Scanes and Comcare (Compensation) - [2023] AATA 3537

Scanes and Comcare (Compensation) [2023] AATA 3537 (31 October 2023)
Division:GENERAL DIVISION
File Number(s): 2021/5381
Re:Noelene Scanes
APPLICANT

AndComcare
RESPONDENT

DECISION
Tribunal:Member W Frost
Date:31 October 2023
Place:Canberra

The Tribunal affirms the decision under review pursuant to section 43(1)(a) of the Administrative Appeals Tribunal Act 1975.
............................[sgd]................................
Member W Frost
Catchwords
WORKERS’ COMPENSATION – Safety, Rehabilitation and Compensation Act 1988 – historical compensable condition – aggravation of ischaemic heart disease – resultant myocardial infarction in 1993 – whether the 1993 incident resulted in death in 2020 – claim pursuant to sections 17 and 18 – payment of death benefit to spouse – payment of funeral expenses to spouse – where there are risk factors – high cholesterol – increased stress – smoking – collateral supply – where the Tribunal is not satisfied that the 1993 incident resulted in death in 2020 – decision under review affirmed
Legislation
Administrative Appeals Tribunal Act 1975 s 43
Safety, Rehabilitation and Compensation Act 1988 ss 4, 5A, 5B, 13AA, 14, 17, 18
Cases
Ilsley v Wattyl Australia Pty Ltd (1997) 75 FCR 1
Kooragang Cement Pty Ltd v Bates (1994) 35 NSWLR 452
March v E & MH Stramare Pty Ltd (1991) 171 CLR 506
Secondary Materials
Comcare, Statutory rates for compensation (Web Page, 17 August 2023) < accessed on 25 July 2023
REASONS FOR DECISION
Member W Frost
31 October 2023
INTRODUCTION

Mr Warren Scanes was employed the Australian Federal Police (AFP) and its predecessors from 1971 to 1995. In 1993, he suffered a ‘myocardial infarction’, commonly known as a heart attack, which was accepted by Comcare to be a compensable condition under the Safety, Rehabilitation and Compensation Act 1988 (SRC Act). This injury was described by Comcare in 1993 as an aggravation of ‘coronary artery disease and resultant myocardial infarction’.[1] In 2020, some 27 years later, Mr Scanes suffered a cardiac arrest and ischaemic heart disease and died aged 71.
[1] Exhibit 1, page 17.
Ms Noelene Scanes is the widow of Mr Scanes. As the accepted ‘dependent’ of Mr Scanes under the SRC Act, Ms Scanes made a claim to Comcare for compensation for an injury resulting in the death of her husband pursuant to section 17 of the SRC Act. This claim was declined by Comcare and that determination was subsequently reconsidered and affirmed by Comcare. As a result, Ms Scanes applied to the Administrative Appeals Tribunal (Tribunal) for review of Comcare’s decision refusing liability to pay compensation under the SRC Act for Mr Scanes’ death.
PROCEDURAL ISSUE
By way of background, the Tribunal sets out below the reason for the regrettable delay between its initial hearing date of 23 November 2022, the resumed hearing on 28 July 2023 and the subsequent provision of a decision and written reasons in this proceeding on 31 October 2023, almost one year after the Tribunal’s first hearing date.
On 23 November 2022, the Tribunal commenced the hearing of Ms Scanes’ application. However, during the early stages of the hearing, one of the medical experts, a cardiologist, who was to be called that day to give evidence became unavailable due to their required attendance at a surgical procedure. As a result, and on the agreement of the parties, the Tribunal adjourned the hearing and, following its provision of suitable dates, re-listed the hearing to resume on 10 February 2023, being the earliest available date for the parties and the Tribunal.
On 6 February 2023, the parties informed the Tribunal that they were each seeking supplementary reports from their respective medical experts in the proceeding and that these reports would not be received before the resumed hearing scheduled to be held later that week.
