the 95% occlusion was to be found. However, in his oral evidence, Dr. Dawkins gave the following reasons for his view that on the balance of probability, the narrowing of the LAD was in the proximal segment: 
i)	As contained in his supplementary report, the patient’s sudden death from a malignant rhythm disturbance; a narrowing in this segment commonly kills young patients suffering from CHD;
ii)	The pathologist’s (unusual) concern for the family;
iii)	Mrs. Mellor’s symptoms; 
iv)	The fact that the pathologist felt able to estimate that the occlusion had been 95%, an estimate more readily made of the LAD before it tapered; a 95% occlusion, meant that only a pinhole was left.
169.	Pulling the threads together, with such a narrowing, the heart muscle could not perform. This would be reflected in chest pain (angina). Other consequences could be a heart attack or unstable heart rhythm. There had here either been a MI (heart attack) or, if not, then the cause of death was that the rhythm was so fast that the heart could not pump; a person could not survive more than two minutes given the lack of output.
170.	Assuming that an angiogram had revealed severe stenosis of the LAD in the proximal segment, Dr. Dawkins’ supplementary report stated that it called for “urgent intervention, either on the same hospital admission, or failing that, within three months”. It was, as he said in evidence, inconceivable that a patient with 95% occlusion in proximal segment would be sent away to return in a year. 
171.	It must be underlined, however, that Dr. Dawkins’ view as to urgency (or prioritisation) depended critically on the location of the occlusion in the proximal segment. In his report following the cardiology meeting, Dr. Dawkins said this:
“ … the presence of a ‘95%’ occlusion of the left anterior descending in such a young patient would have led to urgent revascularisation, on the assumption that the lesion was in the proximal segment of the vessel (which was not specified in the post mortem report). However, had the 95% stenosis been in the mid or distal vessel, she would have had only routine priority.”
172.	Given that a further trigger for mandatory angioplasty was the severity of the occlusion in the proximal segment of the LAD, the question arose as to what was known in this regard.  On death, the PM recorded 95% occlusion at least in one area (though the PM was, as already observed, not more specific). Other than that the occlusion on death was greater than that in life (vivo) and that the stenosis in life would have been severe, it was difficult to say, Dr. Dawkins thought, what that occlusion was in life. Moreover, even if a 65-70% stenosis might not on grounds of severity alone have prompted urgent angioplasty (which Dr. Dawkins did not accept), its character too would have needed consideration (irregular, undercut, fissured). At all events the decision as to angioplasty would be based on a number of factors and, for his part, Dr. Dawkins remained of the view that the lesion was severe enough to warrant intervention, if in the proximal segment, as a matter of urgency. Certainly, in his view, the lesion had been such to provoke malignant arrythmia.
173.	As to the mode of intervention, Dr. Dawkins favoured angioplasty (treatment of the stenosis using a minimally invasive technique with a balloon, with or without stenting to hold the artery open) over by-pass surgery (involving the use of a vein taken from elsewhere in the body to by-pass the coronary stenosis or blockage).  Angioplasty was a relatively safe technique, performed on a single overnight hospital stay.    Angioplasty was very good at dealing with symptoms. There was some dispute as to the impact of angioplasty on life expectancy, there being no definitive trial proof (although, as Dr. Dawkins put it, penicillin had not been subject to any such study). For his part, Dr. Dawkins estimated that had angioplasty been performed, Mrs. Mellor’s life would have been prolonged by some 18-19 years. Clinicians favoured angioplasty on the basis of a mix of science, pragmatism and commonsense. 
174.	Turning to the cause of death, Dr. Dawkins agreed that there was no evidence of MI but was of the opinion that there had not been time for it to develop.  He accepted too that thrombosis had not been observed visually by the pathologist.  He agreed that LVH had been recorded in the PM..   This was significant, in keeping with her hypertension (high BP) and pre-disposed her to arrythmia.  Fibrosis too was seen, was a manifestation of CAD and could have triggered arrythmia. The cause of the arrythmia, however, was inadequate blood supply.   The fibrosis was present at time of death and could have been there for some 2-3 months prior to death.   
175.	As to whether the arrythmia was triggered by a lesion in the proximal segment of the LAD – a lesion somewhere in that artery was undoubtedly present on death – or whether that lesion was simply coincidentally present, Dr. Dawkins thought that, on the balance of probability, there was a lesion in the proximal segment and the pinhole supply was the trigger for the arrythmia which was the immediate cause of death.  It was “far-fetched” or counter-intuitive to say that severe narrowing of the LAD (as found in the PM) was not related to the cause of death. Dr. Dawkins did accept that if the arrythmia had been caused by a MI and if an untreated stenosis in the LAD had precipitated the MI, the mechanism would have been thrombosis and there was no evidence of the pathologist having seen a thrombosis.  As to whether an angioplasty would have served to prevent death on the 1st January, 1998, it was put to Dr. Dawkins that the primary arrythmia was triggered by chronic, long-standing ischaemia and therefore that an angioplasty would have made no difference. Dr. Dawkins disagreed; his view, as already noted, was that an angioplasty would (probably) have prolonged Mrs. Mellor’s life.
176.	The GPs:  At least as expressed in his supplementary report, Dr. Dawkins was of the opinion that:
“ Had a referral been made by the general practitioner in 1992, 1994 or 1995 it is likely that she would have been able to complete an exercise test and that this would be positive for both symptoms and ECG change; then a myocardial perfusion scan would have been positive, and she would have proceeded to coronary arteriography at an earlier date. This would have documented the existence of coronary artery disease, although the extent is likely to have been less severe than in 1997. Having documented the presence of coronary artery disease, the general practitioner and hospital consultant would have been alerted to the importance of the need for close surveillance and the institution of the appropriate medication and or intervention which would have prevented her death in 1998.”
177.	Dr. Dawkins accepted, however, that over the period 1992 – 1995, there were non-cardiac causes which might have explained chest pain, for instance infection; further, reflux oesophagitis could mimic it.  While emphasising that young women presented atypically with angina, Dr. Dawkins agreed that it was difficult to say whether or not in 1992 – 1994 Mrs. Mellor did have angina; even in 1996, some fine judgment was called for. On balance, however, he thought that she probably did have angina, at least from 1994. As he was not in favour of working back from the PM to ascertain the severity of stenosis in life, Dr. Dawkins accepted that guesswork would be involved in such estimation; again, regard would have to be had to Mrs. Mellor’s symptoms. Dr. Dawkins fairly said that it was very difficult to know what to make of the 18 months between April 1994 and November 1995, when there was no recorded complaint as to chest pains;  much, he said, depended on whether Mrs. Mellor in fact had chest pains and used the spray; if she had the symptoms but did not complain that would be consistent with angina.  On the basis that Mrs. Mellor had been referred in November 1995 for her anaemia to be corrected, Dr. Dawkins agreed that it would take some 2-3 months to do so.   
178.	Dr. Saltissi:  He is a Consultant Physician and Cardiologist at the Royal Liverpool University Hospital.  He started doing angiograms in 1977; he performs invasive but not interventionist procedures; accordingly, he does not undertake angioplasties – although he has daily experience of them in the course of his working life. He has a particular expertise in thallium (or nuclear) scans.
179.	In his report, Dr. Saltissi had remarked that Dr. West was “an experienced Cardiologist working within a major teaching hospital who is well versed in cardiological matters and capable of performing his own invasive cardiological tests including coronary angiography without need to refer elsewhere”. Cross-examined by Mr. Gardner on this passage of his report, Dr. Saltissi said that he had met Dr. West some 3 or 4 times at medical meetings and had undertaken a peer review of Dr. West’s unit some 10-12 years previously. Basing himself on this foundation, Mr. Gardner mounted an attack on Dr. Saltissi’s independence;  it was unacceptable that this “association” with Dr. West had remained undisclosed until cross-examination; Dr. Saltissi’s personal knowledge of Dr. West was unique, gave rise to a risk of “bias and unfairness” and raised questions as to whether it was appropriate for Dr. Saltissi to act as an expert in this case.  Having at this stage noted Mr. Gardner’s complaint, it is convenient to defer for the time being my assessment of it. 
180.	Negligence: Dr. Saltissi began with some clarification of the terminology.  Angina, was chest pain attributable to reduced oxygen supply to the heart muscle.  Typical angina pain, exhibited all or almost all of the classical features already mentioned.  Non-cardiac chest pain would exhibit none or almost none of those classical features.  Where some of the classical features were present, the pain was atypical and may or may not signify angina.
181.	Dr. Saltissi agreed that the referral by Dr. Richards demonstrated that the GP needed assistance in assessing the patient. Dr. Saltissi accepted that there was a problem of young women presenting atypically for angina but said that this had come more to the fore recently and had not been as well appreciated in 1996-7. Neither the referral letter nor  Dr. Yellop’s notes (of the 4th July, 1996) could rule out the possibility that Mrs. Mellor’s chest pain was of cardiac origin. Hence the decision taken by Dr. West that Mrs. Mellor should undergo blood tests and perform the ETT. 
182.	As to the ETT,  Dr. Saltissi’s thesis may be summarised as follows. It was common ground that the ETT had not generated abnormal ECG findings or ST segment depressions.  If an ETT results in a ST segment depression when there is chest pain, then myocardial ischaemia will be presumed; if so, the ETT will have been “positive”.  If there is no ST segment depression, then the conclusion is either that there has not been enough exercise (so that the test was simply ineffective) or that there is no CHD. Here, however, Mrs. Mellor had developed her chest pain. If, therefore, her chest pain was angina, then she had done enough exercise to induce ischaemia. But if that be right, then a ST segment depression would have been expected, yet the ETT did not show it.  It followed, said Dr. Saltissi, that a responsible cardiologist could conclude that Mrs. Mellor’s pain was not attributable to CHD.  Pulling the threads together, Mrs. Mellor’s symptoms did not mean that the ETT could be described as positive. The ETT was inconclusive but not negative; that said, the absence of a ST segment depression provided a “lot of reassurance” that Mrs. Mellor’s pain was unlikely to be angina. All the more so if it was to be said that the stenosis was proximal.   Accordingly, the ETT furnished no evidence of ischaemia. The likelihood of any CAD was reduced though it could not be entirely excluded. The likelihood of very severe disease was excluded or minimised.
183.	Neither this analysis nor Dr. West’s decision to discharge Mrs. Mellor was undermined by Mrs. Mellor’s risk factors.  To place these in context, the correct position was that, following the chart, she had a low absolute risk of a coronary event, in the order of 0.5 - 1% per annum (equivalent to 5-10% over 10 years); in other words, there was a 99.5% chance of no event in year 1.  Dr. Saltissi accepted, however, that relative to others of the same age and sex, she had a raised level of risk.
184.	 As to Mrs. Mellor’s performance of the ETT, this could be attributable to a non-cardiac cause: 
i)	First, subjective reasons for a patient “giving up” should not be discounted.  The technician would respond to a patient’s request to stop. Here Mrs. Mellor had completed the first stage (3 minutes) and gave up 4 seconds after a change to a higher workload.
ii)	Secondly, there were a “bunch of factors” which went to explain Mrs. Mellor’s poor exercise tolerance; these were: (a) anaemia; (b) concurrent flu like illness;  (c) acute neurological problems; (d) her subarachnoid haemorrhage; (e) the fact that she was a smoker.
185.	Moreover, there was here a convincing alternative (non-cardiac) diagnosis for Mrs. Mellor’s symptoms of chest pain: namely, reflux oesophagitis secondary to her hiatus hernia.  Such a conclusion was entirely reasonable.  Mrs. Mellor was at low absolute (cardiac) risk; she had been describing atypical chest pain (for angina);  the only positive physical sign had been tenderness in the abdomen. Put together, all these matters pointed to Mrs. Mellor’s pain having a gastro-intestinal cause.
