Scottish Court of Session Decisions

You are here: BAILII >> Databases >> Scottish Court of Session Decisions >> BROWN, AS AN INDIVIDUAL AND AS EXECUTRIX OF THE LATE WILLIAM BROWN AND OTHERS AGAINST DR ALISON SMITH, DR NEIL WRIGHT AND DR JOHN WALLACE, GENERAL PRACTITIONERS PRACTISING IN A PARTNERSHIP AS CRAIG NEVIS SURGERY [2018] ScotCS CSOH_84 (15 August 2018)
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Cite as: [2018] CSOH 84, [2018] ScotCS CSOH_84

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OUTER HOUSE, COURT OF SESSION

[2018] CSOH 84

A652/13

OPINION OF LORD ARMSTRONG

In the cause

(FIRST) EUPHEMIA BROWN, as an individual and as Executrix of the late

WILLIAM BROWN; (SECOND) BRIAN BROWN; (THIRD) WILLIAM BROWN;

(FOURTH) WILLIAM BROWN, as legal representative of his daughter IMOGEN BROWN;

(FIFTH) WILLIAM BROWN, as legal representative of his son CHRISTOPHER BROWN;

(SIXTH) DAVID BROWN; (SEVENTH) DAVID BROWN, as legal representative of his son

AARON YARDLEY-BROWN; (EIGHTH) DAVID BROWN, as legal representative of his

son CALLAN YARDLEY-BROWN; (NINTH) ELIZABETH AYDEMIR; AND

(TENTH) MARSHALL BROWN

Pursuers

against

DR ALISON SMITH, DR NEIL WRIGHT AND DR JOHN WALLACE, General Practitioners

practising in partnership as CRAIG NEVIS SURGERY

Defenders

Pursuers: Milligan QC, Smart; Drummond Miller LLP

Defenders: Smith QC, Pugh; Clyde & Co

15 August 2018

Introduction

[1] The pursuers are respectively the widow, the sons, the sister, and the brother of the

late William Brown (“the deceased”) who suffered a fatal cardiac event on 6 January 2011.

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The defenders are general practitioners who practice together in partnership as Craig Nevis

Surgery, Fort William.

[2] In the case as averred on Record, the pursuers sought damages from the defenders

on the basis that the deceased’s death was caused by negligence on the part of Dr Alison

Smith in the course of the deceased’s attendances with her on 29 December 2010,

31 December 2010, and 5 January 2011. In advance of the diet of proof, it was agreed

between the parties that Dr Smith was negligent, on 5 January 2011, in failing, on that day,

immediately to admit the deceased to hospital for further investigation. Subsequently, on

the basis of evidence elicited, it was further agreed that, on 31 December 2010, Dr Smith was

negligent to the extent that, on that day, she ought to have provided the deceased with

advice that if his chest pain occurred more frequently with little or no exertion or lasted

longer than 15 minutes, then he should call a 999 ambulance (“worsening advice”/“safety

net advice”). In the light of that admission, the pursuers withdrew their allegations of

negligence in relation to the deceased’s attendance with Dr Smith on 29 December 2010.

[3] Beyond the admitted negligence on 31 December 2010 and 5 January 2011, the

pursuers’ cases of fault were that Dr Smith:

(i) failed to diagnose unstable angina on 31 December 2010;

(ii) did not refer the deceased to hospital on 31 December 2010;

(iii) did not prescribe appropriate medication for stable angina, namely low dose

aspirin and beta blockers, on 31 December 2010

[4] In all respects, the issue of causation remained live. The pursuer’s case on causation

was (i) that admission to hospital on or before 2 January 2011 would have resulted in

treatment that would have avoided the fatal cardiac event, and (ii) that admission to hospital

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would have avoided exposure to the cold, a factor which could have contributed to the onset

of the fatal cardiac event, on 6 January 2011. The quantum of damages was agreed.

The agreed facts

[5] The facts admitted on record, and agreed by joint minute, were to the following

effect.

[6] As at 29 December 2010, the deceased had not previously suffered from chest pain.

His first episode of chest pain commenced on Wednesday 29 December 2010, after he had

been walking up and down stairs. His pain eased after five minutes of rest. He attended

Dr Smith, his general practitioner (“GP”), on that day. She noted the circumstances of the

onset of his chest pain. She did not note the site of the pain, nor whether there was any

radiation of the pain. She noted that he was a non-smoker, and that a cholesterol test the

previous year had been normal. She checked his blood pressure and pulse and found them

to be normal. She arranged for him to have an electrocardiogram (“ECG”) test. He had

previously had an ECG in October 2009. Dr Smith’s notes of the consultation were as

follows:

“chest pain this am - came on after going up and down stairs. Eased after sitting for

5 mins - never had anything like it before. felt like when breathing in when cycling

in v cold weather. not sick or sweaty with it. just getting over flu, but no cough etc

now. O/E chest clear, pulse reg 70 BP 120/80, heart sounds 1 + 2 + 0. father MI Willie

never smoked and cholesterol ok last year - for ECG”.

[7] On Thursday 30 December 2010, the deceased attempted to go for a walk but only

got as far as his garden gate, due to chest pain. The pain resolved when he sat down and

rested.

[8] On Friday 31 December 2010, the deceased suffered further chest pain while getting

dressed. His wife arranged an emergency appointment with Dr Smith. The deceased

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attended Dr Smith on that day, complaining of chest pain which she noted he had

experienced after walking for five minutes the previous day. She noted the chest pain to be

retrosternal and localised. She reviewed the deceased’s ECG taken on Wednesday

29 December 2010. She prescribed a trial of glyceryl trinitrate (“GTN”) spray and made an

urgent referral for an exercise ECG or ‘exercise tolerance test’ (“ETT”). She made a review

appointment for him. She did not prescribe low dose aspirin, a beta blocker and a statin.

Dr Smith’s notes from the consultation were as follows:

“Chest pain, as last Wednesday - went for a walk yesterday - sharp retrosternal pain

after 5 mins - had to slow right down. no feeling sick or sweaty or unwell - pain

reasonable localised. no pain moving - has been practicing golf swing - has holiday

to Florida booked for Jan. O/E chest clear PF 550; BP 130/80; pulse reg. Reviewed

ECG from Wed no changes from 2009. for trial of GTN spray and urgent ref for

exercise ECG. Review Wed as planned.”

[9] On Wednesday 5 January 2011, the deceased attended Dr Smith complaining of

continuing chest pains, and of an episode of chest pain while at rest. He complained of an

episode of chest pain the previous night, while lying down. Dr Smith prescribed gaviscon

and omeprazole for suspected acid reflux. Dr Smith’s notes of the consultation were as

follows:

“Patient reviewed pains continue - last night worse lying down - still retrosternal.

took NSAID while had flu O/E abdo NAD. try gaviscon and omeprazole. r/v Mon”

She failed to refer the deceased for admission to hospital, as an urgent referral.

[10] On Thursday 6 January 2011, at 10.45am the deceased attended at the Accident and

Emergency Department (“A&E”) of Belford Hospital, Fort William. His triage notes

recorded:

“67 year old man walked into department c/o chest pain.

1 week Hx of chest pain. Exercise induced. Seeing GP for this - prescribed GTN

1 week ago. Pain got much worse last night - ‘10/10’ at worst point. Pain not

radiating from chest. Pain at moment ‘1/10’. Awaiting exercise tolerance test apt.”

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On further examination, by Dr Bawa, the following was noted:

“1 week history chest pain - on exertion. Has been referred for exercise tolerance

test. Pain started following episode of flu-like symptoms. Pain last night worst at

midnight - when at rest. GTN spray partially improved the pain. Lasted few

minutes, returned again when climbing steps into hospital - now resolved. No

nausea/SOB/sweaty. No cough.”

His vital signs were normal. Troponin I testing was carried out, which was negative. Two

ECGs were carried out, which were normal. He was prescribed gaviscon and discharged, at

2.30pm. At 3pm, after arriving home, the deceased developed chest pain when sitting

down. He collapsed at around 3.30pm. His collapse was witnessed by paramedics from the

Scottish Ambulance Service, who undertook attempts to defibrillate but, upon applying

monitoring electrodes, they discovered that he was in ventricular fibrillation. He was

defibrillated six times. His heart rhythm proceeded to pulseless electrical activity and then

to asystole. At 4.30pm the deceased arrived at Belford Hospital, receiving cardiopulmonary

resuscitation. He was asystolic. The resuscitation in A&E was unsuccessful. He was

pronounced dead at 4.45pm.

A post-mortem examination was carried out on 11 January 2011. The report concluded:

“Post-mortem disclosed an enlarged heart with significant narrowing of the left main

coronary artery. There was also prominent pulmonary oedema in keeping with

acute left ventricular failure. Microscopy has shown evidence of previous

myocardial ischaemia ...

Individuals with an enlarged heart are at increased risk of sudden death, most likely

mechanism of death being the development of arrhythmia.”

The evidence

[11] In all, I heard the evidence of ten witnesses: Dr Smith, Mrs Brown, and,

Ewen Campbell, a family friend, who spoke to the facts of the deceased’s presentation over

the relevant period, and seven expert witnesses, of whom two, Professor Ian Wall and

Dr Philip Gaskell, gave evidence from the perspective of a GP, two, Mr Neil Nichol and

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Dr Graham Johnson, gave evidence from the perspective of an A&E clinician, two,

Professor Stephen Brecker and Dr Kevin Channer, gave evidence from the perspective of a

cardiologist, and Professor Derrick Pounder, who gave evidence relating to post mortem

pathology.

The factual background

[12] (1) Dr Smith gave evidence under reference to her witness statement, dated 23 April

2018. In general terms, the deceased was a man who had enjoyed good health. He had been

an active cyclist and had played golf.

[13] When he attended with her, on Wednesday 29 December 2010, she did not reach a

diagnosis as to what was causing his chest pain. She had considered that one possibility

was a cardiac problem, and for that reason had requested an ECG. She had advised the

deceased to come back to her if his symptoms continued, and arranged a review in

one weeks’ time, in any event, on the basis that, after such a period, it would be clearer as to

whether his chest pain was an isolated incident or was getting worse. Notwithstanding the

terms of the NICE Guidelines on Chest Pain of Recent Onset, which set out the symptoms

which might indicate an acute coronary syndrome (“ACS”), she conceded that she had not

considered the possibly of ACS. Although she had not been considering ACS, she was

considering a possible cardiac diagnosis of stable angina. She accepted that if her diagnosis

had been one of unstable angina, she would have referred the deceased to hospital that very

day. She confirmed that although she had not made any diagnosis, she had not ruled out

one of angina.

[14] When the deceased returned to her on Friday 31 December 2010, that had been

earlier than had been planned for her intended review. He was experiencing more chest

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pain. It occurred with movement on the flat, rather than when going up and down stairs,

and so could be characterised as having become worse. She accepted that in circumstances

where he was experiencing chest pain after only five minutes walking, the pain could be

characterised as being manifest after minimal exertion. Notwithstanding that, she did not

consider ACS, on the basis that the pain was being caused by activity. Her view was that

angina was more likely. When referred to the NICE Guidelines, which indicated that

symptoms which might indicate ACS included:

“new onset chest pain, or abrupt deterioration in previously stable angina, with

recurrent chest pain occurring frequently and with little or no exertion, and with

episodes often lasting longer than 15 minutes”,

she accepted that the deceased’s pain was new onset pain. It had started two days

previously. On that basis he could have been characterised as having stable angina since

Wednesday 29 December 2010. Although the pain could have been described as new onset

pain and manifesting after little exertion, she did not consider ACS, on the basis that the

pain lasted for less than 15 minutes.

[15] She maintained that she had advised the deceased to phone NHS 24 if his symptoms

deteriorated, despite the fact that no mention was made of that in her consultation notes or

in her written statement. She was sure that she would have advised him to that effect. She

accepted that she had not advised him to phone for an ambulance if his symptoms became

worse. Under reference to the report by Professor Wall, dated 12 September 2016, at

paragraphs 8.5 and 8.6, in relation to the appropriate management, given the deceased’s

presentation, she agreed that at the consultation on Friday 31 December 2010 she should

have given advice that an ambulance should be called in the event that the deceased’s

symptoms deteriorated. She did not agree that such advice would have been appropriate on

29 December 2010, on the basis that at that point she had not yet made a diagnosis. She

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accepted, on the basis of her knowledge of the deceased, that if she had given the advice that

an ambulance should be called as appropriate, he would have followed that advice.

[16] On Friday 31 December 2010, she had prescribed GTN spray. She had considered

other options such as aspirin, statins, or a beta blocker but had decided not to prescribe

them. She did not prescribe a beta blocker because the pursuer was using salbutamol for

wheezing, and she did not want to exacerbate that condition. Beta blockers were

contra-indicated where there was asthma. In so far as alternatives to beta blockers were

concerned, they all had side effects and she did not want him to feel worse. In her view, at

that time he was stable. She had not prescribed statins because the previous year’s test

results had indicated that his cholesterol had not been raised. She did not prescribe aspirin

because that can cause indigestion and she was still, at that point, not yet sure if he was

suffering from heart disease, although she was considering it as a likely diagnosis.

[17] Under reference to SIGN 96 “Management of stable angina”: “Pharmacological

Management”, she accepted that she had not followed the guidelines for drug intervention

recommended for first line therapy, except in respect of GTN spray. She had not prescribed

aspirin because it could cause indigestion and was properly viewed as a long-term

prophylactic measure.

[18] At the time she had not made a 100 per cent diagnosis of angina, but rather was

waiting for his response to the GTN spray. Under reference to the NICE Guidelines, at

paragraph 1.2.1.4: “Do not use people’s response to glyceryl trinitrate (GTN) to make a

diagnosis”, her approach had been contrary to the recommended guidelines.

[19] In relation to the deceased’s consultation with her on Wednesday 5 January 2011, she

accepted that, by that time, the deceased was manifesting unstable angina which she

recognised as a form of ACS. On that basis, she accepted that she should have made a

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referral to hospital. She accepted that she had not given advice to the deceased that he

should go to the hospital if his symptoms became worse. She accepted that, at that time,

ACS should have been actively considered and that the deceased should have been referred

to hospital that day for cardiology assessment.

[20] In relation to the attendance on Friday 31 December 2010, under reference to the

report by Professor Wall, at paragraph 8.9, in circumstances where she accepted that pain

after walking for five minutes was consistent with angina, she agreed that the prescription

of low dose aspirin and statins would have been an appropriate preventative measure, but

that she had chosen not to prescribe them. She agreed that she should have made an urgent

referral to hospital.

[21] Although the deceased had been describing pain after exercise which could be

consistent with angina, his description of the pain was atypical of what a patient with

angina would describe. On that basis, since her diagnosis was not certain, she chose not to

prescribe statins. She accepted that she was thinking “he may well have angina”, but she

had not yet made that diagnosis. She accepted that if she had diagnosed angina, she would

have prescribed differently. She would have prescribed low dose aspirin, and statins, and

beta blockers or something similar. However on 31 December 2010 she had not done that

because she was not yet certain that he was suffering from angina.

[22] In cross-examination, Dr Smith confirmed that she had practised consistently as a

general practitioner since 1985, when she graduated MBChB. The practice was situated

two miles from the centre of Fort William, and two miles from the local hospital, Belford

Hospital. It was a district general hospital with medical and surgical consultative services,

an A&E department, and allied health professional services. It had no cardiology

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department. Cases requiring cardiology assessment would be referred to a hospital in the

central belt, most probably in Edinburgh.

[23] She was familiar with the NICE Guidelines which she recognised as providing

guidance on particular illnesses, including angina and chest pain. She did not routinely

refer to them as part of a first line checklist. She was also familiar with the SIGN Guidelines

which were the Scottish equivalent. Her practice, if checking, was to refer to them rather

than the NICE Guidelines. Under reference to SIGN 96 “Management of stable angina”:

“Pharmacological Management”, she agreed that the prescription of beta blockers was an

appropriate first line therapy for relief of stable angina. Under reference to “Management of

stable angina”: “Diagnosis and Assessment”, she recognised that a patient with chest pain

might not necessarily be suffering from angina, and that there could be possible alternative

diagnoses. She confirmed that, when assessing the deceased, she had in mind the type of

discomfort described, its location, its relation to exertion, its duration and other factors

relating to the deceased’s pain, all consistent with the terms of SIGN 96 “Management of

stable angina”: “Clinical assessment”. In relation to his general lifestyle, there had been a

number of factors which it was necessary to take properly into account.