In the circumstances, the following day, on 7 February 2023, the Tribunal held a Directions Hearing. The Tribunal decided to vacate the scheduled hearing on 10 February 2023 and made Directions for Ms Scanes to file and serve a supplementary expert report by 17 February 2023 and for Comcare to file and serve a supplementary expert report by 10 March 2023. The last of these reports was received by the Tribunal on 20 March 2023.
Following the Directions Hearing on 7 February 2023, but on the same day, the Tribunal provided the parties with its availability for a resumed one-day hearing on dates between late March 2023 and mid-June 2023. Unfortunately, the parties had no mutual availability during this period of time. As a result, the Tribunal issued Hearing Certificates for the parties to indicate their availability for a resumed hearing between 19 June 2023 and 28 July 2023. Ms Scanes indicated that her representatives and experts were available in July 2023 and that the latter requested to give evidence on a Friday in that month. Comcare indicated that its Counsel was unavailable until 20 July 2023 and that its expert was available from that date until 28 July 2023. In those circumstances, the Tribunal was left with little option but to list a one day resumed hearing in this proceeding for Friday, 28 July 2023.
The parties’ experts gave oral evidence at the resumed hearing on 28 July 2023. The parties agreed that, due to the nature of Ms Scanes’ application and the detailed medical evidence, they would provide written closing submissions to the Tribunal following the close of the evidence on 28 July 2023, and the subsequent receipt by the parties of the transcript of proceedings. Accordingly, on 9 August 2023, Comcare’s representative informed the Tribunal that it had secured the transcript and the Tribunal therefore made Directions for it to be provided the following day to Ms Scanes and for her to file and serve written closing submissions by 25 August 2023, for Comcare to file and serve its corresponding submissions by 4 September 2023 and for Ms Scanes to provide any reply submissions by 11 September 2023. The Tribunal received the final written submissions on this last date and thereafter reserved its decision in this proceeding and prepared its written reasons.
On 31 October 2023, the Tribunal published its decision and written reasons.
SUBSTANTIVE ISSUE
The substantive issue before the Tribunal was whether the accepted ‘injury’ suffered by Mr Scanes in 1993 resulted in his death in 2020, thereby enlivening Comcare’s liability to pay compensation to Ms Scanes under sections 17 and 18 of the SRC Act.
There was no dispute that Ms Scanes was a ‘dependent’ of her late husband, as defined under section 4 of the SRC Act, and for the purpose of the aforementioned compensation provisions for injuries resulting in death in the SRC Act. For the avoidance of doubt, the Tribunal is satisfied that Ms Scanes was a dependent of Mr Scanes at the time of his death in 2020.
BACKGROUND
Mr Scanes was born on 1 January 1949.[2]
[2] Ibid., page 13.
In 1971, Mr Scanes commenced employment with the then ACT Police in Canberra. He subsequently became an employee of the AFP when it assumed responsibility for ACT policing.[3]
[3] Ibid., page 52.
In July 1985, Mr Scanes was admitted to Woden Valley Hospital.[4] Dr David Craigie, General Practitioner, referred Mr Scanes for cardiac review following ‘two episodes of chest pain and breathlessness’ in December 1984 and July 1985, respectively.[5]
[4] Ibid., page 279.
[5] Exhibit 4.
On 22 July 1985, J. D. Wilson, a Senior Specialist in the Department of Endocrinology at the then Woden Valley Hospital in the ACT, reported to Dr Craigie that Mr Scanes:[6]
was admitted to hospital on the 14^th July with a history of retrosternal chest pain which was associated with shortness of breath. Investigations did not show any evidence of myocardial damage. However, it is noted that he is over-weight and that he smokes 40 cigarettes a day. He has had blood pressures recorded as high as 210/110 mm Hg in the past. He was discharged on the 15^th July. He has been advised to lose weight and to stop smoking…He should also have an exercise ECG done in the near future.
[6] Ibid.