186.	Summarising his views on this aspect of the matter, Dr. Saltissi said that it was the duty of a cardiologist to investigate the symptoms and come to a reasonable and responsible conclusion.  While cognisant of the risks involved, it was unreal to postulate any clinician working on the basis that given any possibility of heart disease, it was mandatory to investigate further. Here it was relevant to have regard to (1) Mrs. Mellor’s low absolute risk, (2) the normal ECG during her pain when performing the ETT, (3) the changed probability of CAD and, a fortiori, serious CAD in the light of the knowledge gained from the ETT and (4) the very convincing alternative diagnosis of a gastro-intestinal cause for her pain. Against this background, it was a reasonable conclusion that Mrs. Mellor did not have CAD. In the circumstances, it was further reasonable and responsible not to investigate further and thus not to expose Mrs. Mellor to the mortality risk of coronary investigation; coronary treatment was not a no risk option.
187.	Causation:  From the outset, Dr. Saltissi’s views here were plain and consistent. In summary:   assuming the exercise of all due care,  it was improbable that Mrs. Mellor would have been prioritised so as to come to angioplasty before the date of her death (on the 1st January, 1998) and, in any event, it was improbable that angioplasty would have been effective to prolong her life and prevent her death.  With regard to prioritisation, Dr. Saltissi made the point that it involved prioritisation over others and questions of “opportunity cost”. 
188.	Thallium scans were, as already noted, a particular expertise of Dr. Saltissi. Such scans did not give information as to prognosis. A scan here would have shown ischaemic changes within the heart, in the territory supplied by the LAD; but a scan would not have shown the location of the focal stenosis within the LAD.  Dr. Saltissi said that he could not recall ever having ordered an urgent angiogram on the basis of a thallium scan.
189.	Had Mrs. Mellor reached angiography “in time”, the question would next have arisen of whether urgent angioplasty would have been mandatory.  In this regard, it was relevant to consider both the severity of any stenosis and its location.
190.	As to severity, Dr. Saltissi’s report (relying on some much praised writing of a Prof. Davies) said this:
“ Had Mrs. Mellor undergone coronary angiography, I agree with Dr. Dawkins that the principal finding would have been an LAD stenosis. The degree of narrowing, however, would have been less than that estimated visually at PM by 25-30% …. During life, an angiogram would therefore probably have found a 65-70% LAD stenosis …. It should also be borne in mind that there would probably have been progression of her coronary atherosclerotic disease in the 18 months between Mrs. Mellor first being seen in Dr West’s clinic and her death. Bearing this and the post mortem discrepancy in mind… coronary angiography, if performed in mid to late 1996, would, on the balance of probabilities… have identified an LAD stenosis of borderline significance (50-60%).”
A 60% occlusion would be significant and could be the underlying cause for angina but in terms of urgency it was not the same as a 95% occlusion.
191.	As to the location of the stenosis within the LAD, Dr. Saltissi regarded neither the fact of sudden death nor the pathologist’s remarks as being of any assistance.  As to sudden death, the LVH revealed on the PM was to be kept in mind; LVH on its own was a potent cause of sudden death.  The pathologist’s concerns as to screening Mrs. Mellor’s family demonstrated good practice but said nothing as to the location of the stenosis.
192.	Turning to the cause of death, it was or became apparent that Dr. Saltissi’s analysis differed in significant respects from that of Dr. Dawkins.  In his report, Dr. Saltissi said this:
“ The PM showed that Mrs Mellor died as a result of pulmonary oedema secondary to a cardiac arrest with no evidence of recent MI pathologically (although this does take time to develop) and, importantly, with no evidence of coronary arterial thrombosis (the underlying pathophysiology of an MI or heart attack). Thus, on the balance of probabilities, it is highly likely that Mrs Mellor’s cardiac arrest (whether ventricular fibrillation, VF or asystole) occurred as a primary arrhythmia and not in the setting of acute MI. She was predisposed to this type of spontaneous and potentially fatal arrhythmia because of her extensive CAD and significant LVH, both shown at PM. ”
Not only did Dr. Saltissi dispute that angioplasty was in general shown to be effective to prolong life but, in the light of this analysis, his view was that there was “no evidence” that an earlier angioplasty would have prevented Mrs. Mellor’s death.
193.	In his oral evidence, Dr. Saltissi explained these opinions as follows:
i)	While it could be understood that there had not been time for a MI to develop, in the absence of evidence of a coronary thrombosis, it could not be said (at least in the vast majority of cases) that there had been a “heart attack”.
ii)	He would attribute the LVH shown on PM as being 90% due to long-standing high BP and 10% due to CAD. 
iii)	Both he and Dr. Dawkins agreed that Mrs. Mellor suffered from CAD and LVH.  They further agreed that by reason of her CAD and LVH, she had scattered fibroses, though in his view, these had developed over 1-2 years rather than a period of months. Further and in his view, LVH was a cause of fibrotic scarring, independently of CAD.  In the area around each one of these scars, the muscle was electrically unstable. When the balance of hormonal and chemical influences was “right”, the electrically unstable heart muscle would spontaneously initiate (more likely) a VF arrest. That was (probably) the cause of death; such spontaneous cardiac events occur in their thousands each year. He disagreed with Dr. Dawkins that there had been an acute ischaemic event; there was no evidence for it.
iv)	The 95% occlusion of the LAD found on PM was not a “coincidence”, in that it contributed to the fibroses over a period of time. But it was not a trigger for Mrs. Mellor’s death.  Dr. Saltissi accepted that severe stenosis in the proximal segment of the LAD (if that is what it was) was associated with an adverse prognosis and that, by itself, inadequate blood supply could give rise to arrhythmia. But the stenosis here could only be presumed as the cause of death if Mrs. Mellor’s LVH was ignored.  With significant LVH and no stenosis, Mrs. Mellor would have been at the same level of risk. CAD was not irrelevant but, given the scarring, it was not likely that an angioplasty would have reduced the risk of sudden death or prevented death.
v)	In any event, unless Mrs. Mellor had complained as to her symptoms, Dr. Saltissi would not have referred her for an angioplasty; in his view, an angioplasty was undertaken to treat symptoms; angioplasties had not been shown to have prognostic benefits.
194.	The GPs: In his report, Dr. Saltissi had said this:
“ Her post mortem ... showed that by the time of her death ... she had already developed fairly severe and widespread atherosclerosis affecting her coronary arteries and cerebral arteries. In particular, she had a very severe narrowing (at least 95%) of her LAD (a vital coronary artery) and a significant 60% narrowing of her LCx.
The process of atherosclerosis is known to require 5-10 years at least to reach this degree and hence we can be sure that it was present for a number of years prior to her death and was certainly present when she was seen by Dr. West in 1996. ”
195.	While Mrs. Mellor had some CHD in 1992 and 1994, some CHD did not mean that she then had significant CHD. In Dr. Saltissi’s view, again drawing on the literature, an occlusion of some 50-70% would be required to cause angina.  If Mrs. Mellor’s LAD had been 60% occluded in January 1997, a deduction of some 10-15% should be made in the previous year, to allow for her progressive atheroma.
196.	Prof. Littler:  In common with the other cardiology experts, Prof. Littler is impressively well-qualified;  suffice to say that he is the Medical Director of the University Hospital Birmingham NHS Trust, a Consultant Cardiologist at that hospital and Professor of Clinical Cardiology at the University of Birmingham. In summarising Prof. Littler’s evidence it is appropriate to adjust the headings, so as to take into account his particular focus on matters relevant to the Sixth and Seventh Defendants (while always bearing in mind that it was not for Prof. Littler, as an expert cardiologist, to evaluate the performance of GPs). 
197.	The GPs:  In 1992, while he could not rule it out, Dr. Littler thought it unlikely that Mrs. Mellor had angina. In 1994, he did not believe that Mrs. Mellor’s symptoms were angina based; they were likely explained by viral and muscular problems. As to the 18 month “gap” between April 1994 and November 1995, it was not usual to have long intervals between episodes of angina. In November 1995, it was likely that Mrs. Mellor did have angina. However, given Mrs. Mellor’s Hb of 8.6, suggestive of severe anaemia, cancer would have been a greater and more immediate concern than any coronary matters.  No ETT would in any event have been conducted on a patient with such a Hb level.   The right course was to treat the anaemia and then re-assess the patient.  As it was likely that such treatment would take 2-3 months, a referral in November 1995 would have produced an outcome not very different from the pathway actually followed.  Commenting on the suggestion that Mrs. Mellor’s stenosis would have developed at 10-15% per annum by reason of her aggressive atheroma, Prof. Littler said that while speculative this was “reasonable speculation”; it was, however, necessary to bear in mind that any such progression may not be linear.  At all events, some 50% narrowing would have been necessary before the symptoms would be observed.
198.	 Had Mrs. Mellor been referred by the GPs to a cardiologist at the various times contended for by the Claimant, Prof. Littler summarised his views of the likely outcome(s) in his  “Supplementary Comments” dated 1st March, 2004:
“ A. Had Mrs. Mellor been referred to a Cardiologist in January, 1992, I do not believe that an exercise test would have been carried out on the basis of the history.  Had an exercise test been carried out, I believe that on the balance of probabilities it would have been negative.
B. Had Mrs. Mellor been referred to a Cardiologist in April 1994, I do not believe that an exercise test would have been carried out on the basis of the history which suggested an infection and musculo-skeletal pain. Had an exercise test been undertaken, I believe that on the balance of probabilities it would have been negative.
C. Had Mrs. Mellor been referred to a Cardiologist in November 1995, I believe that an exercise test would have been carried out but only after her anaemia (Hb 8.6) had been corrected. This could have taken two to three months. I believe that on the balance of probabilities, the result would have been the same as that in 1996, namely inconclusive.”
199.	The position of Dr. West: Negligence:  Prof. Littler was critical of Dr. West. His criticisms proceeded as follows:
i)	 Dr. West had been consulted on the basis of an “excellent” referral letter from Dr. Richards, who was faced with a “diagnostic dilemna”.
ii)	Mrs. Mellor presented with a number of known risk factors for CAD. Her absolute risk was low and this took into account all the factors of which mention had been made; namely, family history, her smoking, high BP and cholesterol level.  However, her relative risk (i.e. relative to other 43 year old females) was high. The risk factors were important, albeit that further investigation was not mandatory on the basis of risk factors alone.  
iii)	Dr. West was wrong to describe the ETT as “negative”. The result of the ETT was neither negative nor positive; it was inconclusive.  There were no significant ECG changes but the patient had not exercised to 85% of her capacity.  While the absence of ST segment depressions reduced the probability of significant CAD, given the inconclusive outcome of the ETT he would not have been happy to discharge the patient.  Further investigation was warranted; it was a breach of duty to fail to do so.