[24] In relation to her consultation with the deceased on Wednesday 29 December 2010,

her recollection was that in describing his chest pain after climbing up and down stairs, he

had indicated that he had been carrying cases at the time. On that basis, she had assessed

that activity as involving more exertion, and more increased effort, than normal.

[25] She had noted the deceased as not feeling sick or sweaty. That was to be considered

in the context of the nature of pain being subjective and often difficult for a patient to

describe. Generally, where there was angina, the patient found the pain difficult to describe,

but often complained of being sweaty or of feeling sick or having a heavy feeling. Patients

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with angina often did not describe pain well. In contrast, the deceased had complained of a

sharp pain which was clearly localised. That was an unusual description from a patient

suffering from angina. She confirmed her understanding, that angina did not usually

present as involving a sharp or stabbing pain, as being consistent with the terms of SIGN 96

“Management of stable angina”: “Non-cardiac chest pain”, at paragraph 2.1.2.

[26] She had considered it significant that he was “just getting over flu”. He had been

unwell, had been in bed for two weeks, had developed a cough, and probably had weaker

musculature as a result. She had taken into account his family history (“father MI”), and the

fact that the deceased had never smoked and had normal cholesterol levels. She had

referred him for an ECG examination, and had considered the possibility that the pain could

be muscular. She accepted however that angina was a common complaint.

[27] She had been aware that, on Thursday 30 December 2010, the deceased had

attempted to go for a walk but had only reached as far as his garden gate before suffering

pain which subsided with rest. In relation to her consultation with him on Friday

31 December 2010, she was aware that he had suffered pain when getting dressed, but that it

had been a sharp pain and that he had not felt sick or sweaty. She had prescribed GTN

spray, requested an urgent ETT, and arranged a review on the following Wednesday. She

confirmed that, at that point, her thoughts were that the deceased was describing the

symptoms of stable angina, involving pain which came on with exercise.

[28] In relation to her consultation with the deceased on Wednesday 5 January 2011, at

which she had noted that he had experienced pain lying down during the night, she had

prescribed gaviscon and omeprazole as measures to counteract indigestion and reduce

stomach acid. She had done so because she was considering acid reflux and dyspepsia in

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the context of his recent viral illness. Her view had been that the pain he described on

Wednesday 5 January was the same pain he had been complaining of earlier.

[29] Where an urgent referral to hospital was required, the mechanism involved would

require Dr Smith to liaise with the hospital by phone, draft a written letter, and arrange a lift

for the patient as transport to the hospital, two miles away, on the basis that an ambulance

would in fact take longer to make the journey.

[30] Where an ETT was required, that could be provided by the local hospital. As at

Friday 31 December 2010, an urgent referral carried with it the expectation that the patient

would be seen within one week, or within ten days, but certainly after the New Year public

holidays. The referral which she had made on Friday 31 December 2010 had been an urgent

referral.

[31] Where there was an abnormal ETT result, further investigation, most probably in the

form of an angiogram, would be required. For that purpose referral to a cardiologist would

be required. That would be necessary before a diagnosis of coronary heart disease (“CHD”)

could be reached. Dr Smith’s view was that, had the deceased been admitted to hospital on

Friday 31 December 2010, and the decision taken that an angiogram was required, it would

have been necessary for the angiogram to be carried out by a cardiologist, most probably in

Edinburgh, which would have been unlikely to happen before several weeks had elapsed.

[32] In re-examination, Dr Smith confirmed her understanding that retrosternal pain was

typical of angina.

[33] She confirmed that she had in the past, on several occasions, referred patients to

Belford Hospital as emergency ACS cases.

[34] (2) Mrs Euphemia Brown, the widow of the deceased, described her former husband

as an active man who played sport, and in particular golf, skiing, walking and cycling. He

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had been in the habit of cycling every Sunday from Fort William to Spean Bridge and back, a

distance of some 20 miles. In December 2010, he had suffered a bout of the flu, but

otherwise, in the recent past, he had experienced no serious health complaints. On

Wednesday 29 December 2010, her husband had gone to his GP, Dr Smith, complaining of

chest pain. He had not had any previous chest pain problems. He had first mentioned his

chest pain to her the day before. He had been moving the dissembled parts of a cot into the

loft of their home, access to which was by a ladder. When he had come downstairs he had

been complaining of pain in his chest. She had phoned the GP and had arranged an

emergency appointment. The fact that he was complaining at all suggested to her that it

must be something significant. He had appeared to be worried, and so she also had become

worried. She did not attend the GP with him on that day. When he returned, he told her

that an ECG had been carried out, but that nothing had showed up. He said that his doctor

had said to him that it could be angina.

[35] On the next day, Thursday 30 December 2010, her husband had not done much at all.

He had not been his usual active self. Whenever he moved, he experienced pain. He had

attempted to go for a walk, but had returned within minutes, complaining that he could not

get further than the garden gate. She had told him to sit down, and when he did so the pain

quickly subsided. Each time he rose from a seated position, the pain returned. When he sat

down, the pain resolved.

[36] On the next day, Friday 31 December 2010, he was complaining of pain again and

went to his GP. That morning he had experienced pain after getting up from bed. He had

not been doing much. Any movement brought on the pain, and so she had phoned his GP.

That evening, which was Hogmanay, she and her husband had not participated in any

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celebrations, but had stayed at home and had gone to bed, having brought in the New Year

on their own.

[37] On New Year’s Day, her husband had done nothing other than to sit on a chair all

day. If he rose from the chair, his pain came back, but subsided when he sat down again.

He was in pain whenever he was not sitting down. Pain was generated even by moving

from his chair to the toilet. On New Year’s Day, it had been the couple’s custom to visit

friends and they did so on that day. They visited their friend Mr Ewan Campbell. Her

husband had struggled to get there on foot, even although Mr Campbell’s home was only

seven to eight minutes’ walk from their own. On the way he kept experiencing pain, and

had to stop several times before being able to carry on. It had been the same pain as that

from which he had been suffering in the previous days.

[38] Mrs Brown had no doubt that if the GP had told him that he should go to the

hospital if things got worse, he would have done so. The weather at that time had been cold

and had remained cold in the days following New Year’s Day. In the days up to 5 January

2011, her husband had done nothing involving any activity.

[39] On Thursday 6 January 2011, Mrs Brown had called an ambulance which had taken

her husband to A&E at Belford Hospital. Her sister-in-law had gone with them. Access to

the A&E at Belford Hospital was by 12 or 13 steps; there was no ground floor entrance. He

had required to ascend and descend the steps when entering and leaving A&E. They had

been dropped off at home, at the garden gate, at 2.30pm. Very quickly, after enough time

only for a cup of tea, her husband had collapsed, and an ambulance was called at 3.00pm.

[40] (3) Mr Ewan Campbell had known the deceased for 44 years, and described him as

an outdoor man with an active life. He had been a keen golfer, hillwalker, cyclist and skier.

He had seen the deceased a few days before his death. The deceased and his wife had

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visited him just after New Year. During the visit, the deceased had not seemed to be his

usual chirpy self. He was a man who had customarily enjoyed New Year, but that was not

the case on this occasion. He seemed slightly downcast. He sat down very quickly on

entering the house. His wife had told Mr Campbell that the deceased had required to stop

two or three times in the course of the journey, which was only a quarter of a mile or so,

because of pain in his chest which was not normal. Mr Campbell described the deceased as

a man who would not normally make a fuss, but rather kept himself to himself. The couple

had stayed with Mr Campbell for two to two and a half hours. Throughout that time, the

deceased had remained seated. He had insisted on having only one dram - which was

uncharacteristic of him. The couple had left at 10.00pm. The weather had been cold and

dry. The temperature had been above freezing, but there had been a cold wind. After that

meeting, Mr Campbell never saw the deceased again.

The expert evidence

[41] It was agreed that in the case of each of the expert witnesses, his report was to be

treated as his evidence in chief, subject to such further examination in chief as the court

might allow.

(i) Diagnosis and treatment by a general practitioner of ordinary competence

[42] (1) Professor Ian Wall gave expert evidence for the pursuers, under reference to his

report dated 12 September 2016. His view was that, in respect of the attendance on Friday

31 December 2010, given the history of chest pain on minimal exertion, and on that history

alone, Dr Smith should have diagnosed ACS until proved otherwise. Such a diagnosis

would have mandated the prescription of a loaded dose (300mgs) of aspirin, and an

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immediate 999 emergency admission to hospital. Such a diagnosis would have been

consistent with guidance given on the Patient.co.uk website: “Assessment for possible acute

coronary syndrome”, where it was stated that:

“Symptoms that may indicate ACS include:

New-onset chest pain or abrupt deterioration in stable angina, with recurrent pain

occurring frequently with little or no exertion and often lasting longer than

15 minutes.”

That description was consistent with what had been noted by Dr Smith in her consultation

notes.

[43] On the hypothesis that it would have been reasonable for her to have reached the

alternative diagnosis of stable angina, then the appropriate treatment would have been the

prescription of GTN spray, low dose aspirin, a beta blocker if no contra-indication, statins,

and “worsening advice” to the effect that in the event of further chest pain with minimal

exertion or at rest, a 999 ambulance should be called.

[44] In relation to the drug therapy offered to the deceased, it was clear that Dr Smith had

prescribed GTN spray. However, Professor Wall did not accept, as having been reasonable,

Dr Smith’s reasons for not prescribing low dose aspirin on the basis that it might cause

indigestion, and that she had not yet reached a certain diagnosis in relation to angina. There

was a need to balance risk and, in that regard, the risk posed by the condition of angina was

potentially very great. To have prescribed low dose aspirin, in these circumstances would

have been standard treatment. No competent general practitioner would not have

prescribed low dose aspirin in these circumstances. If necessary, low dose aspirin could

have been prescribed with other gastro-protective medication to protect the lining of the

stomach. The only reason not to have prescribed low dose aspirin would have been in the

case of the patient being allergic to it.

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[45] In terms of the guidance set out in SIGN 96 “Management of stable angina”, beta

blockers should be used as a first line therapy for the relief of symptoms of stable angina.

That was normal procedure. Professor Wall did not accept, as reasonable, Dr Smith’s reason

for not prescribing beta blockers on the basis that the deceased had been taking salbutamol.

Where the patient was suffering from asthma, that was a contra-indicator for the

prescription of beta blockers, but it was accepted, contrary to the notes made in error in the

deceased’s records, that he had never suffered from chronic obstructive pulmonary disease

(“COPD”). In any event, even if the patient was intolerant of beta blockers, in terms of the

SIGN 96 Guidance, alternatives could be prescribed in the form of rate limiting calcium

channel blockers, long-acting nitrates or nicorandil. There had been no reason not to

prescribe any of these drugs. No reasonably competent general practitioner would have

failed to do so. To do so would have constituted standard management of angina.

Although Dr Smith had been aware that the deceased did not suffer from COPD, she had

noted that he had been “wheezy”. If indeed the deceased had been wheezy at the relevant

time, that would have constituted a contra-indicator for beta blockers, subject to the

available alternatives.

[46] In cross-examination, Professor Wall accepted that before a GP could consider

relevant treatment options, it was necessary to reach a working diagnosis, or a suspected

diagnosis. He did not accept that the deceased’s chest pain could have had a muscular

cause, for the reason that there was no basis for it in the deceased’s notes.

[47] Under reference to his report, at paragraph 6.15, where there was reference to

Dr Smith’s note: “Chest pain - this am - came on after going up and down stairs”,

Professor Wall expressed his view that such activity amounted to minimal exertion. He

accepted that it was possible, in circumstances where the deceased had been carrying cases

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up and down stairs, that muscular pain might have resulted, but, notwithstanding that, he

maintained his view that the fact that chest pain had resulted from exertion was indicative

of angina.

[48] Dr Smith had noted that at that time the deceased had been “not sick or sweaty with

it”. Professor Wall confirmed that such symptoms were associated with heart attack and

ACS, as was vomiting. He accepted that such symptoms were also associated with angina.

The incidence of angina in Scotland was higher than in England and Wales. Under reference

to the SIGN 96 Guidance, the Scottish Health Survey (2003) had reported the prevalence of

angina in males aged 65 - 74 (the deceased’s age group), as 6.7 per cent.

[49] Professor Wall accepted that in determining whether a patient might or might not be

suffering from angina, the history of the patient was critical to an appropriate judgement.

He accepted that Dr Smith had had an advantage in that respect, in that she had had the

opportunity to speak to the deceased, in circumstances where, having been in his presence,

she could assess his presentation and how he was behaving, and had the opportunity to pick

up unspoken signals. He accepted that Dr Smith’s note that the deceased was “just getting

over flu but no cough etc now.” was indicative that she had been considering a chest

infection. He accepted that it was also clear that Dr Smith had been considering the

possibility of a cardiac issue, on the basis that she had noted that the deceased’s father had

suffered a myocardial infarction, and that she had, in the event, referred him for an ECG.

[50] In relation to Dr Smith’s notes of the attendance on Friday 31 December 2010, in

which she had described the pain suffered by the deceased as being “sharp” chest pain,

Professor Wall accepted that the pain associated with angina was often described by patients

as being dull, but in the centre of the chest. He accepted that sharp pain differed from the

classic presentation, but maintained that it did not exclude a diagnosis of angina. In relation

Page 19 ⇓

to Dr Smith’s note that the pain was reasonably localised and was not moving,

Professor Wall accepted that angina was classically associated with radiating pain.

[51] He accepted that on the basis of her conclusions, Dr Smith had put in place a

treatment plan, but he disagreed that its content was reasonable, on the basis that the

deceased had been a man who was physically active, and who could cycle 20 miles

regularly, but was now suffering from chest pain when entering and leaving a loft. These

facts were indicative of something which could be a serious problem.

[52] When producing his report, Professor Wall had been aware of the content of

Mrs Brown’s statement, in particular to the effect that, on Thursday 30 December 2010, the

deceased had attempted to go for a walk but had returned after about two minutes because

of pain and had not gone further than his garden gate, which Professor Wall characterised as

minimal exertion, that, when the deceased had sat down, the pain had gone, that, when he

got up again, the pain returned, and that, on Friday 31 December 2010, the deceased had

again experienced the same pain when getting dressed first thing in the morning.

Professor Wall’s view was that the account by Mrs Brown was a basis for recognition that

the deceased had been continuing to suffer chest pain.

[53] He accepted that Dr Smith’s reference in her notes to the deceased practising his golf

swing, was indicative that she was considering a possible musculo-skeletal failure, and that

her plan to review him on the following Wednesday was part of her treatment plan.

[54] He accepted that, when referring the deceased for an ETT, Dr Smith had indicated

that one reason for urgency was the fact that the symptoms experienced by him had come

on fairly rapidly. In his view, however, when angina was suspected, the referral should

have indicated that the position was urgent rather than “fairly urgent”, as Dr Smith had

stated. Where such referrals were concerned, the standard expectation was that a patient

Page 20 ⇓

might be seen within two weeks or so. On the basis that the need was urgent, the patient

would normally have been seen within a few days. In circumstances in which the timing of

treatment was dependent on the availability of facilities, and the imminent holiday period

would extend from 31 December 2010 until 4 January 2011, Wednesday 5 January 2011 being

the first business day of the year, there had been all the more reason for the provision of

clear worsening advice.

[55] Under reference to Mrs Brown’s description of the deceased’s walk to Mr Campbell’s

home after New Year, he characterised the facts of someone, who could cycle 20 miles

regularly, having to stop because of the onset of pain when walking the relatively short

distance of about quarter of a mile, as being indicative of the onset of chest pain with

minimal exertion.