On 29 July 1985, Dr Peter French, Cardiologist, relevantly reported to Dr Craigie following an exercise test performed on Mr Scanes that:[7]
He was exercised on a Treadmill using the Bruce Protocol and completed 30 seconds of Stage IV before he was stopped by shortness of breath. He did not develop chest pain.
He had normal heart rate response to exertion, pre-existing hyper-tension which rose to significant levels on exertion, and the ECG was negative for ischaemia at peak exercise. Consequently, although he is unlikely to have significant coronary artery disease, the blood pressures recorded are quite significant and I feel that if these pressures are representative of the types of pressures he’d run, then he does have established hypertension and should be treated.
[7] Ibid.
On 6 March 1993, Mr Scanes made a claim for workers’ compensation due to a ‘heart attack’ and ‘work related stress’.[8] Mr Scanes stated that he was a ‘Sergeant Patrol Supervisor’ and that his injury happened, or he first noticed the disease or illness, on 2 March 1993.[9] He further stated that the injury occurred while working at his usual workplace and there had been ‘a build up of police pressures over a 22 year period’.[10] More particularly, in response to requests for details about ‘all the events which led to the injury’ and their contribution, Mr Scanes stated:[11]
A build up of stress & police pressures over a 22 yr period accompanied by drastic budgetary restraints resulting in minimum patrols being available to perform duties to an acceptable level adding further stress to supervisors.
…
Policing is a very stressful occupation & over the years many frightening incidents are attended to that surely effects the health.
[8] Exhibit 1, pages 13-15.
[9] Ibid, page 13.
[10] Ibid.
[11] Ibid., page 14.
On 29 April 1993, Comcare disallowed Mr Scanes’ claim and was ‘unable to find your coronary artery disease and subsequent heart attack was contributed to in a material degree’ by employment, as required under then subsection 4(1) of the SRC Act.[12]
[12] Ibid., page 16.
On 4 June 1993, following Mr Scanes’ request, Comcare reconsidered its determination and was ‘satisfied that the decision to disallow the claim can no longer be sustained’.[13] Accordingly, Comcare decided that ‘there is liability for aggravation of a disease namely coronary artery disease and resultant myocardial infarction’, with the date of the injury being 3 March 1993, when Mr Scanes first received medical treatment for the aggravation.[14] The reconsideration decision referred to the opinion of Dr David Coles, Cardiologist, that Mr Scanes’ ‘reaction to the stress of work was to smoke’ and because ‘his coronary artery disease seemed to be due to his smoking this seemed to form a link with the condition of his employment’.[15] The Comcare decision further stated that:[16]
I am satisfied that the employee’s employment did contribute in a material degree to the aggravation of the disease. The fact that the employee has been under a great deal of stress is not in dispute, and I am willing to accept that part of his reaction to that workplace stress, and his way of coping with it, was to smoke. I also accept that he smoked more heavily at work than at home.
His ‘employment’ therefore, includes his smoking. Consequently, there is a link between the employee’s employment and the aggravation of the coronary artery disease and subsequent myocardial infarction.
[13] Ibid., pages 17-20.
[14] Ibid.
[15] Ibid., page 19.
[16] Ibid.
On 30 June 1995, Mr Scanes ceased employment with the AFP.[17]
[17] Ibid., pages 55 and 117.
In September 1998, Mr Scanes presented to the Emergency Department at Calvary Hospital with what was described as ‘chest heaviness’, tingling down his arm and feeling light headed.[18] The accompanying doctor’s comments noted that Mr Scanes presented with ‘a transient episode of chest tightness’ and ‘the pain was felt on the right side of the chest’, but there was ‘no radiation’, ‘no palpitations’ and a ‘[n]ormal ECG’.[19] Mr Scanes’ past medical history recorded his myocardial infarction in 1993 and ‘very occasionally angina since’.[20]
[18] Ibid., page 153.
[19] Ibid., page 154.
[20] Ibid.
In September 2001, Mr Scanes was referred to the Emergency Department at Calvary Hospital with chest pain, right upper quadrant pain, right shoulder pain and shortness of breath.[21]
[21] Exhibit 2, pages 77-79.