200.	(ii) Causation: Logically, the first question to be explored here was whether, following a thallium scan, Mrs. Mellor would probably have been accorded priority in proceeding to an angiogram or whether she would have been placed on the routine waiting list.  Prof. Littler’s practice was to determine priority by reference to (1) symptoms and (2) performance on the ETT.   As the ETT was “notoriously difficult” for young women and as Mrs. Mellor’s ETT had been inconclusive, the question of whether to proceed from a thallium scan to angiography or to prescribe a full regimen of anti-angina medication on a “wait and see” basis, would turn on her symptoms. Here, there was (as he understood the facts) a genuine difficulty.  Up until 1997 her symptoms were, he thought, inconclusive.  He did, however, have “genuine respect” for the description of her symptoms given by Kerry.  The fact that Mrs. Mellor neither proceeded to angiography nor was prescribed anti-angina medication flowed from Dr. West’s decision to discharge her.  At all events, Prof Littler stood by the answer which he and Dr. Saltissi had given in the report following the cardiology meeting (and which it is convenient to set out in full at this stage):
“ Both experts agree that Susan Mellor died 1 year following her outpatient review by Dr. West on 13/1/97 ... and 17 months following her first outpatient appointment on 4/7/96. It was clear to both experts that by simply summating the waiting times [recorded earlier]...(a total of approximately 2 years 4 months ) then, on the balance of probabilities, Mrs Mellor would have died before undergoing coronary intervention. Furthermore, both experts agree that had a coronary angiogram been carried out in ..[1997] .. on Mrs Mellor, it is unlikely that the findings would have been so prognostically adverse as to have led her medical attendants to credit her with such priority on their waiting list that intervention would have occurred before her death.”
201.	Again logically, the next inquiry is whether urgent angioplasty would have been mandatory following an angiogram (had one been carried out). In his report, when summarising the autopsy, Prof. Littler had written the following: 
“ The left anterior descending artery had a 95% narrowing proximally”  [Italicisation added]
At the very outset of his evidence, Prof. Littler stated that the word “proximally” had been written in error; he could give no reason for the error but what he intended to write was “focally”.  He was at that stage of his report intending to summarise that which had been written in the PM. Understandably, Mr. Gardner probed this error in cross-examination; in particular, he questioned whether it betrayed a view as to what Prof. Littler regarded as probable and realistic.  Though the matter was not entirely straightforward (there were pointers elsewhere in Prof. Littler’s evidence going, arguably, either way), I should say at once that, having seen and heard Prof. Littler give evidence, I unhesitatingly accept his explanation; this was no more than an (uncharacteristic) slip with no deeper significance.  
202.	Prof. Littler went on to express his view as to the location of the stenosis. As appears (at least inferentially) from his answer given in the report following the cardiology meeting (set out above), he could not conclude that it had probably been in the proximal segment of the LAD.   Nor could he agree with Dr. Dawkins as to the matters the latter had relied upon for his conclusion in this regard.  First, the mode of death gave rise to no such indication; there was no particular pattern of coronary disease in patients who die a sudden death; accordingly, sudden death did not give rise to an implication of stenosis in the proximal segment.  Secondly, the pathologist’s remarks owed as much to the family history as to any likely disposition of Mrs. Mellor’s cardiac disease.  Thirdly, the reference by the pathologist to a 95% occlusion was no more than a guesstimate; that reference does not assist as to whether it had been taken at the point where the artery was 3mm or 2mm or 1mm wide.
203.	Turning to the cause of death and the likely advantages of angioplasties, Prof. Littler’s opinion may be summarised as follows:
i)	There was no evidence of a thrombosis or  MI on the 1st January, 1998.
ii)	He agreed with Dr. Saltissi that LVH was a potent risk factor causing sudden death.
iii)	On a balance of probability, the cause of death was a fatal arrhythmia; as he expressed it in his report, “the substrate for the fatal arrhythmia was probably the ischaemic and hypertensive damage of the left ventricle demonstrated … at autopsy”. 
iv)	The fatal arrhythmia could have been triggered without any acute ischaemia.  On the available material, it was impossible to know whether stenosis or LVH had been the cause of death.
v)	 The longer Mrs. Mellor had suffered from hypertension (high BP), the more likely the LVH.  The greater the degree of LVH, the more likely that it would give rise to fibrotic changes. That said, on the balance of probablity, stenosis too was a contributory cause of the fibrosis.  To do so, however, it would have been necessary to have at least 50% stenosis. 
vi)	He was an interventionist as was Dr. Dawkins.  Angioplasty was appropriate for most standard arteries. His experience was that angioplasty had prognostic benefits and he would so advise his patients. He shared Dr. Dawkins’ view that a timely angioplasty would have been likely to prolong Mrs. Mellor’s life by some 18-19 years.
204.	A postscript: Late in his cross-examination of Prof. Littler, Mr. Gardner asked questions of him as to what his treatment of Mrs. Mellor would have involved.  He answered, amongst other possibilities, that (after the thallium scan) he would have prescribed a regimen of drugs and then, depending on the response, he would have considered going on to angiography.    Subsequently, I asked Prof. Littler as to why the drugs would have been prescribed.   He answered that there was a real expectation that they would have improved Mrs. Mellor’s symptoms and some drugs were shown to have beneficial prognostic effects. 
205.	Mr. Gardner then sought to put a further question as to whether (regardless of surgical intervention) the regimen of drugs or medicines would or might have served to prevent the cardiac arrest on the 1st January, 1998 and thereby have prolonged her life.  At this the Defendants vigorously objected and invited me to exclude any such questioning.  Mr. Gardner said that he should be allowed to ask the question and obtain an answer; he could then consider his position. 
206.	I ruled in favour of the Defendants’ objection. My reasons were these:
i)	The case had not been pleaded that way.  More than that, when invited to clarify the Claimant’s case at the start of the trial, Mr. Gardner’s response was as already recorded. On the basis of that response, the Claimant’s case was premised on the fact that Mrs. Mellor’s condition had been such that urgent surgery was mandatory. That was the case in fact pursued during the trial. A contention that a regimen of drugs would probably have saved Mrs. Mellor’s life was not only outwith the Claimant’s case as clarified and pursued, it was fundamentally inconsistent with it.
ii)	Questions relating to the prescription of a full regimen of anti-angina medication let alone any prognostic benefits in terms of the preservation of life, had not been explored with any previous witnesses (or, for that matter, on any systematic basis with Prof. Littler).  Were such an issue to be introduced at so late a stage, it would have been necessary to recall Dr. Dawkins, Dr. Saltissi, Dr. West on any view and, arguably,  Drs. Groves and Richards as well.
iii)	A negative or equivocal answer to Mr. Gardner’s proposed question would obviously take the matter no further.  But a positive answer (i.e. that a regimen of medication would have had prognostic benefits in terms of preservation of life) would likewise have gone nowhere – unless or until the Claimant obtained permission to amend.  
iv)	To my mind, by reason of the matters set out in i) and ii) above, any application to make so fundamental an amendment would have been overwhelmingly likely to fail.  Lateness in this instance could not be cured by orders as to costs. The likelihood of prejudice to the Defendants was real.   The consequences for case management would have been grave indeed.  In all the circumstances, I was amply satisfied that, in the exercise of my discretion, the correct course was to allow the Defendants’ objection.
v)	I add only this.  In the light of the totality of the evidence from all the cardiology experts, it was inherently implausible that, had Mr. Gardner’s questioning been pursued, it would have disclosed a simple  answer to Mrs. Mellor’s condition, short of surgery, which had hitherto eluded all concerned.
THE RIVAL CASES - LIABILITY
207.	Having set out the evidence at some length, I can summarise the rival cases as to liability relatively briefly.  I follow the order of the final speeches.
208.	For the First Defendant, Mr. Holl-Allen’s submissions proceeded as follows. As to negligence, the issue was whether Dr. West had negligently discharged Mrs. Mellor.  The duty of the cardiologist was not to take all steps definitively to rule out cardiac disease; it was instead to investigate the symptoms and then to make a reasonable judgment as to whether to investigate further. Superficially attractive though the Claimant’s risk-benefit argument was, the task of the cardiologist was to distinguish between those who reasonably required further investigation and those who did not. Considerations of opportunity cost arose; so too did the need to take into account the risks of the procedures themselves.  
209.	In considering the decision taken by Dr. West, the relevant test was that contained in Bolitho v City and Hackney HA [1998] AC 232.  This was a case of professional negligence;  what Dr. West had done was defended by Dr. Saltissi a distinguished expert in the field; that went a long way to countering allegations that the course followed by Dr. West had been unreasonable; the mere fact that other experts took a different view was neither here nor there. The decision by Dr. West to discharge Mrs. Mellor had been defensible (i.e. reasonable), not least given the “bunch of factors” outlined by Dr. Saltissi which (even putting to one side his reference to flu) served to explain Mrs. Mellor’s performance on the ETT.  Further, again as explained by Dr. Saltissi, there was a reasonable alternative non-cardiac related diagnosis for Mrs. Mellor’s chest pain. On the basis that Dr. West’s decision to discharge Mrs. Mellor did not constitute a breach of duty, then neither his characterisation of the ETT as “negative” nor the wording of the 13th January letter disclosed an independent head of negligence.
210.	If, contrary to his submissions, Dr. West had been negligent, then Mr. Holl-Allen contended that the Claimant in any event failed to make good his case as to causation.   As expressed in the First Defendant’s written submissions:
“ In order to succeed C must show that with all due care Mrs Mellor would have come [to] surgery (angioplasty) before the date of her death on 1st January 1998 and that angioplasty would have been effective to prevent that death.”
The relevant test was again to be found in Bolitho (supra); first, it was necessary to ascertain what Dr. West would have done had he not discharged Mrs. Mellor; secondly, it was necessary to consider whether Dr. West’s “hypothetical” management was defensible in accordance with the principles set out in Bolam v Friern Hospital Management Committee [1957] 1 WLR 537.  
211.	The stages in the local investigation pathway were clear; such a pathway would have involved a thallium scan, followed by an outpatient appointment, angiography and, if appropriate, angioplasty. There was no sustainable basis for criticising that pathway. Accordingly, having regard to the agreed evidence as to waiting times, the Claimant’s case, said Mr. Holl-Allen, faced grave and ultimately insuperable difficulty.  Against that background, the late evolution in Dr. Dawkins’ evidence on the question of urgency required close scrutiny.  For his part, Mr. Holl-Allen submitted that the correct start date was January 1997 (after the 13th January consultation). There was no cogent basis for arguing that urgent angiography was mandatory; accordingly, it could not be said that Mrs. Mellor would have reached even that stage.  But if that was wrong, it was accepted by all the cardiology experts that there would have been no urgency in proceeding from angiography to an angioplasty unless the angiography had (at least) revealed a stenosis of the LAD which was both severe and proximal.  As to severity it would have been substantially less in life than that found on death; but even if that hurdle was overcome, there was no logical basis for concluding that the stenosis had been located in the proximal segment of the LAD.  Finally, given the uncertainty surrounding the cause of death and Mrs. Mellor’s LVH (a significant risk factor in its own right), it could not be shown that an angioplasty would have been effective to save Mrs. Mellor's’ life.  
212.	For the Sixth and Seventh Defendants, Mr. Hugh-Jones submitted that a GP is to be judged by the ordinary standard of the reasonably competent GP.  Hindsight must be excluded.  It would be simplistic to seek to encapsulate the GP’s duty as being to rule out angina; in particular, allowance had to be made for differences of opinion between responsibly or reasonably held views.  The answers of the GPs themselves as to their own duties should not be taken out of context.
213.	As a matter of fact, it was improbable that Mrs. Mellor had suffered from angina in 1992-1994.   The expert evidence from both Dr. Saltissi and Prof. Littler pointed to that conclusion.  So did the weight of the lay evidence, properly analysed.
214.	As to the case of negligence against Dr. Groves, it turned on whether he made the relevant inquiries in that single consultation of the 9th January, 1992. It was entirely likely that he had done so; not only were those “knee jerk” inquiries but he was also very much alive to the risks facing Mrs. Mellor.