[56] In response to the suggestion that, in the following days, the deceased’s problems

had reached a plateau in their manifestation, Professor Wall’s view was that the pattern,

correctly stated, was that the deceased had been suffering from chest pain, caused by

minimal exertion, over a period of several days. He accepted that the notes from A&E, at

Belford Hospital, from 6 January 2011, recording one week of chest pain, “much worse last

night”, indicated a period of time extending backwards prior to 31 December 2010, during

which the deceased had been struggling with pain on minimal exertion in circumstances

where the pain resolved with rest, and during which the pattern continued until 1 or

2 January 2011 and possibly until 5 January 2011.

[57] He confirmed that in his view the appropriate diagnosis, as at Friday 31 December

2010, would have been that the deceased had been suffering from chest pain on minimal

exertion and was to be considered as suffering from ACS until proved otherwise,

necessitating the prescription of aspirin, and admission to hospital by 999 ambulance.

Page 21 ⇓

[58] Although in his report, at paragraph 8.9, he had stated that, if Dr Smith’s evidence

that the pain came on after walking for five minutes was accepted, the appropriate diagnosis

would have been one of angina, which would have required referral for an ETT on an urgent

basis, his expressed opinion, that the diagnosis should in fact have been one of ACS, with

immediate 999 admission, was based on the fact that he had taken account of the evidence of

Mrs Brown in relation to her descriptions of the symptoms being experienced by the

deceased. Under reference to his report, at paragraph 8.10, his view was that, had a full

history been taken at the relevant time, the appropriate diagnosis would indeed have been

ACS, provoking an emergency 999 admission. Taking into account Mrs Brown’s evidence,

the deceased had been suffering from chest pain on minimal exertion which fulfilled a

criterion for the diagnosis of ACS. In addition to that, he was critical of Dr Smith on the

basis that she had not given any worsening advice.

[59] He accepted that Dr Smith’s diagnosis, that being the first step necessary before

putting in place a care pathway, was predicated on the information made available to her.

He accepted that, on the information which Dr Smith had noted, that pain was coming on

after walking for five minutes, her diagnosis of angina had been reasonable. Against that

however, on the basis of the additional information provided by Mrs Brown’s evidence, his

view was that Dr Smith had failed to take a full history from the deceased. That additional

information included the fact that the deceased had been suffering from pain on minimal

exertion, as illustrated by his inability to walk beyond the garden gate, and his experience of

pain when getting dressed. He reiterated that his criticisms of Dr Smith were that she had

failed to take a full history from the deceased, in particular in relation to the identification of

precipitating factors, and had failed to give him worsening advice. Dr Smith had failed to

elicit from the deceased what was apparent from Mrs Brown’s evidence. In that context, he

Page 22 ⇓

accepted that he did not know what questions had been asked of the deceased by Dr Smith,

and did not know what the deceased’s actual responses had been.

[60] He accepted that the SIGN Guidelines were more relevant for doctors in Scotland

than the NICE Guidelines, but indicated that the matter was often one of personal

preference. Under reference to SIGN 96 “Management of stable angina”: “Diagnosis and

Assessment”, in a passage which stated:

“Those patients who should be considered for early referral to secondary care

include those with new onset angina and those with established coronary heart

disease with an increase in symptoms.”,

he noted that the reference was to “early” referral, rather than to urgent or immediate

referral. He also accepted that further investigations and treatment, such as angiography

and revascularisation were matters to be considered in the context of secondary care

settings. He also accepted that SIGN 96: “Management of stable angina”: “Establishing a

diagnosis” included the statement that:

“A significant proportion of patients with chest pain may not have angina and

assessment should also try to identify alternative diagnoses at an early stage.”

and further:

“Patients with stable angina are usually managed in the primary care setting, but

may present in a number of health care settings. An initial diagnosis of angina can

be made within primary care but this should be supported by further assessment and

risk stratification, which will normally require specialist input”.

He accepted that Dr Smith’s actions in relation to the deceased were consistent with these

passages.

[61] Under reference to another passage in the same document, at paragraph 2.1.2 to the

effect that: “Angina pain is not usually sharp or stabbing in nature.”, Professor Wall

accepted that Dr Smith’s note of the type of pain being suffered by the deceased was not

suggestive of angina. However, given the deceased’s age, and his experience of central chest

Page 23 ⇓

pain, on exertion, which was relieved at rest, his presentation was so typical of angina that a

diagnosis of angina should have been made until proved otherwise, and his case managed

as such.

[62] He accepted that, on Wednesday 29 December 2010, Dr Smith had apparently asked

the right questions, but maintained that she should have reached a diagnosis of angina until

proved otherwise. On that basis, she should have prescribed aspirin, beta blockers - if not

beta blockers, because of prior aspiratory problems, then appropriate alternative medication

- and statins to lower cholesterol in the pulmonary artery. He accepted that the prescription

of statins might take months to be fully effective. Aspirin acted to stop platelets clumping

and causing clots. It would not be immediately fully effective, but its effect was more rapid

than that of statins. It was recognised that, in such cases, there was a general benefit to be

obtained from the prescription of aspirin.

[63] In relation to a report by Dr Gaskell, dated August 2016, in which it was stated that

Dr Smith had been entitled to diagnose stable angina on the basis that the pain was not

occurring frequently and with little or no exertion, Professor Wall’s view was that

Dr Gaskell’s consideration of the matter had been based only on the evidence of Dr Smith,

who had not taken account of the facts referred to in the evidence of Mrs Brown which

indicated minimal exertion, as illustrated by the deceased’s attempt to reach his garden gate

and his pain on getting dressed. Professor Wall accepted that the reference by Dr Smith to

“sharp retrosternal pain after five minutes” indicated pain on exertion, rather than pain on

minimal exertion. Minimal exertion was characterised by activity less than five minutes’

walk. Whereas Dr Smith had noted a history of pain after five minutes, Mrs Brown had

given a history of the deceased suffering from pain on getting dressed and within the

limited period necessary to reach the garden gate. Any reasonable person would consider

Page 24 ⇓

such activity to be minimal exertion. He disagreed with the suggestion that it would only be

reasonable to expect Dr Smith to have reached a diagnosis of ACS with hindsight. In his

view, had she elicited a full history, she would have reached a proper diagnosis. Her failure

to have taken a full history was significant. Professor Wall’s view was that no doctor of

ordinary competence would have reached a diagnosis of stable angina on the basis of the

facts comprising the evidence of Mrs Brown. Although he accepted that patients would not

always give full answers to questions, he would expect a doctor of ordinary competence to

elicit all the necessary and relevant information.

[64] In re-examination, he accepted that, in essence, the difference between him and

Dr Gaskell on the issue of whether or not Dr Smith was negligent, was the fact that in his

report, at paragraph 5.3, Dr Gaskell had attached weight to the statement that “The pain was

not occurring frequently and with little or no exertion”.

[65] On the question of the efficacy of aspirin, Professor Wall agreed with the statement

in the report by Professor Channer, dated 22 February 2016, at paragraph 4.5, to the effect

that the drug reduced mortality by about 25 per cent when taken by patients in the first

24 hours of acute myocardial infarction, and that the benefit is seen almost immediately on

starting the drug.

[66] He considered that, on the basis of the test set out in the case of Hunter v Hanley 1955

SC 200, if Dr Smith had thought that the deceased was suffering from pain after minimal

exertion, then, that being the definition of what constituted ACS, she should not have

reached any other diagnosis.

[67] (2) Dr Philip Gaskell, General Practitioner, gave expert evidence on behalf of the

defenders, under reference to his report, dated August 2016. He confirmed that, in his

Page 25 ⇓

opinion, in relation to the consultation on Friday 31 December 2010, on the basis of the notes

taken by her, Dr Smith had acted appropriately.

[68] He agreed that the SIGN Guidelines were intended for the Scottish context, and that

the NICE Guidelines had no status in Scotland, but were generally useful. Both sets of

guidelines were in effect appraisals of current medical evidence.

[69] In relation to the consultation on Friday 31 December 2010, he confirmed his opinion

that Dr Smith had been entitled to diagnose stable angina, on the basis that the pain was not

occurring frequently and with little or no exertion. He qualified that by suggesting that in

his view, rather than having reached a working diagnosis of stable angina, she had placed

the possibility that the deceased was suffering from that condition at the top of her list of

differential diagnoses. On that basis, he would have expected her, in 2010, to have referred

the deceased for an ETT as a means of confirmation of such a diagnosis. Her referral in that

regard had been appropriate, as had her prescription of GTN spray. In his view the effect of

an “urgent” referral carried with it the expectation that the patient would be seen within

two weeks. In his view the characterisation of the referral as such, was appropriate. In

contrast an “emergency” referral would have involved the patient being seen on the same

day.

[70] On the basis of the deceased’s records, Dr Gaskell’s understanding of the level of

exertion which provoked the pain being suffered by him, as at Friday 31 December 2010, in

the context of the pain remaining in the same area of the chest, being sharp, and not a dull

ache, being the same as on the previous day, and coming on after five minutes, was of the

onset of pain after exercise, but not after minimal exercise. On that basis the history was

suggestive of stable angina. Although it was necessary for a GP to clarify with a patient the

level of exertion which provoked pain, equally, it was reasonable to assume that not all the

Page 26 ⇓

detail would be recorded. Dr Smith should have checked with the deceased whether, when

walking, he was walking briskly or slowly, or was carrying anything. Generally, however, if

pain commenced after five minutes, in a previously fit man, that was suggestive of angina.

[71] In relation to the medication prescribed by Dr Smith, in 2010, it was the practice to

prescribe GTN spray, in that context, as a test of diagnosis. If the GTN spray relieved pain

within two to three minutes, then that provided confirmation of the existence of stable

angina. Although there had been changes in the recommendations since then, such use of

GTN spray was reasonable at that time.

[72] In relation to the fact that Dr Smith had not prescribed beta blockers, Dr Gaskell

confirmed that would have been the appropriate course where a patient was taking

salbutamol in order to relieve breathing difficulties. There was a risk that, where a patient

had asthma, beta blockers would make the condition worse. In a situation where the

deceased was “wheezy”, it was possible that he was suffering from asthma. His view was

that Dr Smith had chosen to avoid the possibility of complicating the presentational picture.

[73] In cross-examination, Dr Gaskell accepted that although the SIGN Guidelines were

specifically preferable to the Scottish context, the NICE Guidelines were nevertheless still

relevant. He had relied on the terms of both the NICE Guidelines and the SIGN Guidelines

in his own report.

[74] In relation to his conclusion that Dr Smith had been entitled to diagnose stable

angina, he accepted that, had the deceased’s pain been occurring with little or no exertion,

then his opinion would have been different. He accepted that if the deceased had been

suffering pain after getting dressed, that would amount to minimal exertion, which would

suggest a diagnosis of ACS, requiring immediate referral to hospital for same day

assessment. Such a set of facts would be regarded as a major warning.

Page 27 ⇓

[75] He confirmed that it would be normal to ask a patient to return, for early review, if

symptoms worsened. In other words, it would be normal to give the patient “worsening

advice”. He would have expected that advice to have been given on each of the

consultations of 29 December 2010, 31 December 2010 and 5 January 2011. That was normal

practice. In the context of this case, he had simply assumed that it had been done. Although

it was usual to do it, in his view it was not something which was normally recorded. At

paragraph 4.18 of his report, he had stated his conclusion that Dr Smith had acted as an

ordinarily competent doctor exercising reasonable care. In response to a question as to

whether in coming to that conclusion, he had included consideration of the need to give

“worsening advice”, his response was that, in his view, the giving of such advice was not a

requirement for the purposes of ordinary competence. It was normal, but was not a 100 per

cent requirement, particularly in circumstances where GPs often worked under pressure.

[76] In relation to the consultation of Friday 31 December 2010, his understanding was

that Dr Smith had placed stable angina at the top of her list of possible differential

diagnoses.

[77] In relation to the SIGN guidance that beta blockers should be used as a first line

therapy, he agreed with that approach, but qualified it to the extent that such an approach

was only appropriate once a diagnosis had been made.

[78] He did not accept that the prescription of aspirin in such circumstances was the

usual practice in 2010. He indicated that the practice had changed since then.

(ii) Accident and Emergency: diagnosis and treatment

[79] (1) Mr Neil Nichol, consultant in emergency medicine at Ninewells Hospital,

Dundee, and at Perth Royal Infirmary, gave expert evidence for the pursuers under

Page 28 ⇓

reference to his report dated 19 April 2018. Amongst his qualifications, he was the lead

author in the chapter “Causes and Pathophysiology of Cardiac Arrest” in the Oxford

Textbook of Critical Care (1999 ed).

[80] On the hypothesis that the deceased had been first admitted to hospital on Friday

31 December 2010, suffering from chest pain brought on by minimal exertion, his view was

that, since the pain was brought on by minimal exercise, and relieved by rest, the obvious

diagnosis would have been one of ACS, which carried with it the risk of sudden death. In

these circumstances initial treatment within A&E would have comprised the prescription of

aspirin, heparin, GTN spray, together with morphine if the patient was in pain. Thereafter

the patient would have been transferred to an acute medical unit within the hospital. On the

basis that the presentation indicated that blood flow to the heart muscle was critically

impaired, with the risk of progression to acute myocardial infarction (heart attack) or cardiac

arrest due to abnormal heart rhythm, the patient would have been kept in hospital. Blood

tests would have been carried out, beta blockers and statins prescribed, high blood pressure

treated, and an ETT carried out.

[81] If later, say on Sunday 2, or Monday 3 January 2011, the deceased, acting on

worsening advice, had been admitted to hospital following attendance on his own account,

the treatment would have been the same, although, against a background that he had

already been seen by his GP who had given worsening advice, the symptoms exhibited

would have presented an even stronger case for admission.

[82] Under reference to the report by Mr Johnson, consultant in emergency medicine, and

expert witness for the defenders, dated 22 September 2016, at “Opinion”: paragraph (ix), to

the effect that:

Page 29 ⇓

“He should also have been provided with appropriate safety netting advice,

specifically to ring 999 and return to hospital if chest pain returned and did not

respond to GTN and persisted more than 20 minutes or came on frequently or with

no exertion.”,

Mr Nichol agreed that had the deceased presented at hospital with stable angina then on

discharge, he should have been given appropriate safety netting advice. He would have

expected the same advice to have been given by an ordinarily competent general

practitioner. The requirement to do so had been reflected in standard teaching from

the 1980s, and the recommended practice had not changed since then.

[83] He confirmed that the SIGN Guidelines were more specifically tailored for the

Scottish context, than the NICE Guidelines. Both sets of guidelines provided

recommendations for the management of common clinical conditions, based on review of

best practice, on the basis of evidence-based current practice, over a period of up to

five years prior to the guidelines coming into force. Their content provided the baseline

standard for the appropriate management of the clinical conditions to which they referred.

[84] Under reference to the deceased’s hospital records from A&E at Belford Hospital,

when admitted at 10.45am on 6 January 2011, it was noted that his blood pressure (170/80)

was higher than the norm (120/80). The explanation for that was that blood pressure

readings were variable in any event, but were influenced, in particular, by stress, pain, and

anxiety, or even simply by the experience of being in hospital. The fact that the deceased

was experiencing chest pain on admission would have been an explanation for his elevated

blood pressure. Where stenosis (narrowing of the coronary artery) was present, there was a

danger associated with raised blood pressure. The effect of stenosis would be to increase the

work rate of the heart, and therefore increase the necessary oxygen delivery requirement.

Where there was stenosis, the supply of oxygen would be inadequate, which could lead to

Page 30 ⇓

ischaemia and chest pain, in turn increasing blood pressure. Against that background, the

deceased’s blood pressure could have been raised simply by walking up the steps to enter

A&E at Belford Hospital.

[85] In Mr Nichol’s view, the deceased would have been kept in hospital on admission

because of his high risk. The core aims would have been to seek to avoid such stressors, and

indeed anything involving an increase in heart work rate, particularly in the form of

exertion. Mr Nichol’s view was that, had the deceased been kept in hospital, and received

appropriate treatment, and kept at rest, then, on the balance of probabilities, the chances of

him suffering a cardiac arrest on 6 January 2011 would have been reduced, but not excluded

entirely.