In December 2005, Mr Scanes presented to the Emergency Department at Calvary Hospital with chest discomfort, tightness, breathlessness and ‘heart racing’.[22] An ECG showed ‘normal sinus rhythm’.[23]
[22] Exhibit 1, page 159.
[23] Ibid.
In June 2011, it was recorded that Mr Scanes experienced chest tightness for one week.[24]
[24] Ibid., pages 416-417 and 609-616.
On 17 March 2014, Mr Scanes made his ‘Last Will and Testament’, which identified his spouse, Ms Scanes, as the sole beneficiary of his estate.[25]
[25] Ibid., pages 84-87.
In 2017, Mr Scanes was diagnosed with emphysema and made a claim for compensation under the SRC Act.[26] In 2018, Comcare declined this claim, which decision it subsequently affirmed upon reconsideration and, in 2019, a differently constituted Tribunal affirmed Comcare’s reviewable decision.[27]
[26] Ibid., pages 21-25.
[27] Ibid., pages 34-40 and 46-80.
In April 2019, Mr Scanes presented to the Emergency Department at Calvary Hospital with ‘[l]eft lateral chest pain’ and was discharged the following day.[28]
[28] Exhibit 2, pages 119-123.
On 12 October 2020, Mr Scanes died, aged 71, at Calvary Hospital, following transportation from his home by ambulance after experiencing chest pain.[29] The ‘Certificate of Cause of Death’ completed on the same date by Mr Scanes’ general practitioner, Dr Leslaw Buczynski, stated that the disease or condition directly leading to the death was cardiac arrest, with ischaemic heart disease as an antecedent cause.[30] The subsequent Death Certificate dated 6 November 2020, stated that the cause of death was ‘cardiac arrest’ and ‘ischaemic heart disease (years)’.[31] The records of the ACT Ambulance Service from 12 October 2020, relevantly stated that:[32]
Pts wife states pt has had flu like symptoms for the past few days with no recent travel outside of the ACT. This morning pt was c/o chest pain and told his wife to call an ambulance. O/E pt GCS 14 – opens eyes to voice. Pt was grey in colour. Pts initial RR was 36 with a clear chest and good air entry. Pt was monitored in a sinus tachycardia of a rate of approx. 130-150. 12 lead ECG showed ST elevation just under 1mm in III and aVF. Pt stated he had CP. Pts GCS then dropped to 4. Pt was lowered to the ground and no pulse could be felt. CPR was commenced and one round of COACHED was completed. Pt had a pulse and was in a junctional rhythm. Pt was extricated. Once in the ambulance pt began to become bradycardic with no BP. Atropine was given with no effect. Pt then went back into cardia arrest. Once in resus a COACHED was due and pt remained in VF, another defibrillation was administered with ACTAS monitor. Pt was then handed over to Calvary hospital.
[29] Exhibit 1, pages 81 and 88 and Exhibit 2, page 333.
[30] Exhibit 1, page 81.
[31] Ibid., page 88.
[32] Exhibit 2, page 333.
On 7 December 2020, Mr Scanes’ widow, Ms Scanes, lodged with Comcare a ‘Claim for Compensation for a Work-related death’ in relation to her late husband and noted that she was his sole dependent.[33]
[33] Exhibit 1, pages 89-97.
On 20 January 2021, Comcare determined that it was not liable to pay compensation under the SRC Act in relation to the death of Mr Scanes.[34]
[34] Ibid., pages 114-118.
On 30 July 2021, following Ms Scanes’ request for reconsideration, Comcare affirmed its determination of January 2021, declining liability to pay compensation in relation to the death of Mr Scanes.[35]
[35] Ibid., pages 148-152.
On 6 August 2021, Ms Scanes applied to the Tribunal for review of Comcare’s decision.[36]
[36] Ibid., pages 9-11.