215.	The starting point for considering the case against Dr. Richards was the care of exceptional quality which she had provided over a number of years. It was plain that she knew her patient well; occasional reticence on Mrs. Mellor’s part paled next to the frequency and regularity of the consultations which took place.  As to the individual consultations forming the subject of criticism, in April 1994 there were ample reasons for not making a referral. Dr. Richards’ caution in prescribing a trial with the GTN spray should not be turned against her.  It was noteworthy that though Dr. Isaac’s first report had fully noted the consultations in question, he had then made no criticisms of this period at all, save for those which were contingent on Mr. Mellor’s evidence;  as with Dr. Dawkins, the late evolution of Dr. Isaac’s opinions required close scrutiny.  There was no proper foundation for the criticisms of Dr. Richards’ monitoring of the use of the GTN spray, themselves formulated only late in the day.   It was a reasonable inference that Mrs. Mellor had not used the spray between April 1994 and November 1995 but, if she had done so and did not tell Dr. Richards, Dr. Richards’ duty did not extend to prising that information out of her.  Dr. Richards’ decision not to make a referral on the 3rd  November 1995, in the light of a single reported use of the spray after an 18 month interval, was defensible.   As to the 29th March, 1996, this was an occasion when Dr. Richards properly, as Mr. Hugh-Jones put it, made “..clinical use of time – deferring any conclusions to await the emergence of symptoms or for time to confirm their absence”. 
216.	As to causation, the case against both GPs was throughout speculative and Prof. Littler’s views were relied upon.  As to November, 1995 in particular, once the 2-3 months were allowed for – so that Mrs. Mellor’s anaemia could be treated – there was no significant difference between a referral then and the pathway actually followed.
217.	For the Claimant, Mr. Gardner QC began by underlining that Mrs. Mellor had died unexpectedly, at a young age, “from CAD”, which she had had for some 5-10 years and which had remained undiagnosed.
218.	Duty:In considering the duty owed by all the medical practitioners, Mr. Gardner emphasised the importance of a risk/benefit analysis in the context of coronary disease.   Such an analysis should have resulted in a high index of suspicion.  Classic angina had four features:  (1) character: a feeling of tightness or pressure; (2) location: in the centre of the chest, often with radiation to the arms, shoulder, back, neck or jaw;  (3) duration: more than a few seconds;  provocation/relief: exercise/ rest.  Faced with a patient presenting with symptoms of chest pain which, not least in the light of other risk factors, might possibly be angina, it was incumbent on a medical practitioner to make appropriate inquiries and to record the answers given, including negatives; in that way a detailed record concerning the patient could be compiled.  A medical practitioner should be aware that young women, in particular, could present atypically and should likewise be alert to the danger that concurrent complaints could mask the presence of a serious condition, such as angina.  The answers given by Drs. Groves and Richards in evidence were revealing as to the extent of their duties.  On the part of a GP, in the case of suspected angina, there should be a low threshold for referral. Once referred to a cardiologist, it was for the cardiologist, who had the necessary means at his disposal, to determine whether a patient did or did not have CHD.    In the case of both the GP and the cardiologist, CHD was to be ruled out, not ruled in.   The aim was to diagnose and treat CHD at the earliest opportunity.
219.	Criticism of experts: Mr. Gardner advanced severe criticism of both Dr. Crouch and Dr. Saltissi. 
i)	In the case of Dr. Crouch, the Claimant’s written Final Submissions said this:
“ ...it is unsatisfactory in the extreme, there being many entirely independent experts available, for the GPs to seek to rely on the opinion of an expert who works for, and receives a stipend from, the GP’s defence society, and may have been involved in the decisions as to the defence of this case.....
Such association not only gives rise to an impression but also a real risk of bias... which the court should take into account when judging what he had to say...”
In answer to an observation from Mr. Hugh-Jones, Mr. Gardner disputed the existence of any practice of calling experts who had a connection with the MPS.
ii)	As to Dr. Saltissi,  his evidence was “unsatisfactory in the extreme”.  The Claimant’s written Final Submissions continued:
“ This was consistent with the fact that he knew and had done an audit of Dr. West’s unit and had formed a view as to his competence.  This view gave rise to the risk that it influenced him when considering the alleged negligence on the occasion in question. Such knowledge on the part of an expert is not only unacceptable and in our experience unique, but gives rise to a risk of bias and unfairness. For this association to remain undisclosed until cross-examination is totally unacceptable and does him little credit...”
iii)	In particular against this background, it was to be borne in mind that the court, not the experts, decided cases.
220.	The GPs: As to Dr. Groves, he had accepted that it would have been a breach of duty not to make the relevant inquiries; but if he had made them, it was extraordinary that he had not noted the answers to them. The absence of any such record was more consistent with a failure to suspect a diagnosis of CAD.
221.	As to Dr. Richards, it was true that she had done good things but her thought processes were inconsistent and confused. Mr. Gardner relied on Kerry’s evidence (in particular) as to Mrs. Mellor’s worsening condition from 1994.  With regard to the 22nd April, 1994 consultation, he drew attention to the reference in the notes to “pressure” and to the reported duration of the pains.  As to the 28th April,1994 consultation and the ensuing 18 month period, the thrust of Mr.Gardner’s criticism focused on the suggested contradiction between prescription of a GT spray and a failure both to monitor its use and to make a referral when told that Mrs. Mellor had used it.  As to the 3rd November,1995 consultation, Dr. Richards had wrongly ignored Mrs. Mellor’s reported use of the spray.  As to the 29th March, 1996 consultation, the clock was ticking; this was not a time to wait and see; Dr. Richards’ failure to refer on this occasion betrayed that her criterion for referral was the probability rather than the possibility of CAD.
222.	As to causation and the Gps, with the exception of the 29th March, 1996 consultation (which was not said to be causative), a timely referral should have led to the diagnosis of Mrs. Mellor’s CHD in sufficient time for it to be effectively treated within the routine timetable.  
223.	Dr. West: Dr. West’s decision to discharge Mrs. Mellor had been illogical and unsustainable.  Mrs. Mellor’s  risk factors told against the decision;  the ETT could not be relied upon in support of it; the “bunch of factors” suggested by Dr. Saltissi were unpersuasive; the alternative diagnosis did no more than suggest a concurrent complaint. Dr. Saltissi’s evidence was to be rejected and did not preclude a finding of negligence against Dr. West.
224.	Following the reassurance given to Mrs. Mellor by Dr. West she had, it would appear, continued to suffer pain but had simply used the GTN spray to alleviate it and (not appreciating its true significance) had not reported it to Dr. Richards or any other medical practitioner.
225.	As to causation, even assuming the reasonableness of undertaking a thallium scan, this was a case which should have been accorded priority when proceeding to an angiogram.  The reason was that Mrs. Mellor was an unusual case, both in terms of age and risk.  Dr. Dawkins’ evidence in this regard should be accepted.  
226.	As to the location of the lesion in the proximal segment of the LAD and hence the requirement of an urgent angioplasty, the starting point was that the pathologist had not said that the stenosis was not located there.  The opinion of Dr. Dawkins (summarised earlier) accorded with commonsense and should be accepted. Further, if the stenosis had a causative effect on the death then it was, said Mr. Gardner, more likely that it would have been in the proximal segment; still further, such a location would have been consistent with the presentation observed by Mr. Mellor prior just before Mrs. Mellor was taken to hospital.   Finally in this regard, Mr. Gardner emphasised “practical” considerations with reference to the dimensions of a nail; the fact that the pathologist was able to estimate – with the naked eye and in the time available - the degree of narrowing at 95% which would present as a pinhole in a 3 mm artery, made it more consistent that the stenosis was to be found in the (wider) proximal segment than in any more narrow downstream segment.
227.	 As to cause of death, Mr. Gardner’s submissions were succinct.  Either there had been a MI directly attributable to the stenosis; or the stenosis was in any event a contributory cause of the fibrosis – if therefore the cause of death was an arrhythmia due to LVH, the stenosis would still have had a causative effect.
DECISION – LIABILITY
228.	(1) The legal framework:   In the course of argument I was helpfully referred to the following authorities (amongst others): Bolam (supra), esp. at pp. 586-7; Maynard v West Midlands RHA [1984] 1 WLR 634, esp. at p.638;  Sidaway v Gov. of Bethlehem Royal Hospital [1985] 1 AC 871, esp. at pp. 892-4; Eckerslie v Binnie (1988) 18 Constr LR 1, esp. at p.79; Bolitho (supra), esp. at pp. 238-243.   Guided by these authorities and informed by the rival submissions (and such evidence as has been relevant thereto), I would venture to summarise the legal framework, for present purposes, as follows: 
i)	An allegation of professional negligence is a serious matter. The burden of proof rests on a claimant advancing such a claim, both as to breach of duty and as to causation.  
ii)	The duty of a medical practitioner is to exercise reasonable skill and care. In the case of a GP, it is to exercise such skill and care as is to be expected from a reasonably competent GP. In the case of a cardiologist, it is to exercise such skill and care as is to be expected from a reasonably competent cardiologist.  This duty is the same whether it arises in contract or tort.
iii)	Where a patient presents to a GP with symptoms which are possibly cardiac-related, it is the duty of the GP to take reasonable care in determining whether and, if so, when to refer such a patient to a specialist cardiologist.   Where a patient has been referred to a cardiologist, it is the duty of the cardiologist to take reasonable care in determining whether to discharge that patient or whether that patient should undergo further investigation and/or treatment and, if so, what investigation and/or treatment and with what, if any, priority. By way of amplification as to the duty and its performance:
a)	If there is no possibility of the patient’s symptoms being cardiac-related, there is plainly no duty to refer, investigate or treat as the case may be; indeed there is the risk that advising unnecessary and inappropriate investigations or treatment may, in some circumstances, itself amount to a breach of duty.  But to my mind, the mere existence of a possibility that the patient’s symptoms are cardiac-related does not, without more, result in a GP coming under a duty at once to make a referral; nor, again without more, does it result in the cardiologist coming under a duty to advise that the patient should undergo further investigation and treatment.
b)	The task of the GP and cardiologist, within their respective spheres, is to exercise reasonable care in distinguishing between those of their patients with possible cardiac-related symptoms who reasonably require referral, further investigation and treatment (as the case may be) and those who do not.
c)	In coming to any such judgment, the GP and the cardiologist are entitled and bound to take into account any other relevant (non cardiac-related) conditions affecting the patient, while taking care to keep in mind that patients may suffer from concurrent complaints and that lesser complaints may, on occasion, mask more serious concerns.  Likewise, in coming to any differential diagnosis, reasonable alternative diagnoses will fall to be considered. Further still, it will no doubt be appropriate for the GP and the cardiologist, in their respective spheres, to take into account the degree of risk faced by the patient in question of suffering a coronary event (heart attack) and the seriousness of the consequences of the risk should it materialise. As to the degree of risk, this extends to both “absolute” risk (i.e. the percentage risk faced by the individual in question, in the light of his/her particular characteristics) and “relative” risk (i.e. how the patient compares with others of the same sex and age). Because the consequences of a coronary event, should one materialise, may be so serious (extending, obviously, to death), these stand as an obvious pointer to the GP and cardiologist, respectively, erring on the side of caution.  But it does not follow that the GP must at once refer to a cardiologist any patient who has any possibility of CAD.  As it seems to me, that would be an abdication of the GP’s own function; not every patient who presents at a GP’s surgery with chest pain should be referred to a cardiologist. Nor does it follow that a cardiologist must at once propel any patient who has any possibility of CAD down a path of further investigation and treatment.  Not least in this regard, it is necessary to bear in mind that there are or may be risks inherent in such investigations and treatment. Conversely, at least in the generality of cases, I very much doubt that it would be right for the GP or cardiologist to await a probability of CAD before proceeding down the pathway of referral, investigation and treatment.