[86] Under reference to the document “Acute Coronary Syndrome”, taken from the

Patient.co.uk website, there were two types of non-ST-elevation ACS. The first, unstable

angina, was recognised where no infarction had occurred, and troponin levels were normal.

The second, non-ST-elevation MI (NSTEMI) was recognised where there was a rise in

troponin levels.

[87] In cross-examination, Mr Nichol was referred to his report at paragraph 2

“HISTORY - from medical records”. On admission to Belford Hospital on 6 January 2011,

the ECG carried out had been normal, as was a chest X-ray. Blood samples had been taken

for troponin analysis (paragraph 2.5). Troponin is a protein present in the cells of heart

muscle. When the muscle is damaged the protein is released and can be measured in blood

samples. The resulting values are indicators of the level of damage to the heart muscle.

[88] The reference at paragraph 2.7 to left axis deviation shown on ECG recordings, also

found to be present on previous ECG recordings, was a reference to comparison with an

ECG recording taken in 2009.

Page 31 ⇓

[89] The deceased’s troponin level was found to be within the normal range

(paragraph 2.8). When asked if that was a reasonable basis for the assumption that no

infarction had taken place, Mr Nichol explained that a single measured value of troponin

was of limited assistance in that context. The analysis required to be repeated. It was not

safe practice to assume heart muscle was intact on the basis of only one measure. While the

recorded single value did not indicate myocardial infarction, on the basis of that measure

alone, it was not possible to rule out unstable angina.

[90] At paragraph 2.11, Mr Nichol had noted that subsequently, on that date, the

deceased had suffered a cardiac arrest at home, had been defibrillated six times, but that

ultimately his heart had become asystolic, and he had been pronounced dead shortly

after 4.45pm.

[91] When considering what might have happened if the deceased had been first

admitted to hospital on Friday 31 December 2010, given his history as at that time, including

two prior attendances with his GP, Mr Nichol confirmed that a diagnosis of ACS would

have been considered, would have been treated as a presumptive diagnosis, and the

deceased would have been prescribed beta blockers, and the case assessed by a senior

physician. ACS presented a high risk. Where there was perceived inadequate blood flow to

heart muscle, the aim was to seek to prevent progression to heart attack or potentially fatal

cardiac dysrhythmia.

[92] He agreed that, in general terms, a heart attack was caused by a clot or plaque

causing the heart to be deprived of oxygen. Arrhythmia was a different, but related,

causation. It might result from a heart attack or from a reduction in blood flow.

[93] In response to the suggestion that the cause of death had been arrhythmic sudden

death in the absence of ACS, Mr Nichol disagreed that ACS had not been present. In his

Page 32 ⇓

view it had indeed been present, and the deceased had died because of inadequate blood

flow to his heart. Arrhythmia could be triggered simply by myocardial substrate, and in the

case of the deceased, at post mortem, previous scarring in the heart muscle had been found

together with hypertrophy, and a narrowed coronary artery. He accepted, that in order for

arrhythmia to be induced, something was required to trigger it.

[94] In that regard, where there was a risk of a clot, in the context of a working or

presumptive diagnosis of ACS, the standard approach would be to prescribe medication to

reduce the attendant risk. Medication would involve the prescription of aspirin and

heparin. Beta blockers would have no effect on clotting.

[95] Where there was not a clot present, aspirin and heparin would have no effect. Beta

blockers, on the other hand could assist. They impact on the receptors of heart muscle, to

reduce heart rate and contractility, thus reducing work rate and reducing the level of oxygen

required.

[96] Under reference to paragraph 5.10 of his report, had the deceased been referred to

A&E on Wednesday 29 December 2010 then, in circumstances in which a second troponin

test proved to be normal, in conjunction with a normal ECG, it was probable that the

deceased would have been discharged home for an ETT to be carried out later in

January 2011, having been given appropriate safety net advice.

[97] Under reference to paragraph 5.11 of his report, however, where he had noted the

evidence of Mrs Brown, to the effect that, on 30 and 31 December 2010, the deceased had

been suffering chest pain occurring on minimal exertion, resulting in a return to his GP, the

question of the degree of necessary urgency required to be considered, in the context of the

fact that 31 December 2010 was a Friday and the next four days were public holidays. An

ETT was a procedure which would not be conducted outwith normal working hours. On

Page 33 ⇓

that basis, the deceased would have been kept in hospital, because of his history and the

imminent holiday period, until at least Wednesday 5 January 2011 which would have been

the earliest date for an ETT to be carried out. Another alternative would have been simply

to proceed directly to transfer to an appropriate hospital for angiography. The timing of

angiography would be some days after input by an A&E consultant.

[98] If the resultant angiogram had indicated a cardiac problem, then the most likely

consequence would have been that the deceased would be referred to the nearest cardiac

centre. Meantime, he would have received full anti-anginal therapy. An identified problem

would most likely be treated by dilating the area of restricted blood flow, and implanting a

stent appropriately, all of which could be done simultaneously during angiography.

[99] Although Mr Nichol indicated that he would defer to a cardiologist as to the cause of

death, he was clearly of the view that beta blockers would have served to reduce the risk of

abnormal heart rhythm.

[100] He disagreed with Mr Johnson’s view that if the deceased had attended hospital on

Friday 31 December 2010, been found to have normal troponin levels, and a normal ECG,

had been prescribed aspirin, beta blockers, heparin, and had been given safety net advice,

then, rather than being admitted, if he was asymptomatic, the hospital would have

discharged him home to rest. The basis of Mr Nichol’s disagreement was that the deceased’s

symptoms of experiencing pain at rest and on minimal exertion had been subject to rapid

progression. If, on the other hand, the deceased at that time, had been in a functioning state

such as to be able to walk without chest pain, then in these circumstances, discharge home

might have been a possible consideration.

[101] At A&E, it had been noted that the deceased was suffering pain at rest on Tuesday

4 January 2011. It was already known that the deceased had suffered pain on minimal

Page 34 ⇓

exertion, in failing to reach his garden gate. These were circumstances of minimal exertion.

In the context of the evidence of Mrs Brown that, after Hogmanay, the deceased, although

having to stop regularly, was able to walk a quarter of a mile, Mr Nichol’s view was that in

the context of covering 440 yards, but having to stop a number of times because of pain,

such activity should be properly characterised as minimal exertion.

[102] In re-examination, he confirmed that stenosis of the coronary artery, resulting in a

reduced blood supply to the heart, would cause pain and could trigger arrhythmia, leading

to death. The onset of arrhythmia required a trigger, which could be a clot or something

else. Where there was no clot, the prescription of aspirin would make no difference, but the

prescription of beta blockers would be effective. Bed rest in hospital would be indicated

regardless of any trigger.

[103] Discharge from hospital would be appropriate only where the patient was able to

exercise and remain pain free. Given the known extent of the deceased’s stenosis, the

question of whether appropriate drug therapy would have made him sufficiently pain free

to allow his discharge, could have been answered only after a trial period to assess his

functioning.

[104] He confirmed that the prescription of aspirin, including in general practice, for cases

of ACS was standard practice for some years prior to 2010.

[105] (2) Mr Graham Johnson, consultant in emergency medicine at St James’s Hospital,

Leeds, was interponed to give expert evidence on behalf of the defenders, under reference to

his report dated 22 September 2016.

[106] He agreed with Mr Nichol that, on the assumption that the deceased had attended

hospital some time after 4.30pm on Friday 31 December 2010, presenting with pain in his

chest on minimal exertion, which resolved with rest, then, at A&E, a presumptive diagnosis

Page 35 ⇓

of ACS would have been appropriate. He agreed that the appropriate treatment would have

been further investigation in the form of an ECG, and the taking of troponin levels, the

prescription of aspirin or other anti-platelet therapy, and heparin as an anti-coagulant agent.

Beta blockers would not have been appropriate where COPD was a factor. Pain relief would

have been prescribed as appropriate.

[107] With such a presenting history, suggestive of ACS, the appropriate treatment plan

would have involved referral to a cardiologist or, in the case of Belford Hospital where no

cardiologist was available, to the appropriate senior physician on call. An appropriate plan

would have been to admit the deceased, not necessarily for bed rest but to exclude exertion,

with ongoing review of medication. The intention would be to confirm coronary heart

disease by means of an ETT, and thereafter to determine its severity. Where there was an

abnormality, the intention would be to define by angiogram, in a cardiology department, the

position of any blockage in the coronary artery. In circumstances where there was no local

cardiology department and, because of the time of year, a resultant delay in carrying out an

ECG, emphasis would be placed on assessing the appropriate necessary medication, prior to

confirmation of the diagnosis. In that regard, beta blockers would be expected to reduce

chest pain in a period of 24-48 hours. The anticipated effect of aspirin would be on a similar

timescale.

[108] In a normal week, the deceased once in hospital, would have been retained as an

in-patient until an ETT had been carried out. In the particular circumstances of his case,

where the weekend was imminent and where in addition, because of the time of year, public

holidays would intervene, where an ECG could not be carried out before the elapse of say,

two to three days, then it was likely that he would have been sent home. That would have

been subject to an assessment of how he was responding to medication. He would have

Page 36 ⇓

been discharged home only on the basis that as a result of the medication, his suffering had

been reduced to an acceptable level.

[109] The incidence of ACS was relatively common. It occurred in two to four per cent of

patients subject to investigation for possible cardiac chest pain.

[110] Although there were three main types of ACS, all presenting with different risks, the

deceased’s presentation was either non-STEMI ACS, or unstable angina. Which diagnosis

was appropriate was dependent on troponin results. In the case of both there was a

recognised variable potential to progress to myocardial infarction and death. The risk was

broadly one of five per cent over 14 days.

[111] In re-examination, Mr Johnson accepted that although that risk was statistically

relatively small, it was nevertheless significant, since it involved the risk of death. It was not

a risk to be taken lightly.

[112] He accepted that where no COPD was present, beta blockers were an appropriate

medication. That would be the case even where the patient, in the absence of COPD was

“wheezy”. In any event, even if there were contra-indicators, alternatives to beta blockers

were available. He agreed that the alternatives of rate limiting calcium channel blockers,

long-acting nitrates or nicorandil, were all reasonable alternatives.

[113] On the basis of the post mortem results, Dr Johnson’s view was that had the deceased

undergone an ETT, its results were unlikely to be normal or, expressed differently, were

likely to be abnormal, and would have triggered referral for angiography.

(iii) Cardiology

[114] (1) Professor Stephen Brecker, Chief of Cardiology at St George’s University

Hospitals NHS Foundation Trust and St George’s, University of London, and Consultant

Page 37 ⇓

Cardiologist at St George’s Hospital, London, gave expert evidence on behalf of the

pursuers, under reference to his report, dated 24 April 2016.

[115] Both he and Professor Channer, the expert witness on cardiology for the defenders,

at a joint meeting held in London on 23 November 2017, had agreed, in terms of their joint

report dated 28 November 2017, that the deceased’s death was caused by changes in the

rhythm of his heart, leading to ventricular fibrillation, possibly having involved preceding

patterns of ventricular tachycardia or arrhythmia. The likely cause of the ventricular

fibrillation was ischaemia, caused by reduced blood supply to the heart muscle, brought

about by stenosis. All of that had been the subject of agreement between Professor Brecker

and Professor Channer.

[116] They did disagree, however, on the issue of the diagnosis which should have been

made in advance of death. Although they agreed that the deceased had been suffering from

ACS, in the form of unstable angina, they disagreed on the timing of the commencement of

the condition.

[117] Under reference to the document “Acute Coronary Syndrome”, located on the

Patient.co.uk website, Professor Brecker confirmed that there was a spectrum of clinical

presentation of coronary disease, which included asymptomatic conditions, stable angina, or

acute coronary syndrome (ACS). Of the two principal classes of ACS the one which was

pertinent to the deceased’s case was non-ST-elevation ACS (NSTE-ACS), which was further

divided into (a) non-ST-elevation MI (NSTEMI), characterised by elevated troponin levels,

and (b) unstable angina, characterised by relatively normal troponin levels.

Professor Brecker and Professor Channer had agreed that, by Wednesday 5 January 2011,

the deceased had been suffering from unstable angina.

Page 38 ⇓

[118] In the context of the attendances made by the deceased on Dr Smith, three scenarios

were put to Professor Brecker:

1. The deceased was referred by his GP for same day assessment to Belford

Hospital on Friday 31 December 2010:

In such a situation the standard treatment would have included assessment in A&E,

including if required, contact with the intake medical team and a cardiologist if one

was present. A diagnosis of ACS should have been made. In a situation where

unstable angina was diagnosed at A&E, but no cardiologist was present, then a

referral would have been made to the senior physician, for confirmation of the

diagnosis as between NSTEMI and unstable angina. The deceased would have been

admitted unless, on appropriate medication, he would have been able to exercise

without pain. In the case of the deceased, that would have been unlikely in

circumstances where, on the basis of the post mortem results, he was at that time

suffering from severe main stem coronary artery stenosis. That would have made it

unlikely that he could exercise even only to the extent of minimal exertion, without

pain. On referral to a senior physician, the deceased would have been admitted,

intravenous access obtained, and anti-platelet and anti-thrombotic drugs

administered, together with aspirin, or an appropriate alternative, to put in place

dual anti-platelet therapy. It would have been standard practice to prescribe beta

blockers in order to reduce his cardiac workload. He would also have been

prescribed vasodilators, to increase blood supply, by widening the coronary artery

and reducing demand on the heart. In this context, nitrates and calcium channel

blockers would have been prescribed in addition to beta blockers. If the deceased

had been continuing to experience pain at rest, intravenous nitrates would have been

Page 39 ⇓

administered. In addition, he would have been given injections of anti-thrombotic

drugs, such as heparin or similar, and would have been started on other drugs with

longer term effects, such as statins to reduce cholesterol levels, and vasodilators such

as ACE inhibitors. All of that would have been standard practice. Had the deceased

received such treatment on Friday 31 December 2010, it is likely that significant

difference would have been made to the supply to and demand on his heart, and that

his level of ischaemia would have been reduced.

2. The deceased was admitted to Belford Hospital on Saturday 1, or Sunday

2 January 2011, having previously received, and acted upon, safety-netting advice

given on Friday 31 December 2010:

In this situation, where the deceased had presented himself to hospital, there would

be no difference from the first scenario. He would have received the same treatment,

with the same effect. The likely outcome would have been the same, resulting in a

reduction in ischaemia over the course of the treatment. A further factor to be taken

into account was that, following admission to hospital, the deceased would have had

several days of treatment involving a combination of therapy and rest in hospital, as

a consequence of which, in Professor Brecker’s opinion, the likelihood of ventricular

fibrillation, would, on the balance of probabilities been removed. The combination

of all of these measures would have removed the ischaemic provocation, which

resulted in ventricular fibrillation, or would have significantly relieved it. In that

context, where stenosis was present, another factor was generally required to trigger

arrhythmia and cardiac arrest. It was not always possible to identify what was that

triggering factor. Ventricular fibrillation was not always predictable. It was

predictable in patients known to be at risk, but the provocative event triggering it

Page 40 ⇓

might not be discernible. In the deceased’s case there had been sufficient substrate,

in the form of stenosis, to trigger ischaemia and sudden death.

3. The deceased was admitted to Belford Hospital, following referral by his GP

on Wednesday 5 January 2011, with a diagnosis of unstable angina:

In that scenario, the treatment would again have been the same as that in respect of

the first scenario. The difference however between the third scenario and the first

two scenarios related to the likely outcome. In the first and second scenarios, the

outcomes were dependent upon the presence of an appropriate therapeutic level of

drugs in the deceased’s blood stream, and the availability of sufficient time for these

medications to take effect. On the basis that such an appropriate period of time was

available, these drugs would have reduced his level of ischaemia. As far as the third

scenario was concerned, where there was a more limited period of time available,

until the critical date of 6 January 2011, it was not possible to say that the risk of

ischaemia could have been avoided. The risk of ischaemia would have been

reduced, but it would not be possible to conclude that in a limited timescale the

medications administered would have achieved their maximum effect. The drugs

would have had some effect, which would have been more than negligible. The

effect of the medication would have been not insignificant, but it was not possible to

say its effect would be more than 50 per cent likely to have achieved its desired aim.