LEGISLATION
Subsection 14(1) of the SRC Act relevantly provides that Comcare is liable to pay compensation in accordance with the SRC Act ‘in respect of an injury suffered by an employee if the injury results in death’.
The Tribunal notes that ‘injury’ is defined in subsection 5A(1) of the SRC Act to mean:
(a) a disease suffered by an employee; or
(b) an injury (other than a disease) suffered by an employee, that is a physical or mental injury arising out of, or in the course of, the employee’s employment; or
(c) an aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment;...
Section 17 of the SRC Act sets out the manner in which compensation is payable for injuries resulting in death, relevantly as follows:
(1) This section applies where an injury to an employee results in death.
…
(3) Subject to this section and to sections 16 and 18, if the employee dies leaving dependants some or all of whom were, at the date of the employee’s death, wholly dependent on the employee, Comcare is liable to pay compensation in respect of the injury of $400,000[37] and that compensation is payable to, or in accordance with the directions of, Comcare for the benefit of all of those dependants.
…
(9) A reference in this section to a dependant of a deceased employee shall be read as a reference to a dependant by or on behalf of whom a claim is made for compensation under this section.
[37] Pursuant to section 13AA of the SRC Act, this compensation amount is indexed by reference to the Wage Price Index. At the time of Mr Scanes’ death on 12 October 2020, this amount was $575,364.35. See accessed on 25 July 2023.
Subsection 4(5) of the SRC Act relevantly states that a person who, immediately before the date of an employee’s death, lived with the employee and was the spouse of the employee, shall be taken to be a person who was wholly dependent on the employee at that date.
Finally, section 18 of the SRC Act provides for compensation in respect of funeral expenses, as follows:
(1) Where an injury to an employee results in death, Comcare is liable to pay compensation in respect of the cost of the employee’s funeral to the person who paid the cost of the funeral or, if that cost has not been paid, to the person who carried out the funeral.
(2) The amount of compensation is the amount, not exceeding the amount determined in accordance with subsection (4), that Comcare considers reasonable, having regard to:
(a) the charges ordinarily made for funerals in the place where the funeral was carried out; and
(b) any amount paid or payable in respect of the cost of the funeral under any other law of the Commonwealth.
(3) Where a person is liable to pay the cost of the funeral of an employee, any amount paid under this section to the person who carried out the funeral is, to the extent of the payment, a discharge of the liability of the first‑mentioned person.
(4) The maximum amount of compensation under subsection (2) is:
(a) $9,000; or
(b) if the regulations prescribe a higher amount—that amount.
Note: The amount of $9,000 is indexed under section 13.[38]
EVIDENCE
[38] Pursuant to section 13 of the SRC Act, this compensation amount is indexed by reference to the Consumer Price Index. At the time of Mr Scanes’ death on 12 October 2020, this amount was $12,491.46. See accessed on 25 July 2023.
Dr David Coles – Cardiologist
On 9 March 1993, Dr Coles wrote to the Medical Officer of the AFP relevantly as follows in relation to Mr Scanes:[39]
We thought that his inferior infarct probably started about three days ago. Accordingly I took the opportunity to study him fairly soon after his admission.
His problem is coming from a totally occluded right coronary artery. This seemed to be full of fresh clot but there was good retrograde filling in the left system. This latter implied that the narrowing that precipitated the total occlusion had been present for some time. He had well preserved left ventricular function and so his outlook should be reasonable.
[39] Exhibit 1, pages 201 and 927.

On 13 April 1993, Dr Coles wrote to Mr Scanes’ general practitioner, Dr David Craigie, relevantly as follows:[40]
It is now about a month since his acute inferior infarct and he reports to be feeling very well. He is exercising regularly and has had no further chest pain.
…
There was no sign of cardiac failure or cardiomegaly.
…
The ECG showed sinus rhythm with the older inferior infarct.
I was pleased with his progress and the fact that he has remained off cigarettes…I have no worries about his cardiac health, but would be concerned if he went back to a smoking environment too quickly. I would be grateful if you could check his fasting cholesterol and triglyceride levels in another month or so, and if appropriate use lipid lowering agents.