d)	In my view, therefore, while the objective of the GP and cardiologist must undoubtedly be to diagnose and treat CAD at the earliest opportunity, the relevant duty cannot be encapsulated into any simple formula, such as definitively “ruling out” CAD.  In any event, any such formula would necessarily require qualification so as to recognise that the duty resting on a medical practitioner is one of reasonable care rather than strict.  
iv)	With specific reference to GPs, there is a duty to make relevant inquiries of a lay patient arising out of the history given by the patient, together with the symptoms with which the patient has presented and to record those inquiries and the answers to them. Some times (there can be no universal rule), the recording of negative answers will itself be significant. The importance of this duty to record inquiries and answers lies not so much in any arid questions of note taking but rather in the compilation (for future use) of a detailed record as to the patient’s history.  The duty resting on the GP to make inquiries is, however, necessarily limited.  It is one thing to probe that which the GP is told or can reasonably observe or already has reason to monitor; it is quite another to suggest that a GP comes under a duty to cross-examine a reticent or unwilling patient; as it seems to me, the former is but the latter is not, at least generally, within the scope of any duty resting on the GP.   Furthermore, the mode of performance of any duty to monitor may depend on the nuances of the GP - patient relationship in the individual case; in an appropriate case, the GP’s duty may not extend beyond a request to the patient to monitor the use and effect of medication and to report back. 
v)	Any consideration of whether a GP or cardiologist has performed the duty resting upon him/her, is accordingly and necessarily fact sensitive.  The wisdom of hindsight must be excluded. Especially in the field of diagnosis and treatment, ample allowance must be made for differences in responsible and reasonable professional opinion; there is seldom only one correct answer to problems of professional judgment.  Provided the decision of a medical practitioner accords with a body of competent professional opinion, the practitioner will not be negligent merely because the conclusion to which he has come differs from that of other medical professionals or even another body of competent professional opinion; nor will he be negligent, simply because the court prefers another body of professional opinion.  While the court is not bound by the opinion of an expert, however distinguished: 
“ …In the vast majority of cases the fact that distinguished experts in the field are of a particular opinion will demonstrate the reasonableness of that opinion. In particular, where there are questions of assessment of the relative risks and benefits of adopting a particular medical practice, a reasonable view necessarily presupposes that the relative risks and benefits have been weighed by the experts in forming their opinions. But if, in a rare case, it can be demonstrated that the professional opinion is not capable of withstanding logical analysis, the judge is entitled to hold that the body of opinion is not reasonable or responsible.”
Bolitho (supra), per Lord Browne-Wilkinson, at p.243.
Finally in this regard, not every error of judgment constitutes negligence.
vi)	It is not always appropriate or necessary to have recourse to Bolam or Bolitho (supra), in order to determine whether or not there has been negligence. Where there is no applicable general and approved practice, the question is simply whether, in all the circumstances of the particular case, the relevant act or omission was negligent: Jackson & Powell on Professional Negligence (5th ed.), at para. 12-115.
vii)	Turning to causation, a claimant must establish his case that the injury, loss and damage flow from the negligence alleged. As already remarked, the burden of proof rests on him.  The standard of proof is a balance of probability; the authorities do not suggest that this issue is to be determined on the basis of a “loss of a chance” and, certainly, there was no such contention in the present case. In addressing causation following a negligent omission, two questions arise. The first is the purely factual question: what would have happened (on a balance of probability) if the negligent omission had not occurred? The Bolam test (supra) is irrelevant to this inquiry.  The second question is whether that which would have happened would itself have been negligent.  The Bolam test is “central” to this second inquiry.  See, Bolitho (supra), at pp. 239-240. 
229.	(2) The expert  witnesses:  Before coming to my conclusions of fact and to the application of the relevant legal principles to the facts as found, it is appropriate to say something of the expert witnesses as to liability.
230.	In summary:
i)	I am satisfied that all the expert witnesses as to liability were honestly seeking to assist the court.  Their opinions, as stated in evidence, were genuinely held.  
ii)	With regard to the experts called by the Claimant, Dr. Isaac and Dr. Dawkins, I do have a very real concern as to the significant evolution in their thinking as expressed in their supplementary reports prepared at about the time of or shortly after the commencement of the trial.   If I may say so and emphatically without suggesting any impropriety, the impression which I have formed is that this has at least something to do with the rather late but obviously energetic entry of Mr. Gardner into the case.  At all events, it is striking that the experts have gone considerably further in their supplementary reports than they were prepared to go in their first reports. In the case of Dr. Isaac, criticism of the April 1994 consultations did not feature before, save for matters contingent on Mr. Mellor’s factual evidence.  In the case of Dr. Dawkins, an implicit acceptance of a wait for routine angiography and neutrality on the location of the stenosis, have been replaced by strongly expressed views supporting an urgent requirement for both angiography and angioplasty.  On the one hand, it is important that the Claimant should not suffer because only late in the day the expert witnesses have been required to focus on the real issues. On the other hand, such noteworthy developments in expert thinking require very close scrutiny; honest and genuine experts can succumb, all too often and however inadvertently, to hindsight based over-enthusiasm.
iii)	 As to Dr. Crouch and Dr. Saltissi, the Claimant’s criticisms have already been recorded.  There was no application to debar either from giving expert evidence.  But that said, when considering the weight to be given to Dr. Crouch’s evidence and notwithstanding my view that he sought to give his evidence entirely fairly, it will be necessary to take carefully into account his close connection to the MPS.  Such a connection could very easily have a sub-conscious effect on his perspective.  As a relative outsider to this field, I am wary of any general pronouncements; but having regard to experience in other areas of the law, I cannot avoid saying that Dr. Crouch’s links to the MPS strike me as disquieting.   
iv)	So far as Dr. Saltissi is concerned, I acquit him of the charges advanced by the Claimant. I think he was neither biased nor unfair; it is true that he gave certain of his answers vigorously but that is a reflection of his temperament rather than a disclosure of any partiality. Moreover, I think that much of the Claimant’s criticism missed its mark; Dr. Saltissi’s peer review of Dr. West went to his general competence. But Dr. West’s general competence was not in issue in this trial. The issue in the trial was whether Dr. West, an otherwise competent cardiologist, was negligent on this single occasion.  What remains was Mr. Gardner’s criticism that Dr. Saltissi’s peer review of Dr. West’s unit should have been disclosed prior to cross-examination; to my mind, that criticism had force; it is unfortunate that, for whatever reason, timely disclosure was not made.   The impression that late disclosure may have created was avoidable and should have been avoided.
v)	Finally here, it is necessary to keep well in mind the danger, in a case such as this, of expert witnesses eliding their own practices and preferences with their opinions as to the demands of reasonable or responsible practice.
231.	(3) The case against Dr. Groves:  I have no hesitation in dismissing the case against Dr. Groves. 
232.	With regard to alleged negligence, as has become clear, it turns exclusively on the consultation of the 9th January, 1992. Further still, it comes down to the factual question of whether Dr. Groves made appropriate inquiries designed to exclude IHD and angina and received satisfactory answers; Dr. Groves, it will be recollected, did not dispute that if such was not the case, then he had failed in his duty. It was alleged that had Dr. Groves asked the relevant questions, then the answers given would and should have led him to refer Mrs. Mellor to a cardiologist. Conversely, it was not or not seriously in dispute that if Dr. Groves asked the appropriate questions and received satisfactory answers, then there was no duty on him to refer. 
233.	For my part, I regard it as wholly implausible that Dr. Groves did not make the appropriate inquiries. He was well aware of the risk factors impacting on Mrs. Mellor; the questions were of the knee jerk variety; he had himself acted decisively in 1988 and caused Mrs. Mellor to be admitted to hospital. Against this background, it is overwhelmingly unlikely that he simply overlooked questions as to suspected IHD or angina.  I conclude that on the balance of probability he did ask the necessary questions and received satisfactory answers. It is true that Dr. Groves failed to record the questions put and the answers given; he plainly should have done; I view Dr. Crouch’s evidence (as to the contrast between the “ideal” and “real” worlds) as explaining but not excusing that breach of duty; if and insofar as Dr. Crouch’s evidence went further, I would be unable to accept it.  The failure to record is not, however, the gravamen of the Claimant’s case against Dr. Groves – not least because in terms of causation it does not go anywhere. Accordingly, as the Claimant fails to make good any allegation of relevant breach of duty against Dr. Groves its case against him must fail.
234.	Even had I concluded that Dr. Groves had been negligent, the Claimant’s case against Dr. Groves would in any event have failed on causation grounds. First, I accept the evidence of Prof. Littler that it was unlikely that Mrs. Mellor had angina in 1992; such evidence is reinforced by Dr. Saltissi’s view that even if Mrs. Mellor had some CHD in 1992, it did not mean that she had significant CHD then.   For completeness, Dr. Dawkins’ evidence was, at its highest, equivocal as to Mrs. Mellor’s condition in 1992.   Secondly, viewed in this light, I regard as wholly persuasive Prof. Littler’s opinion as to the likely outcome of a referral in 1992 – namely, it is unlikely that an ETT would have been carried out and that, if carried out, it would probably have been negative.  The reality is that the Claimant’s case in terms of causation against Dr. Groves was, at best, speculative.
235.	(4) The case against Dr. Richards:  On all the evidence, the picture presented of Dr. Richards is that of a competent, caring and attentive GP;   Dr. Isaac himself accepted that her notes were (generally) of a high standard; her referral letter (of 29th April, 1996) attracted praise across the spectrum of the witnesses and was described by Prof. Littler as “excellent”.   Nonetheless, the claim against Dr. Richards must be considered without pre-conceptions; competent professionals can have uncharacteristic lapses.   Having approached the claim against Dr. Richards in this manner, I have reached the clear conclusion that it fails; I am not persuaded that Dr. Richards was negligent but, if I am wrong and she was, any negligence on her part was not causative. My reasons follow.
236.	 Alleged negligence:  I start with the consultation of 22nd April, 1994. I am wholly unable to accept the submission that it was negligent of Dr. Richards not to refer Mrs. Mellor to a cardiologist following this consultation.
i)	Dr. Richards’ view at the time was that Mrs. Mellor did not then have angina.  That view now enjoys the support of Prof. Littler, reinforced (at least inferentially) by Dr. Saltissi.   On 1994, Dr. Dawkins was again equivocal.   It is not altogether easy to see how a claim for negligence in respect of a failure to refer in April 1994 can get off the ground, faced with the weight of the expert evidence as to Mrs. Mellor’s actual condition; albeit with the aid of hindsight evidence, the probability is that Dr. Richards was correct in her diagnosis that Mrs. Mellor did not then have angina. It may be that this conclusion is sufficient to dispose of the allegation against Dr. Richards in respect of April 1994 but I do not leave the matter there;  it is appropriate instead to address the argument that the suspicion of angina was such as nonetheless to warrant a referral in April 1994.  For this purpose, I turn to the evidence of Mrs. Mellor’s condition at the time.
ii)	I start with the evidence of family members, namely Mr. Mellor and Kerry.   While in his evidence in chief Mr. Mellor had taken April 1994 as the start of Mrs. Mellor’s chest pains, spoke of her using the GTN spray to relieve those pains and described other symptoms consistent with angina, in cross-examination he accepted that he was not sure why he had done so.   He accepted that he was uncertain as to dates. It seems unlikely, to put it no higher, that Mrs. Mellor would have used her mother’s GTN spray even before one had been prescribed for her.  Mr. Mellor was doing his best to assist the court; however, to my mind and although he resisted the suggestion and indeed also said (curiously) that he could not be sure whether she had chest pain in 1997, his description provides a broadly accurate picture of Mrs. Mellor’s condition in 1996-1997, rather than 1994. 