[119] In a situation where the deceased’s condition had been deteriorating over several

days, these several days would have been available for the appropriate drugs to take full

effect. Therefore, had he been admitted on Friday 31 December 2010 or Saturday 1, or

Sunday 2 January 2011, ventricular fibrillation would probably have been avoided. That

was to be contrasted with the scenario in which he had been admitted on 5 January 2011, in

Page 41 ⇓

the context of which all that could be said was that there would have been a continuing

reduction in his level of ischaemia. It was also significant that, in relation to the first and

second scenarios, at the time when medication would have been commenced the deceased

would have been in better physical condition, and would have responded better to

medication than would have been the case by Wednesday 5 January 2011, by which time he

would have deteriorated and would have been experiencing more frequent and prolonged

pain.

[120] Professor Brecker fundamentally disagreed with Professor Channer’s view that the

deceased had been suffering from stable angina on Wednesday 29 December 2010,

progressing to unstable angina on Wednesday 5 January 2011. In so far as the deceased’s

condition on Wednesday 29 December 2010 was concerned, it was not possible to

characterise it as stable where there had been no known period of stability. Such a diagnosis

could only be made in circumstances whereby it was known that the condition had not

changed over time. It was not possible to characterise a condition as stable in a period of

only a few days. A better description would have been to characterise the condition as

“recent onset angina”. But notwithstanding that, however, where it was plain that pain was

brought on by minimal exertion, the correct diagnosis was unstable angina.

[121] Professor Brecker did not accept a progression which began with stable angina,

developing into unstable angina, and resulting in death within a matter of days. In the

context of ACS, a better and more logical analysis was that the angina being suffered by the

deceased had been unstable from its commencement. It was relevant to note that patients

with stable angina could remain stable for years. The fact that the deceased had previously

been fit and healthy was a further significant factor. Given his prior state of health, it was

clear that, in relation to his heart function, something had changed.

Page 42 ⇓

[122] Professor Brecker adhered to the terms of his report, dated 24 April 2016. Nothing

had come to his attention, since then, which had altered his view as there expressed.

[123] He accepted the view expressed by Professor Pounder, consultant pathologist, to the

effect that the deceased’s fatal cardiac event had not had a thrombotic cause, but rather was

the result of vasoconstriction, in combination with a provocational trigger, as being very

plausible. He also accepted that exposure to cold could have constituted the provocational

trigger. It was recognised that cases of stable angina in which pain was brought on by

exertion, specifically in cold weather, were common. Further, had the deceased been

admitted to hospital at an earlier stage, he would not have been exposed to cold, the

provocation to vasoconstriction would have been removed and, as a result, in all probability,

there would have been no ventricular fibrillation. He confirmed however that although he

regarded the suggestion by Professor Pounder as a plausible explanation, it did not alter his

own opinion.

[124] In cross-examination, Professor Brecker was referred to the A&E notes relating to

the deceased’s attendance at Belford Hospital on Thursday 6 January 2011. The noted

history indicated that there had been one week of chest pain induced by exercise, following

an episode of flu-like symptoms. Pain had been much worse “last night”, when at rest.

Professor Brecker accepted that the terms of the history indicated a change in symptoms,

from what had previously been the case. He attached importance to what had been noted,

as the described symptoms were significant and plainly worse than had been the case.

Where there was pain at rest, it would be appropriate to consider the possibility of

myocardial infarction.

[125] He did not consider that the described symptoms were such as to raise the

immediate possibility of coronary vaso-spasm. That was on the basis that pain at rest was a

Page 43 ⇓

classic symptom of ACS which would prompt consideration rather of coronary artery

disease. In relation to that, on the suggestion that there was a dispute between him and

Professor Channer in relation to whether the deceased’s condition had been ACS,

Professor Brecker indicated that not to be his understanding. Professor Channer had told

him that his view was that the deceased had been suffering from ACS on Wednesday

5 January 2011.

[126] Pure coronary spasm was a rare condition in the absence of coronary disease.

Against that, however, cardiac pain at rest was a recognised classic symptom of ACS.

Although spasm was an alternative possible cause of cardiac chest pain at rest,

Professor Brecker doubted that, clinically, a differentiation could properly be made between

cardiac pain at rest in the absence of ACS, and unstable angina.

[127] Under reference to Professor Channer’s report, dated 22 February 2016,

Professor Brecker considered that it was possible that Professor Channer may have been

using the term “ACS” to describe only troponin positive syndromes, and was removing

unstable angina from that class of conditions. Be that as it may, unstable angina, involving

normal troponin levels and chest pain was generally considered to be part of the recognised

category of ACS.

[128] Professor Brecker did not accept that his opinion, on the possibility of the deceased

surviving with appropriate treatment, was predicated on the cause of death having been

caused by a blood clot. Rather, his view was that death had been primarily caused by

ischaemia in conjunction with other factors. It was significant that no clot had been found

post mortem. Notwithstanding that, it was possible that there had been microscopic clots

which had contributed to death, but Professor Brecker’s opinion did not depend on that

having been the case. In his view the primary cause was ischaemia.

Page 44 ⇓

[129] Under reference to the joint report by Professor Brecker and Professor Channer dated

28 November 2017, at Question 4, Professor Brecker had referred to an article “The

Pathophysiology of Acute Coronary Syndromes”, by Davies, in which it was stated:

“A significant proportion, but not all, of samples from unstable angina contain

thrombus, while most samples from stable angina, but not all, do not contain

thrombus. The absence of thrombus in unstable angina is in part related to the time

delay between acute symptoms and atherectomy.”

Whereas it appeared that Professor Channer was excluding unstable angina on the basis that

no thrombus was present, Professor Brecker had referred to the article, as support for his

opinion that the deceased had been suffering from unstable angina, on the basis that it

indicated recognition, following research, that in ACS, presenting as unstable angina,

thrombus need not necessarily be present. On that basis, Professor Brecker’s opinion was

not dependent on the presence of thrombus.

[130] Against that background, at paragraph 6 of the joint report, Professor Channer had

stated that, on Wednesday 5 January 2011, the deceased had reported pain when at rest,

which would be compatible with the diagnosis of unstable angina. Further, at Question 8,

Professor Channer had stated, in relation to the attendance at A&E on 6 January 2011:

“Troponin was negative so the final diagnosis of 6 January 2011 was troponin negative

unstable angina. An elevated troponin level would be expected in patients suffering

from an ACS.”

On the basis of these two contradictory positions, Professor Brecker characterised

Professor Channer’s approach as being inconsistent. Professor Channer’s approach

appeared to be that unstable angina should be excluded where there is no thrombus, but

also that, notwithstanding the absence of thrombus, the deceased was suffering from

unstable angina.

Page 45 ⇓

[131] Under reference to an article relied upon by Davies, as support for the statement in

his article, Professor Brecker accepted that the evidence justifying Davies’ conclusions had

been based on conditions in living patients. It was stated in the article relied upon by Davies

that:

“There are a number of possible explanations for the absence of thrombus in

atherectomy samples taken from unstable angina patients. One explanation is that

pure coronary spasm may have been responsible for the angina.”

Another explanation was that, over the passage of time, the body was able to break down a

thrombus. Professor Brecker accepted that such a situation was different from that where

there was post mortem examination following recent death, in the course of which it would

be routine to identify any blood clots. Although Professor Brecker accepted that the

statement in the Davies article was based on research involving living patients, he

maintained that there could be many explanations why no thrombus might be present in

cases of angina. Clearly the question of time-interval absorption by the body could not

apply where death occurred, but other explanations such as pure coronary spasm or a clot

missed in the course of post mortem examination, were other possible explanations.

[132] Professor Brecker accepted that in a situation where no clot had been present,

prescription of aspirin would have had no effect. In such circumstances, he also accepted

that blood thinning products would have had no effect on the deceased. He maintained,

however, that even where there was no blood clot, the prescription of beta blockers would

have had some immediate anti-arrhythmic effect but, in particular, would have served to

reduce cardiac demand and workload.

[133] He accepted that it was possible for ventricular fibrillation to occur without a

provocational trigger. In the circumstances of the deceased’s case, in the absence of a clot, a

provocational trigger could have been constituted by what appeared to be a clear substrate

Page 46 ⇓

for ischaemia, that being 70 per cent stenosis of the left main stem coronary artery in

conjunction with pain on minor exertion. Such facts would tend to suggest a conclusion of

resultant ischaemia. In the circumstances of sudden cardiac death, it was logical to link

ischaemia as the causative factor for ventricular fibrillation. Where there was 70 per cent

stenosis of the left main stem coronary artery, significantly reducing supply to the left

ventricle, it would not be reasonable to suggest that stenosis and the resulting ventricular

fibrillation were not related. In general, left main stem disease would be regarded as a red

flag warning to any cardiologist.

[134] In considering whether beta blockers would have impacted on the effect of stenosis,

Professor Brecker took into account the high level probability that ischaemia had triggered

the ventricular fibrillation. Where ischaemia was brought about by stenosis, whether or not

in circumstances involving a blood clot or spasm, beta blockers would serve to reduce the

level of ischaemia by reducing the cardiac workload. In his view, the administration of beta

blockers would have served to reduce the overall level of ischaemia to significant effect.

[135] Professor Brecker accepted Professor Channer’s view that beta blockers would have

no effect on spasm as a causative factor for ventricular fibrillation. It was significant,

however, that the administration of nitrates can relieve spasm.

[136] Professor Brecker differed from Professor Channer in his stated view that the only

mechanism for cardiac chest pain at rest, absent ACS and unstable angina, was spasm. In

Professor Brecker’s view that was but one mechanism. Relevant texts all indicated that ACS

could be defined by coronary pain at rest. Where there was cardiac chest pain without

coronary disease, the appropriate descriptor was “vasospastic angina”. In the case of the

deceased, however, it was known that he had coronary disease.

Page 47 ⇓

[137] It was not possible to offer an opinion on the isolated effect of beta blockers on

patients with ACS because all of such patients would necessarily be simultaneously

prescribed all the other necessary medications to treat their condition. It remained

Professor Brecker’s view, however, that the medication which the deceased would have

been prescribed in hospital, as treatment for ACS, together with the fact of simply being in

hospital, would, on the basis of his clinical experience and on the balance of probabilities,

have prevented ischaemia and therefore ventricular fibrillation. He accepted that, given the

limitation on assessing the effect of beta blockers in isolation, it was at least theoretically

possible that such patients would survive in any event, even if beta blockers had not been

prescribed. He thought that more likely, though, where a presentation different to that of

the deceased was the case. Here, the deceased had the classical substrate for ischaemia and

sudden death, in the form of left main stem coronary artery stenosis. That comprised the

condition clinically most associated with sudden death, and indeed was known colloquially

in the profession as “the widow maker”.

[138] In so far as the timing of the effect of medication was concerned, Professor Brecker

considered that the relevant period was probably one of about three days. Thus, if the

deceased had been admitted to hospital on Friday 31 December 2010, death on Thursday

6 January 2011 would have been avoided. Where the effect of medication had been over the

period of only one day, it was not possible to say that the medication would have made a

50 per cent difference. Although, after administration, drugs such as aspirin, beta blockers

and nitrates would have had a material effect on the level of ischaemia within hours, on the

balance of probabilities about three days would have been required as the minimum period

to achieve alteration of the eventual outcome.

Page 48 ⇓

[139] On the hypothesis that the deceased was suffering from ACS on Wednesday

29 December 2010, the differences between Professor Brecker and Professor Channer, as to

the probable cause of ACS in his case, were set out in their respective answers to Question 7

in their joint report dated 28 November 2017.

[140] Professor Brecker accepted that it would not have been appropriate to administer

intravenous nitrates in hospital where the patient was pain free at rest. If a patient

presented with a history of pain at rest, intravenous administration of nitrates would be

appropriate on admission, but subject to discontinuation when the patient became pain free.

[141] In re-examination, Professor Brecker noted that Professor Channer had stated in his

report, dated 22 February 2016, at paragraph 6.1, that the deceased had died following

cardiac arrest after a short history of unstable angina. Unstable angina was a form of ACS.

[142] In their joint report, in answer to Question 8, Professor Channer had stated that the

deceased’s history at Friday 31 December 2010, of exercise related chest pain, was

compatible with a diagnosis of angina, and that his reported chest pain at rest on 5 January

2011 was compatible with a diagnosis of unstable angina. Professor Brecker agreed that

recognition of unstable angina was a clinical diagnosis rather than a pathological one.

[143] Although Professor Channer held the view that the deceased’s post mortem

examination excluded ACS, he had also stated that the deceased was suffering from

unstable angina. Professor Brecker’s response was that although, at times,

Professor Channer appeared to seek to exclude unstable angina from the general class of

ACS , equally his position seemed to be that since there was no ACS, there was no unstable

angina.

[144] Professor Brecker confirmed that his opinion was not dependent on the existence of a

thrombus. Rather, his view was that the deceased had been suffering from ACS and that

Page 49 ⇓

appropriate treatment would have prevented ischaemia and therefor ventricular fibrillation.

In his answer to Question 4 of the report of his joint meeting with Professor Channer,

Professor Brecker had stated that, although in ST-segment elevation myocardial infarction

(STEMI) one would expect to find thrombus, in unstable angina thrombus may or may not

be present. In that respect, the absence of thrombus was not conclusive. It was also

significant that thrombus was something discoverable only post mortem. It was not possible

to know of the existence of thrombus in life.

[145] It was significant that in his experience, with appropriate treatment, the majority of

patients presenting with left main stenosis and ventricular fibrillation survive.

[146] (2) Professor K S Channer, Honorary Professor of Cardiovascular Medicine, Sheffield

Hallam University, Consultant Physician and Cardiologist, gave expert evidence for the

defenders under reference to his report, dated 22 February 2016, and the report of the joint

meeting between him and Professor Brecker, held on 23 November 2017.

[147] He was asked to consider a set of circumstances in which, at some time between late

afternoon on Friday 31 December 2010 and midnight on Sunday 2 January 2011, the

deceased had been admitted to hospital with a diagnosis of ACS. He accepted that in such

circumstances, standard treatment would have been as described by Professor Brecker,

including the administration of beta blockers. On that basis, where the risk was of

myocardial infarction, caused by a blood clot, beta blockers would have been given early in

order to reduce the risk of death by 10-15 per cent, but the benefit was not acute and risk

reduction occurred only after 15 days. If the risk had been ventricular fibrillation, then there

was evidence that beta blockers did not significantly reduce risk until the elapse of six days

from the occurrence of myocardial infarction. Reference was made to the MIAMI study,

reported in the European Heart Journal (1985). Where cardiac arrhythmia had occurred, in

Page 50 ⇓

the absence of myocardial infarction, there was no evidence that beta blockers would reduce

the risk of sudden death, except in cases of a severely damaged heart.

[148] In cross-examination, Professor Channer stated that he had retired from clinical

practice in the NHS in April 2012, and that since 2014 he had been engaged only in

medico-legal matters. He had not been involved in the clinical treatment of NHS patients

for over six years. He was instructed in medico-legal matters principally on behalf of

defenders. Over a recent period of 12 months, less than 20 per cent of his reports had been

instructed on behalf of claimants. He accepted that he had a reputation for being supportive

of doctors, and that he sat on the Council of the Medical Defence Union. He accepted that a

style report, produced by him, and dating from 2012, but similar to the report prepared by

him for the present case, was available on the internet, but that he had not published any

corresponding style report appropriate for a claimant’s case.

[149] He accepted that unstable angina was a form of ACS, or at least, was one of the

manifestations of ACS. Under reference to the paper “Acute Coronary Syndrome” available

on the Patient.co.uk website, a paper he had not previously seen, he accepted that unstable

angina was characterised by normal troponin levels.

[150] In his view, ACS involved acute pathology, most commonly in the form of a

ruptured plaque in the coronary artery, with associated thrombus. ACS could be caused by

unstable angina, involving pain at rest, but could also be caused by coronary artery disease

in association with thrombus. There were two types of unstable angina. In terms of the

NICE Guideline 2010, as set out in the report of the joint meeting between him and

Professor Brecker:

“The term ‘acute coronary syndrome’ encompasses a range of conditions from

unstable angina to ST-segment elevation myocardial infarction (STEMI), arising from

thrombus formation on an atheromatous plaque.”

Page 51 ⇓

ACS was therefore a coronary event involving thrombus formation on plaque rupture. He

did not agree that ACS was a clinical diagnosis rather than a pathological one. When

referred to the joint report, where the NICE Guidelines, at paragraph 1.2.1.3, were quoted to

the effect that, of the symptoms which may indicate ACS, one set was:

“New onset chest pain, or abrupt deterioration in previously stable angina, with

recurrent chest pain occurring frequently and with little or no exertion, and with

episodes often lasting longer than 15 minutes.”,

he agreed that, on that basis, unstable angina was a clinical diagnosis based on exhibited

symptoms.

[151] Where, as in the present case, at post mortem examination there had been no evidence

of thrombus in the coronary artery, there was no pathology for the most common cause of

unstable angina. Nevertheless, it was possible that the deceased could have been suffering

from unstable angina by Wednesday 5 January 2011, without such pathology. Where that

was the case then, prior to that date, the deceased would have been suffering from recent

onset angina. His understanding was that the deceased’s unstable angina, involving pain at

rest, had developed on 5 January 2011, and that before that his angina had been brought on

by exercise. With hindsight, he considered that when the deceased attended his GP,

complaining of chest pain on exercise, on Wednesday 29 and Friday 31 December 2010, he

had been suffering from angina. He characterised pain on minimal exertion as angina,

rather than unstable angina. Where “crescendo” angina was experienced, the condition fell

to be characterised as unstable angina.

[152] At paragraph 2.6 of his report, Professor Channer had noted on that, on Friday

31 December 2010, the deceased had reported chest pain which was sharp and retrosternal,

lasting five minutes, precipitated by walking. He had assumed that what was being

Page 52 ⇓

described was normal walking. In contrast, what Dr Smith had noted at the consultation

was “chest pain, as last Wednesday - went for a walk yesterday - sharp retrosternal pain

after 5 mins”. He accepted that what had been recorded was pain after five minutes of

walking, rather than pain lasting five minutes. When asked whether he would define

walking for 5 minutes as minimal exertion, his response was that any answer would depend

on the definition of “minimal”. He accepted that unstable angina was defined by pain at

rest, or pain of a crescendo pattern, which was getting worse. His preference was to

describe the condition of experiencing pain after minimal exertion as new onset exercise

related angina. He accepted that a pattern of changing pain on walking was crescendo in

nature. Where the pattern of pain changed on exercise, and became crescendo in nature,

that fell within the pattern of unstable angina.

[153] Under reference to his report at paragraph 3.6 “Unstable angina or acute coronary

syndrome”, he had characterised ACS as being caused by a sudden reduction in coronary

blood flow because the narrowed artery had been intermittently blocked by a thrombus or

clot attached to the atheromatous deposit or plaque, resulting in the heart muscle being

acutely starved of blood.

[154] At paragraph 3.7, under reference to the European Society of Cardiology

(“ESC”) ACS guidelines 2007, he had stated that in most cases of unstable angina, the chest

pain occurs at rest, and that, by definition, the pain must last for more than 20 minutes for

the diagnosis of unstable angina to be accepted. When referred to the ESC ACS

guidelines 2007, at page three, he accepted that the reference to persistent pain lasting more

than 20 minutes was in relation to ST-elevation ACS which was not the condition from

which the deceased had been suffering. At page six, paragraph 4.1, of the ECS ACS

guidelines 2007, the clinical presentation of NSTE-ACS was described as including

Page 53 ⇓

prolonged (more than 20 minutes) anginal pain at rest, but also three other separate sets of

exhibited symptoms. His explanation for not including the other three presentations at

paragraph 3.7 was that the most common presentation involved chest pain at rest for more

than 20 minutes. He characterised the other presentations as being not common. He

accepted that in considering unstable angina, he would not exclude the other presentational

patterns. He accepted that the deceased had been suffering from severe angina. He

accepted that, since that was one definition of unstable angina, the deceased had been

suffering from unstable angina.

[155] At paragraph 3.14 of his report, he had stated that in about two thirds of cases of

sudden coronary death, the death had occurred as a consequence of an acute coronary

syndrome, having occurred in the early stage of a thrombotic occlusion of the artery. He

accepted that only in the last sentence of the paragraph had he stated that, overall, sudden

death is the first and fatal manifestation of coronary artery disease in about one third of

cases. He confirmed that such cases would involve no evidence of thrombus, and that death

most probably resulted from malignant arrhythmia.

[156] At paragraph 4.19 of his report, in relation to the question of whether Dr Bawa had

been negligent in discharging the deceased from hospital on Thursday 6 January 2011, while

he considered that a diagnosis of unstable angina would have been reasonable, his opinion,

nevertheless, was that she had not breached her duty of care by discharging him. That was

contrary to the opinions of Dr Johnson and Mr Nichol, both accident and emergency

consultants, and contrary to an admission of liability, made earlier in the case, by Dr Bawa’s

employers. Against that, Professor Channer maintained that he had reached his own

opinion on the matter.

Page 54 ⇓

[157] He agreed that the case of the deceased involved a longstanding condition

comprising stenosis of the left main stem coronary artery, left ventricular hypertrophy, and

scarring from previous endocardial changes, in an active man who had previously lived

asymptomatically, impacted by a trigger which had caused arrhythmia, leading to death, in

the absence of thrombus. He agreed that in those circumstances, an appropriate trigger was

necessary for death to result. He agreed, in particular, that the condition had progressed to

ischaemia and that something would have been required to trigger arrhythmia. He accepted

that although thrombus was one possible trigger, it was not the only cause, and that one

third of comparable cases had other pathology. He accepted that the four precipitating

factors identified by Professor Pounder, being exercise, significant emotion, exposure to

cold, and ingestion of a large meal, were factors which could promote the occurrence of

unstable angina.

[158] On the hypothesis that the deceased had been admitted to hospital with unstable

angina, notwithstanding a normal ECG result and negative troponin, the standard treatment

to be expected would have involved the administration of aspirin, anti-platelet medication,

heparin statins, beta blockers and nitrates. He accepted that beta blockers have an

anti-ischaemic effect, the maximum effect of which occurs within two to three days of

administration. Calcium channel blockers would not have been administered unless there

was a contra-indicator for beta blockers. Beta blockers reduced demand on the heart,

correcting any supply/demand imbalance likely to cause ischaemia. Pain relief would have

reduced the risk of arrhythmia where the patient was experiencing continuous pain. Pain

was associated with sympathetic activation that caused vasoconstriction and increased the

workload of the heart (ESC-AMI guidelines 2012, at paragraph 3.2). Accordingly, the

administration of pain relief would reduce the risk of ischaemia. He accepted that a

Page 55 ⇓

combination of all of the above treatments would have had the effect of reducing ischaemia

which in turn would have reduced the risk of arrhythmia.

[159] Whether any failure to provide such treatment in the case of the deceased had

contributed to the development of ischaemia was dependent on how long he might have

been in hospital. Where an ETT or angiogram had disclosed a significant problem, he would

have been referred for surgery and would most likely have survived. His experience was

that, of patients presenting with stressors similar to those impacting on the deceased, who

received such treatment, the majority would survive. Given the obvious prohibition on an

unethical trial, there was no evidence to indicate the proportion of such patients who would

survive without such treatment.

[160] In re-examination, on the hypothesis that the deceased had received such treatment

on the basis of a diagnosis of ACS, in circumstances where in fact he was suffering from a

different condition, Professor Channer’s view was that in circumstances where the standard

treatment for ACS was administered, all of the drugs prescribed to treat thrombus, that is to

say aspirin, heparin and anti-platelet therapies, would have had no effect. That would leave

anti-ischaemic drugs such as beta blockers, and nitrates which were vasodilatory. If the

deceased had presented at hospital on Friday 31 December 2010, Professor Channer

anticipated that if he was experiencing severe exercise related pain, which came on early but

without pain at rest, then the clinicians would be looking for ACS confirmation by means of

ECG and troponin testing. If these tests had produced abnormal results he would have been

admitted. His presentation would have suggested cardiac pain but the employment of these

risk stratification tools would have been necessary for a fuller understanding of his

condition.

Page 56 ⇓

[161] Where there was no diagnosis, and he might have been suffering chest pain for some

reason other than ASC, then, subject to a medical test, he would have been treated on a

putative diagnosis of angina, but not kept in hospital if his ECG and troponin levels were

normal. Such results would have indicated a low risk.

[162] In the absence of a blood clot, a possible pathological mechanism which could have

resulted in the necessary provocation to induce arrhythmia could have been the blocking of

the critical artery by spasm, which could have occurred spontaneously at the site of

narrowing of the artery. Such a spasm would lead to ischaemia, which itself would lead to

ventricular fibrillation. It was possible that such a spasm could be caused by exposure to

cold, especially on the face, but it could also be caused by sympathetic aggravation brought

about by the experience of, for example, anger or excitement.

The pathological perspective

[163] Professor Derek Pounder, Professor Emeritus of Forensic Medicine, at Dundee

University (retired) gave expert evidence for the defenders, under reference to his report

dated 10 March 2018. Under reference to the report of the post mortem examination carried

out on the body of the deceased, Professor Pounder confirmed that, of the two authors, he

knew Dr Mark Ashton, consultant pathologist, personally, and had no reason to doubt his

skill as a forensic pathologist. He confirmed that no evidence of occlusive thrombus was

found post mortem. The relevant findings in relation to the heart were as follows:

“The heart was enlarged with mild left ventricular hypertrophy and it weighed 475g.

The left main stem coronary artery showed marked atherosclerosis with

approximately 70 per cent narrowing and there was also significant narrowing of the

proximal anterior descending branch. The left circumflex branch and the right

coronary arteries showed mild atherosclerosis. There was no evidence of an

occlusive thrombus. The cardiac valves were unremarkable.”

Page 57 ⇓

He agreed in general with the opinions expressed in the report of the post mortem

examination.

[164] Under reference to his own report, he confirmed that the assessment of the cause and

mechanism of death required consideration of both the clinical history and the post mortem

findings, and that the core of the clinical history in the present case was exercise induced

chest pain for a period of about one week, culminating in an episode of chest pain leading to

a cardiac arrest due to ventricular fibrillation. Post mortem, there had been evidence of

hypertensive heart disease, with increased muscle mass of the main pumping chamber of

the heart (left ventricular hypertrophy), resulting from the increased work required to

maintain a higher than normal blood pressure. The heart weight of 475g was above the

maximum expected and would have resulted in an increased demand for blood flow to the

heart muscle (myocardium), and an increased risk of ischaemia (caused by an imbalance

between myocardial oxygen demand and supply, resulting in myocardial hypoxia which, in

turn, produced electrical instability). The extent of the increased heart muscle mass was not

sufficient in itself to constitute a likely cause of ischaemia and electrical instability. In

general, a heart weight of 500g or more would be required to firmly entertain that

possibility. Notwithstanding that, the left ventricular hypertrophy found post mortem in the

present case would have exacerbated the risk of ischaemia arising from atherosclerotic

coronary artery disease.

[165] He described the standard method of dissection of the heart, and examination of the

coronary artery, by slicing at 3mm intervals in order to allow identification of disease in the

artery wall or in the lumen. The colour of the interior of the artery, being off-white, provided

a contrast to the red colour of any clot which might be present. While he accepted that there

was always the possibility of human error, in his view, failure to identify a clot which was

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present would amount to incompetence on the part of the examining pathologist. On death

following a cardiac event, a pathologist would always concentrate on looking for a clot. Clot

formation was a potential cause, although never concluded to be the cause, unless all other

possible factors were excluded. On the other hand, where a clot was found, it would usually

be the cause of death.

[166] Where no clot was found post mortem, the possible mechanisms of death involving

heart disease, particularly in the case of sudden deaths, were coronary artery disease,

atherosclerosis, or, generally, chronic longstanding disease without any acute manifestation,

such as severe narrowing of the coronary artery, or enlargement of the heart as in the

present case. In such circumstances, where such conditions led to arrhythmia, the likely

cause would be some dynamic factor imposed on the longstanding abnormality.

[167] Ventricular fibrillation was caused by electrical instability which resulted in

disruption of the regularity of the heartbeat as it moved through the heart muscle.

[168] Ischaemia was caused by the imbalance between demand from the heart muscle and

the supply of blood flow from the coronary artery. Such an imbalance could occur where

increased muscle mass increased demand, in the form of increased rate of heartbeat, in

circumstances where, as the result of stenosis in the coronary artery, or the existence of a clot

occluding the artery to any extent, there was a reduced blood supply to the heart. In the

present case, increased heart size would have resulted in increased demand, which, coupled

with the noted stenosis of the coronary artery, which would have reduced blood flow,

would have resulted in an electrical imbalance within the heart. Heart muscle would have

become ischaemic, through lack of oxygen, resulting in instability which would have

affected muscle contraction and led to arrhythmia.

Page 59 ⇓

[169] Under reference to his report, he confirmed that where, as here, the lumen of the

coronary artery was reduced by approximately 70 per cent, it was to be noted that such a

figure was at the lower end of the range of narrowing likely, in itself, to account for

ischaemia. Having said that, however, the presence of left ventricular hypertrophy

increased the likelihood of ischaemia developing. As he put it, these circumstances were

certainly enough to account for ischaemia. At a later stage in his evidence, he described

these facts as being borderline for the risk of the development of ischaemia, or sufficient to

account for ischaemia. His final position was that where these circumstances were present,

and the patient was already suffering from angina, then the risk of sudden death by

ischaemia was significantly increased.

[170] It was significant that focal scarring was found on the inner surface of the muscular

wall of the left ventricle (sub-endocardial fibrosis). The development of such scarring was

the result of ischaemia due to reduced blood supply, possibly exacerbated by a rapid heart

rate. The presence of the scarring, a form of necrosis, was an indicator of a previous

myocardial infarction. Its presence was also significant in that it increased the likelihood of

the future development of cardiac arrhythmia, even in the absence of acute ischaemia.

[171] In the absence of a blood clot, the combination of these factors, comprising the

presence of focal severe coronary atherosclerosis in the left main coronary artery, left

ventricular sub-endocardial scarring from previous myocardial infarction, and left

ventricular hypertrophy, were sufficient anatomical findings to account for myocardial

ischaemia and an ischaemic sudden death consequence upon an arrhythmia, all as

suggested by the given history of collapse in the case of the deceased.

[172] On the other hand, it was significant that, at post mortem examination, there was an

absence of evidence of fresh myocardial infarction which was in keeping with the known

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normal ECG result and the negative troponin levels recorded in hospital some hours before

death. No thrombus was found within the major coronary arteries and the atherosclerotic

plaques within the coronary arteries showed no surface features which would have

suggested the formation of a previous thrombus subsequently dissipated. These findings

suggested that death had been caused by an electrical imbalance leading to dysfunction of

the left ventricle, due to factors other than the presence of a blood clot.

[173] ACS was an umbrella term which embraced a spectrum of atherosclerotic coronary

artery disease (ACAD) including unstable angina, myocardial infarction, and ischaemic

sudden death, but not including stable angina. As used currently in clinical practice, the

term included unstable angina and myocardial infarction. It was not a term used by

pathologists who, instead, would make anatomical diagnoses of ACAD, coronary

thrombosis or myocardial infarction as explanations for ischaemic sudden death. There was

a distinction to be drawn between the role of the pathologist in making an assessment of the

cause of death, as against clinical diagnosis of a condition in life. Unstable angina was a

clinical diagnosis and not a pathological diagnosis; it is a clinical syndrome, and not a

specific disease. It is angina in a crescendo pattern induced by limited physical activity or at

rest. To distinguish it from stable angina required a clinical interpretation of the patient’s

historical account of their angina, and was therefore a subjective clinical symptom. It had

been noted authoritatively that:

“the distinction between new angina, worsening angina and unstable angina is

notoriously difficult and based on a clinical assessment and a careful and full clinical

history.”