iii)	On the appearance presented by her evidence, Kerry Mellor was a witness with strength of character and I have anxiously considered what she had to say. Again, I have no doubt that she was seeking to assist the court.  On the balance of her evidence, though Mrs. Mellor did have some chest pains in 1994 and 1995, they worsened in 1996-1997.   Kerry had a framework for fixing dates; she used the birth in 1995 of her first son, Jordan, as a point of reference.  Notably, Kerry said that in 1995, when visiting her mother daily while pregnant with Jordan, she had not noticed anything in particular about her mother’s mobility.  
iv)	It follows in my judgment, that the evidence from family members, while demonstrating some chest pains in 1994 and 1995 points to significant worsening in 1996-97. The “family” evidence does not, to my mind, demonstrate significant use of the GTN spray in 1994 (other than that referred to in Dr. Richards’s notes, to which I shall shortly come).
v)	These conclusions as to the evidence given by Mr. Mellor and Kerry are fortified when regard is had to various hospital notes relating to Mrs. Mellor’s admissions in respect of her other complaints.  On the 27th September, 1994, it was noted that Mrs. Mellor had “no problems” with breathing and no chest pains.   By contrast, on the 29th November, 1996, there are stark references to central chest pain, its relationship with exertion and the use of the GTN spray to relieve it.  In between these two dates, there is of course the evidence from Dr. Yellop’s notes of the history given to her by Mrs. Mellor herself on the 4th July, 1996.  In those notes, Mrs. Mellor spoke of six months (not two years) intermittent chest pain.  
vi)	I turn next to Dr. Richards’ notes of the consultation in question, with the perspective furnished by her own evidence as well as that given by Dr. Isaac and Dr. Crouch. The background was that Mrs. Mellor had been complaining of a “flu like” illness.  Dr. Richards was sufficiently concerned (and diligent) to make a home visit.   With regard to possible CHD, there were admittedly some worrying symptoms – the reference to pressure and the duration of the pain, recorded as a few minutes. Conversely, however, the burning pain, the fact that it occurred at different points along the arms and the fact that it was (expressly) not related to exertion, were all inconsistent with or atypical of angina.  For my part, against this background, I cannot fault Dr. Richards’ reaction; she did not think Mrs. Mellor had angina but she wished to prescribe the GTN spray as a trial.  Some GPs would have prescribed the spray while others would not have done so; Dr. Richards could not have been criticised either way.  In my judgment it is both unfair and fallacious to suggest that Dr. Richards’ position disclosed a dilemma – either there was no need to prescribe the spray or she was dutybound to make a referral. That approach, with respect, stands the reality of the situation on its head. It was instead entirely appropriate for Dr. Richards to form a view that Mrs. Mellor did not have angina but to prescribe the spray out of an abundance of caution and to review the matter in due course.
vii)	It follows that I am unable to accept Dr. Isaac’s criticisms of Dr. Richards with regard to the 22nd April consultation.  As to his first report, his criticisms were contingent on Mr. Mellor’s evidence –which, as I have already concluded, is properly referable to a much later date. As to Dr. Isaac’s supplementary report, I fear, with respect, that impermissible hindsight has swayed his judgment.  
viii)	On the material available at the time, Dr. Richards’ conclusion that Mrs. Mellor’s pain was not ischaemic and her decision not to refer at the time were reasonable and responsible. 
237.	I come next to the 28th April, 1994 consultation.  As already set out, the notes for this consultation refer to “chest ok” and “used GTN spray 1x Monday 25th not since”.    For my part, I accept Dr. Richards’ evidence as to this consultation and (bearing in mind fully the need for caution, given Dr. Crouch’s connection with the MPS), I prefer Dr. Crouch’s evidence to that given by Dr. Isaac. In summary:
i)	Dr. Richards did not record whether the use of the spray had been successful. She should have done. But having gone to the trouble of prescribing the GTN spray, it would have been curious if she had not recorded the fact that the use of the spray had been successful, if indeed it had been.  
ii)	It can hardly be said of Dr. Richards that she failed to refer because she had overlooked the possibility of angina; she had herself prescribed the spray.  Nor can it be said that Dr. Richards was (say) stubbornly resistant to making referrals; she readily made a number of referrals over the period during which she cared for Mrs. Mellor.
iii)	In any event, had the pain been symptomatic of angina, it is further surprising that the spray had only been used once in six days. 
iv)	It remained the case that there was no reported link between the reported pain and exertion.  In all the circumstances, a single use of the spray did not make a referral mandatory.
238.	I come next to the interval between April 1994 and November 1995. As the trial and Dr. Isaac’s evidence developed, so too did criticism of Dr. Richards’ alleged failure to monitor use of the GTN spray.  I do not think that such criticism was either warranted or made out.
i)	I accept Dr. Richards’ evidence that she had asked Mrs. Mellor (albeit not on every occasion when she saw her) to tell her if she had used the spray. 
ii)	Even though (as will be apparent) I regard the duty to record significant inquiries and answers as an important duty resting on a GP, I am not persuaded that the absence of a reference to “monitor” in Dr. Richards’ notes of the 22nd April or 28th April was significant. That is to stretch the duty too far.   It is true that there was a reference to “monitor” in Dr. Richards’ notes of the 29th March, 1996 consultation; I decline however to construe Dr. Richards’ notes as if they were a statute, so that the absence of a reference to “monitor” is to be taken as implying that Dr. Richards had not asked Mrs. Mellor to report back on any use. Similarly, while certainly with hindsight it would have been preferable if Dr. Richards had recorded questions and negative answers over this 18 month interval, having regard both to Dr. Richards’ evidence and her general conscientiousness, I am not prepared to conclude (contary to her evidence) that she asked no such questions over the entire period. Nor would I be prepared to accept that over the many meetings between Dr. Richards and Mrs. Mellor during this period, it was incumbent on Dr. Richards to record every inquiry and every answer received, including negatives; the suggestion involves a loss of proportion as to the GP’s duty to record significant inquiries and answers; it also entails losing sight of the true rationale of that duty, as explained earlier.
iii)	Mrs. Mellor was seeing Dr. Richards frequently over the period in question, in connection with other matters. If she had used the spray, there is no good reason – certainly at that time – why she would not have mentioned it. On all the evidence of Mr. Mellor and Kerry, I do not think it probable that Mrs. Mellor was making unreported use of the spray over this period. Further, if Mrs. Mellor had used the spray regularly over this period, it is remarkable that she reported only one use at the 3rd November, 1995 consultation (see below); there could have been no good reason at that stage, for Mrs. Mellor to report inaccurately.
iv)	Given the relationship between Dr. Richards and Mrs. Mellor, I do not think it was unreasonable for Dr. Richards to rely on Mrs. Mellor reporting back if she had used the spray.
v)	If Mrs. Mellor had used the spray but chose not to report that fact to Dr. Richards, it was, in the circumstances, no part of Dr. Richards’ duty to prise that information from Mrs. Mellor.
vi)	In all the circumstances, faced with a period of 18 months without any reported use of the spray, Dr. Richards was entitled to approach the 3rd November, 1995 conference with a degree of reassurance that Mrs. Mellor had not been suffering from angina.  Had Mrs. Mellor been suffering from angina over this period, it must be likely that the spray would have been used more often over this period. The reason is straightforward;  as already mentioned, angina is pain consequent on a restricted oxygen supply to the heart; once the blockage is sufficient to cause such pain, it is inherently likely that the pain will recur from time to time, prompting repeated use of the spray.
239.	The 3rd November, 1995 consultation requires careful consideration. By now, Prof. Littler’s evidence, which I accept, was that Mrs. Mellor probably did have angina.  At the time, Dr. Richards of course did not know that. Was Dr. Richards negligent in not referring Mrs. Mellor to a cardiologist at this stage?   I am not persuaded that she was.  First, for the reasons already given, Dr. Richards was entitled to be reassured by the passage of 18 months without a reported incident of chest pain or the use of the spray. A single use of the spray after such an 18 month interval did not oblige Dr. Richards to refer;  it may well be that some GPs would have done; but I cannot say that Dr. Richards was in breach of duty for not doing so.  Secondly, to my mind, it was on all the evidence, entirely reasonable at this juncture for Dr. Richards to regard the anaemia and concern as to cancer as taking priority. For completeness, I have not lost sight of the criticisms as to Dr. Richards’ notes of this consultation;  while I accept that they do leave something to be desired, they do not undermine the conclusions to which I have come in respect of Dr. Richards’ actions arising out of this consultation.
240.	Finally, I turn to the 29th March, 1996 consultation, as to which I can express my conclusions very briefly.  By now there had been repeated and effective use of the spray.  To my mind, the facts as they then appeared would have required a referral but for one matter; namely, the “clinical use of time” to adopt Mr. Hugh-Jones’s phrase; for the 29th March consultation cannot properly be evaluated without having regard to the fact that Dr. Richards arranged to see Mrs. Mellor again in three weeks’ time.  That Mrs. Mellor did not attend on the 19th April, so that the consultation had to be postponed to the 23rd April, is neither here nor there.   I do not accept that it was unreasonable of Dr. Richards to keep the matter under review in this fashion;  once hindsight is removed, it was not reasonably apparent that the clock was ticking (Mr. Gardner’s phrase). Nor do I think that by proceeding in this way, Dr. Richards was applying the wrong test of only referring on a probability of angina.
241.	Causation: For all these reasons, therefore, I have concluded that the case of negligence against Dr. Richards must fail.  If, however, I was wrong about that, then it seems plain to me that the case against Dr. Richards must in any event fail on causation grounds.  My conclusions here can be summarily expressed:
i)	For the reasons given by Prof. Littler, it is improbable that a referral in 1994  would have resulted in an ETT but, if it had, it is probable that any such test would have been negative.  To the extent that Dr. Dawkins, in his supplementary report (but not before) and orally expressed a contrary opinion, I view his evidence on this topic as no more than speculative.
ii)	With regard to November 1995, it is improbable that an ETT would have been carried out until after Mrs. Mellor’s anaemia had been corrected. As that would have taken some 2-3 months, the difference between the hypothetical pathway that would then have been followed and the pathway actually followed is, in my judgment, immaterial. Furthermore, it is probable that the result of any such ETT would have been the same as that carried out in August, 1996 – to the characterisation of which I shall shortly be coming.
iii)	The failure to refer on the 29th March, 1996 was, realistically, not said by Mr. Gardner to be causative of any loss or damage, bearing in mind that the actual referral was made on the 29th April, 1996.
242.	(5) The case against Dr. West:   Negligence:  I agree with Mr. Holl-Allen that the issue here is whether the Claimant can show that Dr. West was negligent in discharging Mrs. Mellor.  As it seems to me, the characterisation of the result of the ETT and the terms of the 13th January letter are simply part and parcel of the same issue; they do not give rise to independent grounds of negligence. 
243.	As I have already underlined, the allegation of professional negligence is a serious matter.  I remind myself that a mere difference of professional opinion or the preference for one course of action over another, does not disclose negligence.  On all the evidence, which I have anxiously weighed, my conclusions as to the picture presented to Dr. West after Mrs. Mellor had undertaken the ETT are as follows:
i)	The case had been referred to him by a respected GP practice, on the basis of an excellent referral letter; plainly, the GP concerned faced, as Prof. Littler put it, “a diagnostic dilemma”.  Dr. West needed to address that dilemma.
ii)	As to risk factors, it was true that Mrs. Mellor had a “mild” absolute risk of a coronary event: 5-10% over 10 years, or 0.5% - 1% per annum. But her relative risk was high;  as a young woman, suspected of having angina, she made an unusual patient.
iii)	The history given to Dr. Yellop contained some features which supported a diagnosis of angina and others which were not typical.  The location of the pain (central chest), its radiation into the back and right shoulder, its relationship with exertion and the fact that there was now a history of such pain for 6 months with the pain occurring three times per week, all pointed to angina.  Conversely the duration of the pain (seconds) and its unpredictable nature told against angina.  That said, on the evidence I have seen, Dr. West appreciated or certainly ought to have appreciated, the risk of young women presenting atypically. There was certainly enough here to warrant, at the least, a real suspicion of angina.  That that is so is confirmed by Dr. Yellop’s annotation of the risk factors and her subsequent letters to Dr. Richards of 4th July and 2nd August, 1996.  At all events, there was sufficient concern to prompt Dr. West himself to direct that an ETT should be undertaken, a decision which was undoubtedly correct and which has not been the subject of any criticism.
iv)	Over-dramatisation is to be avoided but, to my mind, Mrs. Mellor’s performance of the ETT should have given rise to real concern. In colloquial terms, it is striking that a 43 year old woman should be capable of accomplishing no more than 1.7 mph at an elevation of 5.  It reveals, as Dr. Dawkins put it, a “profound” reduction in exercise capability; indeed all the cardiology experts were, as noted, agreed that the ETT showed Mrs. Mellor to have “a very restricted exercise capability indeed”. 
v)	With respect, I am unable to accept Dr. Saltissi’s “bunch of factors” as serving to explain Mrs. Mellor’s performance or as suggesting a non-cardiac cause.   Even making allowance for subjective factors impacting on performance of an ETT, such considerations were only part of a much larger picture and should have been outweighed by other concerns.   Nor was I persuaded that Mrs. Mellor’s anaemia (mild at the time), or her neurological problems or history, could adequately explain her performance, or her chest pain or her breathlessness.   As to Mrs. Mellor having a concurrent flu like illness, Mr. Holl-Allen realistically accepted that this was a false point; had Mrs. Mellor  indeed been suffering form such an illness, the test would not have been undertaken at all.  As to Mrs. Mellor being a smoker, I found Dr. Dawkins’ analysis unanswerable;  the test is only performed by those who are suspected of having CHD;  more than 50% of the patients undergoing the test are smokers; there was no evidence of lung disease;  other than showing that Mrs. Mellor was unfit, smoking had no relevance; but Mrs. Mellor’s performance was way below that expected for an unfit person of her age and gender. As to a convincing alternative diagnosis (of a gastric or gastro-intestinal nature), for my part, I can understand keeping an open mind on it;  but, given the possibility of concurrent complaints and the weight of suspicion as to angina, I cannot accept that the possible alternative diagnosis could or should have led to the ruling out of angina at this stage.
vi)	A more formidable point raised by both Dr. West and Dr. Saltissi was the fact that although Mrs. Mellor’s symptoms (chest pains and SOB) had been reproduced by the test, the ETT had not generated abnormal ECG findings or ST segment depressions; this, it was said, provided reassurance that Mrs. Mellor’s pain was not angina.  The difficulty, here, however, is that insufficient exercise had been undertaken; accordingly, the reassurance that would otherwise have been provided was necessarily limited.  For my part, this feature of the ETT did not entitle Dr. West to rule out or discount CAD;  the correct conclusion was that this feature demonstrated a reduced probability of significant CAD. 
vii)	In my judgment, the ETT was neither positive or non-contributory (Dr. Dawkins) nor negative (Dr. West). It was instead inconclusive (Dr. Saltissi and Prof. Littler).  Very fairly, Dr. West accepted that, with hindsight and with the classifications now in use, the test was to be characterised as equivocal.  For completeness, the danger in describing the ETT as “negative sub-maximal” (Dr. West’s notes) is that it is not at once apparent to anyone other than Dr. West as to what is meant by it.
viii)	Pulling the threads together, this was a young person, with multiple risk factors for CAD and severely reduced exercise tolerance.  The ETT had proved inconclusive; it had not been able to establish a cause for that reduced exercise capability. Bearing in mind the reason for commissioning the ETT in the first place, namely, a real suspicion of angina, I regret that I can see no logically sustainable reason for the decision to discharge Mrs. Mellor without further investigations. The ETT simply could not have given sufficient confidence that cardiac pain could be ruled out or discounted.  The position reached in August 1996 was fundamentally different from that (for instance) facing Dr. Richards when she prescribed the GTN spray trial in April 1994.  In August 1996 and January 1997, as it seems to me, Mrs. Mellor’s case necessitated further investigations.
244.	 It follows that, in my judgment, Dr. West, on this occasion, failed to exercise reasonable skill and care in his treatment of Mrs. Mellor. He should not have discharged her without further investigation.  Even taking into account the risks inherent in further coronary investigation and treatment, there was no good reason for not at least proceeding to a thallium scan.  The risk/benefit calculation for taking such a course pointed overwhelmingly towards doing so.  I accept that Dr. West gave his evidence honestly and fairly; I accept further that he genuinely and strongly believed that Mrs. Mellor’s problems were not cardiac in nature; still further, that what the GP required of him was a decision, not an expression of his doubts.  What I am unable to accept however, is that there was any tenable analysis of the facts which justified a decision to discharge Mrs. Mellor without more. In that regard, it cannot seriously be suggested that the second paragraph of the 13th January letter cured the defects in the decision taken; plainly it did  not.
245.	In coming to this conclusion, I have not overlooked that Dr. West’s decision to discharge Mrs. Mellor was supported by Dr. Saltissi.   With respect, on this aspect of the case, his views do not deter me.  First, because here, I am not at all sure that the question of any applicable general and approved practice arises; the issue is simply whether in all the circumstances the decision to discharge was negligent.  On such an issue, the view of an expert, no matter how eminent, cannot be determinative.  Secondly, because even if Bolam (supra) is applicable to this issue, then on the analysis to which I feel driven, any practice of discharging a patient in the circumstances in question would not be logically sustainable. Thirdly, I have already acknowledged the force of Dr. Saltissi’s observations as to the absence of significant ECG changes in the course of the ETT, notwithstanding the reproduction of Mrs. Mellor’s symptoms. For reasons already given, essentially going to the limitations of the ETT, on the question of negligence, I regard that point as decisively outweighed by others; I shall return to it, however, when dealing with causation, a sphere in which it is of not inconsiderable significance.
246.	By way of a postscript as to negligence, following the reassurance provided by Dr. West’s decision to discharge Mrs. Mellor, she did not subsequently complain to Dr. Richards or other doctors as to her chest pains.  I accept in this regard Kerry’s evidence and conclude that Mrs. Mellor did indeed suffer from worsening chest pains in the course of 1997 (along, no doubt, with a variety of other complaints); that Mr. Mellor could not now recall such pains is neither here nor there.  During this period too, I am satisfied that Mrs. Mellor did make more frequent use of a GTN spray but she did not report it to Dr. Richards; the likelihood is that Mrs. Mellor now used the spray because it gave relief but, having been told that her pain was not cardiac related, she saw no need to report its use and effect.
247.	Causation:  To recap, the inquiry here, as correctly formulated by Mr. Holl-Allen, is whether, with the exercise of all due care and had Dr. West not discharged her, (1)  Mrs. Mellor would have come to angioplasty before the date of her death on 1st January, 1998 and (2) that angioplasty would have been effective to prevent her death.   Unless the Claimant succeeds on this area of the case, the claim against the First Defendant must fail.
248.	There was no doubt as to the stages in the pathway which Dr. West would have followed:  (1) a thallium scan; (2) an outpatient appointment; thereafter, if required: (3) angiography; (4) angioplasty.   Further and certainly by the conclusion of the trial, there was no or no serious suggestion that this pathway would itself have been negligent.  Still further, there was no suggestion that the routine waiting times (set out earlier) were unreasonable.  
249.	What remains is the critical dispute as to whether Mrs. Mellor would and/or should have been accorded priority treatment (so as to override the routine waiting times) and whether, if so, such treatment would in any event have been effective. It is here, in my judgment, that the Claimant’s case against the First Defendant breaks down.  I am not persuaded that, as a matter of probability, Mrs. Mellor would have reached angiography before the 1st January, 1998; the highest I would put it, is that there was a possibility that she would have done so. Without the benefit of hindsight, a failure to proceed to urgent angiography would not have given rise to any proper criticism of Dr. West (or the First Defendant). But even if I am wrong about angiography and its timing, I cannot see any logically cogent basis for concluding that the stenosis was in the proximal segment of Mrs. Mellor’s LAD; and unless it was, then all the cardiology experts agree that Mrs. Mellor would (perfectly properly) only have had routine priority for angioplasty and would not have come to angioplasty before the 1st January, 1998. Finally, given Mrs. Mellor’s significant LVH, I am unable to conclude that angioplasty in this case would have been effective to save Mrs. Mellor’s life; it would certainly have been attractive to try angioplasty; it may well have succeeded; but I cannot say that, as a matter of probability, it would have succeeded.  Any one of these conclusions is fatal to the Claimant’s case against the First Defendant;  a fortiori, all of them.  The claim against the First Defendant must accordingly be dismissed. I turn to my reasons.
250.	(1) The start date, the thallium scan and angiography:  At the outset here, some cautionary remarks are appropriate.  First, there should not be a search for spurious precision when considering the hypothetical timetable.  Secondly, when assessing what Dr. West would have done, the relevant assumption is that Dr. West had not thought it right to discharge Mrs. Mellor; instead, he had determined that further investigations were appropriate. Accordingly, Dr. West’s hypothetical mindset would have been different from his actual mindset.  Thirdly, however, a distinction must be drawn between the need to investigate further and the urgency which such investigation demanded.  
251.	There was no or no substantial criticism of the January 1997 start date for the hypothetical timetable. As recorded, that was the date given by Mr. Gardner early in the trial when pressed on the point; it ties in with the 13th January, 1997 consultation and letter of the same date in which Dr. West communicated his decision to discharge Mrs. Mellor. It is fair to say that Dr. Dawkins contended for an August 1996 start date, linked to the time when the result of the ETT became known; he did so on the premise that, in the 13th January, 1997 consultation, Dr. West did no more than communicate a decision already made.  Even assuming that Dr. Dawkins is right on that latter point, there is no proper basis for assuming an earlier start date than January 1997, unless either it is to be inferred that Dr. West would have brought forward his consultation had he decided on further investigations or the waiting time for that consultation is to be criticised.   To my mind, it cannot be inferred that Dr. West would have brought forward the date of the consultation.  Nothing in his evidence suggested that he would have done so; moreover, here, the fact that there were no  significant ECG changes during the ETT would, in my judgment, have told against Dr. West prioritising that consultation.   As already indicated, there is no foundation for any criticism of the waiting time for the January 1997 consultation.
252.	It follows that time for the hypothetical timetable starts running from January 1997.  Some 2-3 months were then required waiting for a thallium scan.  Even allowing no additional time for an outpatient appointment, it follows further that unless angiography was to be prioritised, on the basis of a one year routine waiting time, it would not have been reached before the 1st January, 1998.   
253.	Would angiography have been prioritised?  It is unnecessary to repeat the evidence which has already been set out but its tenor can be shortly summarised.  Dr. West would not have accorded it urgency.  Dr. Saltissi plainly would not have done so; he could not recall ever having ordered an urgent angiogram based upon a thallium scan.  Prof. Littler’s answer seemed to me understandably equivocal in that his view would likely have turned on a precise analysis of the symptoms of the individual case, though he stood by the answer which he and Dr. Saltissi had given in their report following the cardiology meeting, premised on a routine waiting time for angiography.  Dr. Dawkins, to my mind, plainly contemplated in his report following the cardiology meeting that routine waiting times would have been applicable.  In his supplementary report and in oral evidence, he vigorously contended for urgent angiography. 