[174] Again under reference to his own report, in circumstances where, following post

mortem examination, there was no basis for the conclusion that a transient thrombus had

arisen from an atherosclerotic plaque, that being the most usual pathological basis of

Page 61 ⇓

unstable angina, there were four other possible causes of unstable angina, only one of which

was referable to the present case. That cause was one of dynamic constriction of the relevant

vessel (vasoconstriction) which could not be visualised post mortem. In the present case the

time interval between the exhibited symptoms and death had been very short. No thrombus

had been identified and no active smooth muscle proliferation, which would have indicated

prior thrombus formation, had been noted as being present on any atherosclerotic plaque (a

“culprit plaque”). On the other hand, the fact that no clot had been found at post mortem

examination was not surprising. Research indicated that no clot was found in 20-30 per cent

of comparable cases.

[175] In the absence of a “culprit plaque” or a coronary artery thrombus or fresh

myocardial infarction, there was no evidence to suggest that in this case, the pathway to

death had been by thrombotic occlusion or partial occlusion of the coronary artery. Where

that was the case, death could arise as a result of the concurrence of fixed or dynamic

factors, the latter being impossible to assess during an autopsy, although sometimes to be

inferred from a history of physical exertion or high levels of emotion. Vasoconstriction was

a dynamic phenomenon in the living which could not be seen after death. Similarly,

stress-induced reduction in the activity of the autonomic innervation of the heart (reduced

parasympathetic vagal tone) could facilitate the development of ventricular arrhythmia

which could not be assessed post mortem. A rapid heart rate increased susceptibility to

sub-endocardial ischaemia and arrhythmia. An acute rise in blood pressure as a result of

exposure to cold could also increase myocardial oxygen demand and increase the risk of

ischaemia and arrhythmia.

[176] In considering why it was that the deceased died on 6 January 2011 rather than at an

earlier date, it was possible only to view the matter in hindsight by informed speculation.

Page 62 ⇓

Circumstances immediately prior to his collapse could have increased demand on his heart.

The experience of being in hospital could sometimes be stressful, resulting in increased

blood pressure and increased heart rate. Physical activity would also increase demand on

the heart. Exposure to cold would have increased demand, by a rise in blood pressure

without a commensurate fall in heart rate. In short, it was not possible to say definitively

how the necessary factors combined at 6 January 2011. In theory, the deceased could have

died at any time whilst engaging in the ordinary activities of life such as walking, running

for a bus or, if he was sensitive to cold, by walking outside in winter weather.

[177] In response to the suggestion that had the deceased been an in-patient in hospital

between 31 December 2010 and 2 January 2011 then, being in a warm environment with the

benefit of bed rest, he would have avoided any exposure to cold which could therefore be

eliminated as a possible cause of death, Professor Pounder qualified any answer as being

one involving retrospective speculation. Even if the deceased had been sensitive to the cold,

and the weather had been particularly bad, it was not possible to say definitively what

would have happened. Even the experience of severe emotion could be enough to cause

someone suffering from angina to collapse. The condition from which the deceased was

suffering was the most common cause of sudden natural death. Although there was a

possibility that some part of the hospital environment might have triggered a fatal cardiac

event, it was to be noted that, in hospital, there was, of course, the potential for immediate

resuscitation.

[178] In cross-examination, he accepted that the deceased had been suffering from a

longstanding background condition which, as a result of a provocative trigger factor, had

progressed to arrhythmia. He also agreed that it was not surprising that the deceased had

been asymptomatic until only one week before his death. Even accounting for the

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deceased’s condition, comprising focal severe coronary atherosclerosis in the left main stem

coronary artery, left ventricular sub-endocardial scarring from previous myocardial

infarction, and left ventricular hypertrophy, it had not been inevitable that he would die of

these conditions. Appropriate treatment would undoubtedly have reduced the risk of that.

[179] On the basis that unstable angina was a clinical diagnosis rather than a pathological

diagnosis, in circumstances where there could be no obvious pathological basis for the

presence of unstable angina, it was not possible to rule out unstable angina on the basis of

pathological findings. The identification of unstable angina was a matter for a clinician, on

the basis of the history given by a patient and the clinician’s interpretation of the

information provided.

[180] Of the five possible causes of unstable angina, vasoconstriction of the coronary

artery, because of its dynamic nature, could not be confirmed at post mortem examination,

and therefore could not be excluded as a cause of unstable angina leading to death on the

basis of pathological findings. A comparable example was that of the limitations of post

mortem examination in a case of fatal epilepsy. In Professor Pounder’s view, on the basis

that unstable angina had been the correct diagnosis, then vasoconstriction was the only

possible explanation for death.

[181] Under reference to the A&E notes of Belford Hospital, in relation to the deceased’s

attendance on 6 January 2011, he accepted that the deceased’s increased blood pressure

at 10.45am (170/80), could have been caused by the experience of attending hospital and

having negotiated the steps to the entrance of A&E, which in turn could have triggered

arrhythmia.

[182] The possibility that exposure to cold could cause an acute rise in blood pressure,

increasing myocardial oxygen demand and the risk of ischaemia and arrhythmia, was

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supported by the relevant epidemiological research. There was no doubt that there was

evidence to support that theory.

[183] It was commonly accepted that there were four principal precipitating causes for

angina in susceptible patients. Such patients were warned against the risks involved in

exercise, experiencing heightened emotion, exposure to cold, and the consumption of large

meals.

[184] He confirmed that acceptance of a clinical diagnosis of unstable angina was not

dependent on confirmation by pathological findings. Although discovery of thrombus

would generally be expected as the most common cause of death in unstable angina,

in 20 per cent of the referable cases there were other explanations.

[185] Although it was possible, in the generality, that very small or tiny clots could be

formed, causing unstable angina, subsequently resolving so as not to be present at post

mortem examination, in the present case there were none of the features in the atherosclerotic

plaques which would be expected if that had occurred. If a thrombus had not dissolved, or

had otherwise been assimilated by the body, but had become detached and moved

downstream through the coronary artery, then the resulting occlusion, or partial occlusion

would have resulted in a myocardial infarction. Viewed in the round, at post mortem

examination, there had been no evidence of thrombus, and no evidence that there had ever

been a thrombus. On that basis, his view was that any suggestion that there had been a

thrombus was not well founded.

[186] In hindsight, the symptoms experienced by the deceased in the week before his

death could be explained by the extent of the narrowing of the coronary artery and the

enlargement of his heart which, together, were sufficient for the development of ischaemia,

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particularly where there were added factors such as additional strain on the heart through

exercise by, for example, moving up and down stairs.

Discussion

[187] Senior counsel for both parties adopted their respective written notes of argument,

the content of which, together with the submissions made at the bar, is reflected in what

follows.

[188] I accepted the witnesses to facts, namely, Dr Smith, Mrs Brown, and Mr Campbell, as

being credible and reliable in their evidence. In my assessment, Dr Smith presented as a

frank and open witness who, very responsibly, was doing her best to assist the court.

[189] In relation to the proper assessment of expert evidence, I was referred to Kennedy v

Cordia 2016 SC (UKSC) 59. Applying the principles to be derived from that case, I found

each of the expert witnesses, albeit to varying extents, and with the exceptions of Dr Gaskell

and Professor Channer, to be appropriately qualified and experienced witnesses who gave

authoritative evidence in an appropriately measured, detached and professional manner. In

general, their views were coherent and clearly expressed.

[190] In contrast, I found both Dr Gaskell and Professor Channer to be unsatisfactory

witnesses. Since Dr Gaskell’s opinion was based solely on the content of the notes recorded

by Dr Smith, and took no account of the totality of the deceased’s symptoms as described, in

particular, by Mrs Brown, it was in effect predicated on a basis which was contrary to the

evidence which I accept, namely, that, by Friday 31 December 2010, the deceased’s pain was

occurring frequently and with little, minimal or no exertion. There were significant

inconsistencies in his evidence. Although he made positive references to the SIGN 96 and

NICE Guidelines in his report, his oral evidence, in relation to the appropriate use of GTN

Page 66 ⇓

spray and beta blockers was inconsistent with their terms. Contrary to the guidance of

NICE 2010, which he accepted was relevant to practice in Scotland, he considered GTN

spray to be appropriately used as a diagnostic tool. Notwithstanding the advice set out in

SIGN 96 “Management of Stable Angina”, to the effect that beta blockers should be used as

first line therapy in cases of stable angina, he approved of Dr Smith’s reasoning in not

prescribing beta blockers and was not critical of her failure to prescribe available and

appropriate alternatives. Somewhat surprisingly, given the strong views expressed by

almost all the other experts on the importance of the matter, he expressly stated that he did

not regard the provision of worsening advice to be a necessary requirement of ordinary

competence. Contrary to other evidence which I accept, in particular from Mr Nichol, he

did not accept that in the context under consideration, the prescription of aspirin was

standard practice in 2010. I assessed him, as a witness, to be overly defensive of Dr Smith’s

actions, and indeed not obviously impartial. To the extent that his opinion differed from

those of the other experts, I attached little weight to his views.

[191] Professor Channer had retired from NHS clinical practice in 2012, and, since 2014

had been engaged solely in medico-legal matters, instructed principally by defenders. He

accepted that he had a reputation as being supportive of doctors. Although, in his report, he

found that in the case of the deceased, death had been caused after a short history of

unstable angina, and accepted in cross-examination, as was agreed between the parties, that

unstable angina was a form of ACS which could be characterised by normal troponin levels,

at other points in his evidence he appeared to consider ACS only to include troponin

positive syndromes and to remove unstable angina from that class. In my assessment, the

differentiation which he sought to draw in the context of the issue in this case, amounted to

little more than a distinction without a difference, and, viewed more critically, was

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unhelpful and unnecessarily obfuscatory. He was selective in his use of medical literature;

in one instance he sought to characterise unstable angina by reference to one definition, in

circumstances where, of the three other cited definitions, one more closely fitted the facts of

the case. He was not familiar with the Patient.co.uk website. Although he recognised that

the deceased, on Wednesday 5 January 2011, had been suffering from unstable angina

involving pain at rest, his assertion that, prior to that day, the deceased was suffering merely

from angina brought on by exercise was inconsistent with the evidence of Mrs Brown. In his

report, he had noted that, at Friday 31 December 2010, the deceased had been suffering from

chest pain lasting five minutes, precipitated by walking, whereas in fact what Dr Smith had

noted was that the deceased was suffering chest pain after five minutes of walking. His

evidence was internally inconsistent. He appeared reluctant to characterise the deceased’s

pain as having been brought on by minimal exertion, expressing the view that whether or

not that had been the case depended on how minimal exertion was to be defined. Although

he characterised chest pain brought on by minimal exercise as angina, rather than as

unstable angina, on the basis that unstable angina was manifested by a crescendo

presentation, he accepted that unstable angina can be defined not just by pain in crescendo

pattern, but also by pain at rest which was getting worse, consistent with the deceased’s

condition. He accepted that changing pain on walking amounted to a crescendo pattern,

and that crescendo pain on exercise was indicative of unstable angina. On the evidence, by

Friday 31 December 2010, the deceased was exhibiting such a presentation. In my

assessment of him as a witness, I found Professor Channer to be insufficiently neutral,

independent and objective. As with Dr Gaskell, to the extent that his opinion differed from

those of the other experts, I attached little weight to his views. By comparison, I had no such

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reservations about the evidence of Professor Brecker, whose evidence, in relation to the

issues on which they were each asked to express opinions, I prefer.

[192] My findings as to the agreed issues for determination by the court are set out in what

follows. Unless the contrary is indicated, the evidence to which I have referred is evidence

which I accept.

(i) What symptoms did the deceased suffer from between 29 December 2010 and 6 January

2011?

[193] On the agreed facts and the evidence which I accept, the deceased, having previously

been a healthy, fit and active man, who participated regularly in golf, skiing, walking and

cycling had the following symptoms at the relevant dates:

Wednesday 29 December 2010: He experienced the first episode of chest pain when

moving up and down stairs in his home. The pain eased after five minutes rest.

Thursday 30 December 2010: He experienced chest pain when walking on the flat,

over the short distance from his front door to the garden gate, the pain resolving on

rest. Dr Smith noted the incident as indicating more chest pain. She accepted that

such pain experienced after five minutes walking was equivalent to pain on minimal

exertion. Viewed objectively, since he was now experiencing pain on the flat, rather

than when moving up and down stairs, his condition had worsened. Mrs Brown

described the deceased, on that day, as not doing very much, not being his usual

active self, and that, whenever he moved, he experienced pain. Each time he rose

from a seated position, the pain returned and, on sitting again, the pain resolved.

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Friday 31 December 2010: The deceased experienced chest pain when getting dressed.

The pain was retrosternal and localised. His wife described the situation as being

that any movement on his part appeared to bring on pain.

Saturday 1 January 2011: Mrs Brown described the deceased as suffering pain

whenever not sitting down. Walking to Mr Campbell’s home, he continued to

experience pain as before.

Wednesday 5 January 2011: The deceased was experiencing continuing chest pain and

chest pain at rest including at night when lying down.

Thursday 6 January 2011: The pain experienced by the deceased, at rest, had been

much worse (10/10) during the previous night. He had by that point been suffering

chest pain for one week.

(ii) What symptoms did the deceased report to Dr Smith on 29 and 31 December 2010?

[194] On the basis of her recorded notes, Dr Smith noted the deceased as having reported

as follows:

Wednesday 29 December 2010: The deceased had suffered chest pain after going up

and downstairs, which had eased after sitting for five minutes. He had not been

feeling sick or sweaty.

Friday 31 December 2010: The deceased had suffered sharp retrosternal chest pain

after walking for five minutes. He had to slow right down. He did not feel sick or

sweaty or unwell.

Page 70 ⇓

(iii) What condition or conditions was the deceased suffering from between 29 December

2010 and 6 January 2011?

[195] As disclosed at post-mortem, the deceased had been suffering from focal severe

coronary atherosclerosis in the left main stem coronary artery, left ventricular

sub-endocardial scarring from previous myocardial infarction, and left ventricular

hypertrophy.

Wednesday 29 December 2010: On the basis of the evidence of Professor Brecker: new

onset unstable angina.

Friday 31 December 2010: I accept the evidence, in particular, of Professor Brecker

that, at this date, the deceased was suffering from ACS. Support for his opinion is

provided by the evidence of Professor Wall which was to the effect that chest pain on

minimal exercise should be taken as indicating ACS, until proven otherwise, and by

Dr Nichol and Dr Johnson who agreed that pain on minimal exercise or at rest,

relieved by rest, ought to have given rise to a presumptive diagnosis of ACS.

Professor Brecker’s evidence was that the deceased should have been diagnosed as

suffering from ACS, in the form of unstable angina, since 29 December 2010. I accept

his analysis that, on the known facts, the concept of a progression from stable angina

on 29 December 2010, progressing to unstable angina subsequently, was not

appropriate.

Wednesday 5 January 2011: Both Professor Brecker and Professor Channer agreed

that, certainly by that date, the deceased was suffering from ACS in the form of

unstable angina.

Thursday 6 January 2011: Death following a history of unstable angina.

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(iv) Whether Dr Smith failed to act properly in seeking to obtain a medical history which

would have resulted in the deceased disclosing that he had pain in the chest on minimal

exertion? Whether Dr Smith breached her duty of care to the deceased on 31 December 2010

by failing to diagnose ACS?

[196] Both the SIGN 96 and the NICE Guidelines indicate that at the stage of assessment

and diagnosis, in relation to patients with suspected angina, there is a clear requirement for

a detailed clinical assessment and a detailed history. Mr Nichol’s evidence was that,

particularly in relation to patients presenting with chest pain, the taking of a proper history

was the cornerstone of diagnosis, and that, as set out in his report, such a history should

include the noting of details of the type of pain, whether it is new or a progressive symptom,

its duration, its distribution and radiation, its alleviating and aggravating factors and all

other associated features. The histories noted by Dr Smith on Wednesday 29 and Friday

31 December 2010, given the possibility of a life-threatening condition, were inadequate in

these respects. In that context, given the imminent holiday period, and the high risk

associated with a serious, unstable and potentially fatal condition, it was incumbent on

Dr Smith to adopt a proactive approach in taking the deceased’s history, which should have

involved appropriately refined and penetrating questioning, and a recognition of the

limitations, in that context, of a reliance on the passive recording of his reported symptoms.