254.	The matter is not easy.  On the one hand, Mrs. Mellor’s age (making her an unusual patient with a high relative risk) and the sizeable defect which in Dr. Dawkins’ view the thallium scan would have revealed, point to the fact that some doctors would have proceeded to urgent angiography. Assuming in Dr. Dawkins’ favour that his supplementary report and oral evidence reflect his true views, it can be inferred that he would have accorded Mrs. Mellor priority. Again, if Mrs. Mellor’s symptoms had worsened significantly and had been appropriately reported, Prof. Littler might have moved from prescribing a regimen of medication to urgent angiography. But conversely, given Mrs. Mellor’s low absolute risk and the absence of significant ECG changes during the ETT,  I cannot conclude that Dr. West would have done so. Nor, on all the evidence, could I begin to conclude that it would have been negligent not to proceed to urgent angiography. As it seems to me, this is a classic instance where, without the advantage of hindsight, reasonable and responsible medical professionals might have held divergent opinions.
255.	In summary, unless I can conclude that either (1) the start time would or should have been brought forward to August 1996 or (2) that angiography would or should have been accorded priority, then I cannot say that Mrs. Mellor would have reached angiography before the 1st January, 1998.  For the reasons already given, I cannot arrive at either conclusion (1) or (2).  The most that can be said is that some cardiologists might have prioritised angiography, although, even then, it would remain unlikely that angiography would have been reached until well into 1997.   If I am right so far, then the Claimant’s case against the First Defendant must fail on this ground alone; but in case I am wrong I turn to the question of whether urgent angioplasty would have been mandatory. 
256.	(2) Angioplasty: To my mind the position here is relatively clearcut and, by itself, destructive of the Claimant’s case on causation. Important though this topic is, my conclusions can be shortly stated:
i)	There is no factual evidence that the stenosis was in the proximal segment. The pathologist did not say it was. 
ii)	In the report following the cardiology meeting, Dr. Saltissi and Prof. Littler were emphatically of the view that urgent angioplasty was unlikely.  In the same report, Dr. Dawkins was studiously neutral on the location of the stenosis and hence neutral on the need for urgent angioplasty.  I regard that as telling. There is no good reason why Dr. Dawkins, if he thought that the stenosis was in the proximal segment, should not then have said so.  Conversely, Dr. Saltissi and Prof. Littler have consistently maintained that the location of the stenosis cannot be determined.
iii)	The reasons which Dr. Dawkins has subsequently advanced in support of the argument that the stenosis was in the proximal segment, with respect, lack cogency.  They strike me, again with respect, as afterthoughts. To my mind, Prof. Littler’s reasons  for disagreeing with these later thoughts of Dr. Dawkins are compelling; no inference as to location can be drawn from the cause of death; nor from the pathologist’s remarks as to screening the family; nor from the guesstimate given by the pathologist as to percentage occlusion.
iv)	For completeness, nothing in Mrs. Mellor’s condition immediately prior to going to the hospital on the 1st January, 1998 (a point canvassed by Mr. Gardner in his final submissions) assists at all on the location of the stenosis.
v)	In the event, there is simply no proper basis on which I could infer that the stenosis was, as a matter of probability, located in the proximal segment of Mrs. Mellor’s LAD.   On this footing, as is by now apparent, all the experts agree that Mrs. Mellor would not have reached angioplasty (even with the exercise of all due care) by the 1st January, 1998.   Regardless of any other conclusion as to causation, that is an end to the claim as against the First Defendant.
vi)	Finally (and for completeness), I have not lost sight of a point emphasised in particular by Dr. Saltissi, going to the severity of the stenosis.  I am persuaded that in life, the severity would probably have been reduced by some 25-30%, so that in mid- late 1997 it would likely have been of the order of 65-70%.  I would not, however, on that ground have ruled out the need for and likelihood of urgent angioplasty, had it been established that the stenosis was located in the proximal segment of the LAD.
257.	(3) The effectiveness of angioplasty in this case:   In case it should be necessary to do so, I go on to consider this topic (on the assumption that angioplasty was reached “in time”).  I preface my remarks by saying that nothing which follows is intended to or should cast doubt on the likely effectiveness of angioplasty generally in terms of prognostic benefits. So far as the generality of this matter is concerned, I prefer the views expressed by Dr. Dawkins and Prof. Littler to those of Dr. Saltissi. 
258.	Reverting to this case, the starting point here must be the cause of death.  Having regard to the PM, there is difficulty in supporting the suggestion of a “heart attack”; while the absence of evidence of MI can be explained (there was not time for it to develop), the absence of any evidence of a thrombosis is significant. If there was no heart attack, then, in the circumstances, the probable cause of death was a fatal arrhythmia.  Dr. Dawkins thought it “far-fetched” to conclude that the stenosis was unrelated to the cause of death; but, as it seems to me, the matter does not permit so simple an answer. There was force, both in Dr. Saltissi’s view that stenosis could only be presumed as the cause of death if Mrs. Mellor’s LVH was ignored and in Prof. Littler’s observation that, on the available material, it was impossible to know whether the cause of the arrhythmia was stenosis or the significant LVH.  Even assuming that the stenosis was itself (as well as the LVH) a contributory cause of the fibrosis, it seems inescapable that the LVH caused fibroses independently of CAD (and hence independently of any omission on the part of Dr. West).
259.	That brings me to the nub of the present issue: whether an angioplasty, unblocking a focal stenosis would  have served – as a matter of probability -  to save Mrs. Mellor’s life, given the significant LVH found on PM.  In colloquial terms, the angioplasty would have been addressing an important part, but still only a part, of the problem.  In my judgment, having regard to the carefully reasoned evidence from Dr. Saltissi (in particular) on this part of the case, I do not feel able to conclude that an angioplasty would probably have prevented death.  I repeat that this is no reflection on the generality of angioplasties.  Here, however, I must have regard to the fact that with her significant LVH and (assuming) no stenosis, Mrs. Mellor would have been at the same level of risk.  Any one of the fibroses could, as I understand the evidence, have given rise to the fatal arrhythmia.  Against this background, an angioplasty eliminating the stenosis in the LAD would have left untouched a part of the problem independent of it. If in fact the fatal mechanism was independent of the stenosis in the LAD, then it is unlikely that an angioplasty would have prevented Mrs. Mellor’s death. On the available evidence, I do not see how such a hypothesis can be described as improbable.
260.	In summary, had the relevant stage in the pathway been reached, an angioplasty would have been worth trying. It might have been successful in saving Mrs. Mellor’s life. But, given her significant LVH, I cannot say that it probably would have been.  For this reason too, the Claimant’s case on causation cannot succeed.
QUANTUM
261.	In the light of my conclusions so far, quantum is of course academic. I therefore do no more than record summarily my conclusions on the major issues, essentially for completeness and out of deference to the arguments advanced.
262.	(1) Past pecuniary loss:  This figure was agreed at £36,500.
263.	(2) Past Emotional support: This was a claim brought in respect of alleged emotional support provided by Kerry to Mr. Mellor, in particular in the light of his depression.  The Defendants disputed this claim arguing that Kerry spent time with her father because neither wished to be alone; in short, the time spent amounted to mutual support and did not give rise to any recoverable claim. If the claim was well-founded, then an hourly rate of £6.25 was agreed.  In my judgment, an amount would have been due under this heading but much reduced from the £30,000 odd claimed. Doing the best I can, I would have allowed 10 hours a week for 1998 but nothing thereafter.  The total figure would therefore have amounted to 52 x 10 x £6.25 = £3,250.00.
264.	(3) Loss of future services of wife:  On the basis of a life expectation of 19 years, a multiplier agreed at 8.97 and a multiplicand agreed at £4,500, this claim would have amounted to £40,365.00.
265.	(4) Emotional support for the Claimant for the future:  This claim for £28,000 odd was advanced in respect of future emotional support to be provided by Kerry to Mr. Mellor. I would have disallowed this claim. 
266.	(5) Loss of maternal care and attention for Kirk:   I would have allowed this claim in the (ultimately) agreed amount of £5,000.00.
267.	(6) Loss of Mrs. Mellor’s care and attention of Mr. Mellor:  This was disputed by the Defendants in principle; if recoverable, quantum was agreed at £5,000.00.  On the bases that this claim is logically distinct from the claim for loss of services and that it was confined to a very modest amount, I would have allowed it in principle. As to quantum, I would not have quibbled with the £5,000.00 agreed.
268.	(7) Funeral expenses, Mr. Mellor’s continued travel to the cemetery and continued purchase of flowers for Mrs. Mellor’s grave: The Defendants, responsibly in all the circumstances, were minded to agree this claim at £9,000.00 but on terms that it was not a precedent and on the ground that argument as to this claim would have been disproportionate. I agree.
269.	(8) Bereavement: This claim resulted in an agreed figure of £7,500.00.
270.	(9) Cost of therapy for Mr. Mellor:  This claim was agreed at £2,500.00.
271.	(10) Mrs. Mellor’s pain and suffering:   On the assumption that I had reached the same conclusions as to liability as already set out but that I had decided causation in favour of the Claimant as against the First Defendant, I would have awarded £3,000.00 under this heading in respect of 1997.
272.	(11) Nervous shock:  Under this heading the Claimant claimed £30,000.00 and the Defendant was ultimately prepared to pay £10,000.00.  Some brief observations are appropriate:
i)	Intriguingly, though he was criticised by the Claimant for his connections to the MPS, Dr. Bradley, the psychiatrist called by the First Defendant, gave evidence more favourable to the Claimant than did Dr. Hayes, the psychiatrist called by the Claimant.
ii)	The key question here was whether the Claimant’s nervous shock could be separated out from the “ordinary” grief flowing from bereavement.  After Dr. Bradley had given evidence, the First Defendant indicated its readiness to agree this claim in principle.
iii)	For my part, I would have allowed it in the amount which the First Defendant was prepared to pay, namely £10,000.00.  In all the circumstances, that was an ample sum. 
iv)	I add only this. One of the key components of this claim, was the shock suffered by the Claimant when shown his wife’s body at the Rotherham District General Hospital; I have summarised the facts when dealing with Mr. Mellor’s evidence and it is unnecessary to repeat them here.  I bear in mind of course that that hospital is not one for which the First Defendant is answerable. But with a view to the future, I am bound to observe that, on the basis of the Claimant’s account of these events,  consideration should be given by all concerned as to how such sensitive matters could be more thoughtfully handled.
v)	I record that the Sixth and Seventh Defendants advanced an argument that any claim for nervous shock was, against them, too remote. It is unnecessary to express any view on this contention and I do not do so.
CONCLUDING OBSERVATIONS
273.	As is apparent, Mrs. Mellor’s widower and daughter gave evidence in this matter and, I should add, attended court regularly throughout the trial. If I may say so, they conducted themselves throughout with dignity.  
274.	For the reasons already given, the Claimant’s claim fails against both Dr. Groves and Dr. Richards; in both cases, neither breach of duty nor causation has been established.
275.	Also for the reasons given, I have concluded that Dr. West, the cardiologist, for whom the First Defendant is answerable, should not have discharged Mrs. Mellor on the 13th January, 1997 and was negligent by doing so. That said, no causative link has been established between this breach of duty and Mrs. Mellor’s death.  The Claimant’s claim therefore fails against the First Defendant.
276.	The sad fact is that Mrs. Mellor was in a variety of unfortunate respects a very ill woman.  Her death at so early an age was a tragedy but not one which any of the Defendants could have avoided by the exercise of due diligence.
277.	I shall be grateful for the assistance of counsel in connection with drawing up the order and all questions of costs.