Given the known facts, comprising, in particular, the detail of Mrs Brown’s evidence in

relation to the deceased’s symptoms over the period to Friday 31 December 2010, Dr Smith

clearly failed to do that. Her notes do not record that he was suffering pain on minimal

exertion, or that his condition had worsened. In relation to the taking of the deceased’s

history, she failed to act properly.

Page 72 ⇓

[197] Dr Smith’s evidence was that although she did not consider ACS at the time, despite

the recent onset of the deceased’s pain, she accepted that, having been previously fit and

active, he had presented to her with pain which had become worse over the previous

two days and which arose on minimal exertion. These were symptoms in a previously

active and fit man, indicating recent onset chest pain and therefore indicative of a potentially

serious problem. Professor Wall’s evidence was that in a previously fit man, where there

was no proper basis for any muscular cause, a description of chest pain on exercise should

have raised the question of possible angina. History was critical in the diagnosis of angina.

The incidence in Scotland of angina was 6.7 per cent, or 1/15, within the relevant age group.

I accept the evidence of Professor Wall that, by Friday 31 December 2010, chest pain

experienced on minimal exercise was indicative of ACS, until proven otherwise, and should

have required immediate referral to hospital; the evidence of Mr Nichol, that a presumptive

diagnosis of ACS should have been made; and that of Professor Brecker, that, had the

deceased been admitted to hospital on Friday 31 December 2010, a diagnosis of ACS would

have been made. On the basis of that evidence, I find that, by failing, on 31 December 2010,

to diagnose the condition of ACS, Dr Smith breached her duty of care to the deceased.

(v) If it was reasonable not to diagnose ACS, what treatment should Dr Smith have

provided to the deceased?

[198] Dr Smith’s evidence was that on Wednesday 29 December 2010 she had considered

one possibility to be a cardiac problem and, in particular, had considered a possible

diagnosis of stable angina. She had not ruled out angina. By 31 December 2010, she had

considered angina to be more likely. On Friday 31 December 2010, she prescribed GTN

spray, as a diagnostic tool, contrary to the NICE Guidelines, and made an urgent referral for

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ETT. In that regard, she accepted that, except in relation to her prescription of GTN spray,

she had not followed the SIGN 96 Guidelines in relation to the drug intervention

recommended for first line therapy in the management of stable angina. Professor Wall’s

evidence was that, in cases of stable angina, the appropriate first line intervention was the

prescription of GTN spray, low dose aspirin, beta blockers, statins, and, given the very great

risks posed by angina, the provision of appropriate warning advice. Had it been reasonable

for Dr Smith not to diagnose ACS, but rather stable angina, that is the course of treatment

she should have provided. Her evidence was that she had not prescribed beta blockers

because the deceased had been “wheezy”, had already been prescribed salbutamol, and

because, in cases of asthma, beta blockers were contra-indicated. In any event, she did not

consider the possibility of prescribing any of the available alternatives to beta blockers.

Professor Wall’s evidence was that where a patient was intolerant of beta blockers, no

reasonably competent GP would have failed to provide an alternative drug. The effect of

beta blockers or the available alternatives would have been to reduce the level of cardiac

ischaemia, by reducing the heart’s workload, and thereby reducing the risk of ventricular

fibrillation. Both Professor Brecker and Professor Channer expressed the view that the

maximum effect of such drugs would be achieved within about three days. Although there

was reference in the evidence to a longer relevant period, in particular in relation to the

findings of the MIAMI international trial, reported in the European Heart Journal (1985), I

have not placed weight on these findings as they related to patients, who, unlike the

deceased, were suffering from acute myocardial infarction.

[199] It was accepted that, on Friday 31 December 2010, Dr Smith ought to have provided

the deceased with worsening advice, but failed to do so. In the course of the evidence, what

that worsening advice ought to have been was expressed in a variety of different ways.

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Dr Smith indicated that it would have been appropriate that the deceased be told to call an

ambulance or go to hospital if his symptoms deteriorated, and Dr Gaskell’s view was that

the advice should have been to seek an earlier review if they worsened. It was suggested on

behalf of the defenders that by Friday 31 December 2010, the deceased’s symptoms had

reached a plateau and did not in fact become worse prior to Wednesday 5 January 2011, but,

rather, during that period maintained a constant level. However, Professor Wall, Mr Nichol

and Professor Johnson all spoke of the very great risks associated with angina, and taken

together with the context of the imminent holiday period, I prefer the evidence of the

witnesses other than Dr Smith and Dr Gaskell, to the effect that the appropriate worsening

advice should have been more extensive. Professor Wall’s view was that the deceased

should have been advised to call a 999 ambulance in the event of further chest pain on

minimal exertion or at rest. Mr Johnson, in his report, referred to advice specifically to

ring 999 if chest pain returned and did not respond to GTN spray and persisted more than

20 minutes or came on frequently or with no exertion. Mr Nichol, in his report referred to

advice in relation to pain at rest, on minimal exertion, lasting for 15 minutes, or being

unresponsive to GTN spray. Given the deceased’s condition at Friday 31 December 2010,

and on the basis that a full history had been taken, the tenor of that evidence is, in effect, that

the appropriate advice should have been to call an ambulance if there was no improvement,

in the sense that his symptoms continued as they currently were. On that basis, in the

context of the high risk symptomatology associated with angina, the concept of symptoms

having reached a plateau has no application in relation to the issue of causation following

failure to give such advice.

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(vi) What was the cause of the deceased’s cardiac arrest on 6 January 2011?

[200] Although there was reference to the fact that the most common cause of death in

cases of coronary artery disease involves the presence of thrombus, I am satisfied that death

did not occur in that way in the case of the deceased. At post mortem examination, no blood

clot was found to be present, and, in the absence of evidence of any active smooth muscle

proliferation which might indicate prior thrombus formation on atherosclerotic plaque,

there is no basis from which to conclude that there ever was thrombus present. The issue of

any thrombus having been dissipated or assimilated by the body does not arise given the

timescale of the deceased’s sudden death. Since the matter was raised, if only incidentally,

in the course of the proof, for completeness, I would add that, in the context of no clot

having been found at post mortem examination, I find there to be no persuasive basis from

which it could be inferred that either of the two pathologists concerned was negligent in that

regard. I find, rather, in circumstances in which the deceased had been suffering from

longstanding focal severe coronary atherosclerosis in the left main stem coronary artery, left

ventricular sub-endocardial scarring from previous myocardial infarction, and left

ventricular hypertrophy, death was caused by ventricular fibrillation which, in turn, was

caused by ischaemia brought about by reduced blood flow to the heart muscle, resulting

from stenosis of the left main stem coronary artery. That conclusion was common ground

between Professor Brecker and Professor Channer. The evidence of both of these witnesses,

taken with that of Professor Pounder, was to the effect that the ischaemic nature of the heart

muscle, however it was triggered, was the principal precipitating factor, in that it was

ischaemia which caused the ventricular fibrillation leading to sudden death. In

Professor Brecker’s view, the primary cause of the ventricular fibrillation was ischaemia. He

considered that there had been sufficient substrate, in the form of the extent of the noted

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stenosis, coupled with pain on minimal exertion, to trigger ischaemia and thereafter sudden

death, absent another provocational trigger. In Professor Pounder’s view, increased heart

size coupled with stenosis of the coronary artery would have reduced blood flow to the

heart, rendering the heart muscle ischaemic, and leading to cardiac arrhythmia. In

circumstances in which the stenosis present was reducing the lumen of the coronary artery

by 70 per cent, and was coupled with the noted left ventricular hypertrophy, these factors

together, in his opinion, were sufficient to account for ischaemia of the heart muscle. Where

the deceased had, in addition, been suffering from angina, the risk of sudden death brought

about by ischaemia was significantly increased.

(vii) What difference, if any, would treatment or advice offered by Dr Smith on either

31 December 2010 or 5 January 2011 have made to the outcome?

[201] If, on Friday 31 December 2010, Dr Smith had prescribed beta blockers or an

appropriate alternative, the deceased would have had the benefit of their anti-ischaemic

effect. On the basis that their maximum effect would have been in place within about

three days, the likelihood of a fatal cardiac event, the principal cause of which was

ischaemia, would have been significantly reduced, and, on the evidence of

Professor Brecker, reduced to the extent that it would have been prevented.

[202] If on Friday 31 December 2010, Dr Smith had immediately referred the deceased to

hospital, then, under reference to my findings in relation to Issue (viii), below, with the

benefit of hospital treatment, death on 6 January 2011 would have been avoided.

[203] If, on Friday 31 December 2010, Dr Smith had provided appropriate worsening

advice, the deceased, on her evidence and that of Mrs Brown, would have followed it, and

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would have been admitted to hospital, following the events of New Year’s Day as described

by Mrs Brown, or, at the latest, following their visit on foot to Mr Campbell.

[204] If, on Wednesday 5 January 2011, Dr Smith had prescribed beta blockers or an

appropriate alternative, the deceased would have had the benefit of their anti-ischaemic

effect, but to a lesser extent. On the evidence of Professor Brecker, even if the deceased had

been admitted to hospital on that date, it would not be possible to say that the risk posed by

ischaemia could have been avoided. It could have been reduced, but it could not be said

that the medication would have reached its maximum effect. The effect would have been

more than negligible, and not insignificant, but it could not be said that more than 50 per

cent of its desired effect would have been achieved prior to the time of death.

(viii) On a hypothesised attendance at Belford Hospital between 31 December, after

attending Dr Smith, and the end of 2 January 2011, what difference, if any, would treatment

have made to the outcome?

[205] I accept the evidence of Mr Nichol, largely agreed by Mr Johnson, that if the

deceased had attended hospital on Friday 31 December 2010 , a diagnosis of ACS would

have been made, prompting the prescription of aspirin, heparin, and GTN spray, together

with morphine if the deceased was in pain. Thereafter the deceased would have been

transferred to an acute medical unit within the hospital. On the basis that the presentation

would have indicated that blood flow to the heart muscle was critically impaired, with the

risk of progression to acute cardiac arrest due to abnormal heart rhythm, the deceased

would have been kept in hospital. Blood tests would have been carried out, beta blockers,

or where there was a contra-indication, appropriate alternatives, and statins prescribed,

high blood pressure treated, and an ETT carried out. In broad terms, Professor Channer

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agreed that such a course of treatment would have been put in place. Professor Brecker’s

evidence was that the deceased would have been admitted, intravenous access obtained,

and anti-platelet and anti-thrombotic drugs administered, together with aspirin, or an

appropriate alternative, to put in place dual anti-platelet therapy. It would have been

standard practice to prescribe beta blockers in order to reduce his cardiac workload. He

would also have been prescribed vasodilators, to increase blood supply, by widening the

coronary artery and reducing demand on the heart. In the case of the deceased, nitrates

and calcium channel blockers would have been prescribed in addition to beta blockers. If

the deceased had been continuing to experience pain at rest, intravenous nitrates would

have been administered. In addition, he would have been given injections of

anti-thrombotic drugs, such as heparin or similar, and would have been started on other

drugs with longer term effects, such as statins to reduce cholesterol levels, and vasodilators

such as ACE inhibitors. All of that would have been standard practice. The deceased

would have been kept in hospital on admission because of his high risk. The core aims

would have been to seek to avoid stressors, and indeed anything involving an increase in

heart work rate, particularly in the form of exertion. Mr Nichol’s view was that, had the

deceased been kept in hospital, and received appropriate treatment, and kept at rest, then,

on the balance of probabilities, the chances of him suffering a cardiac arrest on Thursday

6 January 2011 would have been reduced, but not excluded entirely. Professor Brecker’s

evidence was that even in the absence of thrombus, the prescription of beta blockers would

have had immediate anti-arrhythmic effect but, in particular, would have served to reduce

cardiac demand and workload. In so far as the timing of the effect of medication was

concerned, he considered that the relevant period was probably one of about three days.

In cross-examination, Professor Channer agreed with that. He accepted that beta blockers

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have an anti-ischaemic effect, the maximum effect of which occurs within two to three days

of administration. Calcium channel blockers would not have been administered unless

there was a contra-indicator for beta blockers. Beta blockers reduced demand on the heart,

correcting any supply/demand imbalance likely to cause ischaemia. On the same analysis,

Professor Brecker’s evidence, which I accept, was that if the deceased had been admitted to

hospital on Friday 31 December, the medication which he would have been prescribed, as

treatment for ACS, together with the fact of simply being in hospital, on the basis of his

clinical experience, and as I find on the balance of probabilities, would have prevented

ischaemia and therefore ventricular fibrillation. Death on Thursday 6 January 2011 would

have been avoided. Although it was suggested by Mr Johnson that the deceased might

have been discharged home, that was contradicted by both Mr Nichol and

Professor Brecker. On the basis that the deceased would not have been admitted, or would

subsequently have been discharged only if, on appropriate medication, he would have

been able to exercise without significant pain, Professor Brecker’s view was that given the

post mortem findings indicating severe main stem coronary artery stenosis, discharge home

would have been unlikely.

[206] Both Mr Nichol and Professor Brecker were of the opinion that had the deceased

attended hospital later, for these purposes up to the end of Sunday 2 January 2011, the

treatment he would have received would have been the same. In Professor Brecker’s view,

the effect, and likely outcome would have been the same in that death would have been

avoided.

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(ix) What difference, if any, would the non-drug treatment associated with being in hospital

on 6 January have made to the outcome?

[207] On the evidence of Mr Nichol, the deceased when in hospital would have had the

benefit of being kept in bed rest, and would thus have been protected from any exposure to

the consequences of physical exertion which might have provoked cardiac arrest.

[208] On the evidence of Professor Pounder, the possibility that exposure to cold could

cause an acute rise in blood pressure, increasing myocardial oxygen demand and the risk of

ischaemia and arrhythmia, was supported by relevant epidemiological research. If in

hospital on Thursday 6 January 2011, the deceased would not have been exposed to the low

temperature out of doors and would have been protected from that risk.

Conclusion

[209] On the basis of the relevant case law to which I was referred, namely Hunter v

Hanley 1955 SC 200, Bolitho v City and Hackney Health Authority [1998] AC 232, Honisz v

Lothian Health Board [2006] CSOH 24, and Amanda McGuinn v Lewisham and Greenwich NHS

Trust 2017 EWHC 88 (QB), and my findings in relation to the agreed issues, I find that

Dr Smith was professionally negligent and breached the duties of care which she owed to

the deceased, in that on Friday 31 December 2010, she (i) failed to diagnose unstable angina,

(ii) failed to refer him immediately to hospital, (iii) failed to provide appropriate worsening

advice, and (iv) failed to prescribe the medication appropriate for a diagnosis of stable

angina. Having considered the further authorities to which I was referred, namely Wright v

Cambridge Medical Practice [2013] QB 312; Hughes-Holland v BPE Solicitors [2017] 2 WLR 1029;

and South Australia Asset Management Corp. v York Montague Ltd [1997] AC 191, and applying

the principles to be derived from them to the facts of this case, I am satisfied, given my

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findings in relation to the agreed issues, that it is proved that these failures were materially

causative of death, in that their consequences were that the deceased was denied the

appropriate treatment which, on the balance of probabilities, would have reduced his level

of cardiac ischaemia to the extent that ventricular arrhythmia would have been prevented. I

find, in addition, that in any event, if the fatal cardiac event on Thursday 6 January 2011 was

caused by exposure to cold, as a provocational trigger, her failures were responsible for him

being denied the protection from such exposure which admission to hospital would have

provided.

Decision

[210] For these reasons, I find in favour of the pursuers. I sustain the pursuers’ first and

second pleas-in-law, repel the defenders’ third, fourth and sixth pleas-in-law, and award to

the pursuers the sums agreed. I reserve, meantime, all questions of interest from the date of

proof, and expenses. The case will be put out By Order to allow these matters to be

addressed.