[40] Ibid., pages 924-925.
On 20 April 1993, Dr Coles provided a report to Comcare which stated that:[41]
Mr Warren Scanes was admitted to Woden Valley Hospital with chest pain earlier this year. He had had a history of pain for several days before presenting. He had an acute inferior infarct and subsequent coronary arteriography showed a total occlusion of his right coronary artery. He claims that this was due to stress.
In discussing this, it seems as though the stress may be working through his cigarette smoking. He says that when he is at work he smokes up to 60 cigarettes a day, but when he is at home he smokes only about 15 cigarettes in a day.
This seems to cover all the questions in paragraphs 1, 2 and 3. In regard to paragraph 4, he is now recovering from his infarct and gradually returning to normal physical activities. He is taking a small dose of beta blocker and half an Aspirin a day. He has mild residual mitral incompetence due to papillary muscle dysfunction, but no evidence of cardiac failure. His blood pressure is satisfactory. He thus has evidence of the infarct affecting his heart and this will probably continue indefinitely.
In summary, this man’s chest pain presented at work where he claims he is under stress. He supports this claim by giving evidence of his cigarette consumption when at work compared to home. While this connection is valid, I do not think stress has definitely been shown to play any part in the development of coronary artery disease.
[41] Ibid., page 27.
Dr Coles did not give evidence in this proceeding.
Professor Michael O’Rourke – Cardiologist
On 24 May 1994, Professor O’Rourke provided a report to Comcare’s then solicitors relevantly as follows:[42]
[42] Exhibit 5.
Mr Scanes showed me the copy of his coronary arteriogram report and still frames of the coronary arteriogram itself. I noted that left ventricular ejection fraction was excellent on March 4, 1993, despite recent infarction. The right coronary artery was completely occluded, but it filled promptly with abundant collaterals from the left injections.
…
I was surprised by the normal left ventricular ejection fraction in the coronary arteriogram performed on the day of admission with diagnosis of acute myocardial infarction, and also by the angiographic finding of a completely occluded right coronary artery with abundant collaterals providing excellent filling from the left coronary system at this time. Hence I called for the notes of the hospital admission at Woden Valley Hospital on March 4, 1993. These notes paint a rather different picture than presented to me by Mr Scanes at his appointment with me.
The hospital notes describe from two observers the onset of symptoms on the evening of Monday, March 1, with a continuation of pain over the Tuesday and Wednesday and with this taking on a different character suggesting pericarditis when admitted to the hospital on Thursday, March 4. There is no mention at all in these notes of excessive stress. On the contrary, the referring letter from the Police doctor described the pain as being intensified by laughing and the admitting officer made the same comment. The initial electrocardiogram was described in the Discharge Summary as showing old inferior myocardial infarction. Centrally there was no progression of the electrocardiographic features of myocardial infarction while in hospital. The diagnosis of myocardial infarction however was made on the basis of elevated cardiac enzymes (CK and LDH), both of which were elevated to more than twice the upper limit of normal. In his angiographic report of March 9, 1993, Dr Coles made the same interpretation about onset of inferior infarction some days previously and drew attention to the possibility that high grade obstruction of the right coronary artery had been present for quite some time, allowing development of collateral vessels such that acute occlusion caused a very small myocardial infarction. Mr Scanes suffered no complications of myocardial infarction while in hospital, apart from some recurrence of chest pain while watching football on television some days before discharge.
…
In my view, on the balance of probabilities, Mr Scanes’ work as a Police officer did not contribute to myocardial infarction which apparently commenced on the evening of Monday, March 1, with continuing symptoms of myocardial ischaemia and possibly of pericarditis up until the morning of March 4. Mr Scanes had other risk factors for myocardial infarction, including heavy drinking, heavy smoking, past hypertension and possible family history.
…
I agree with the claimant’s medical treatment. Coronary arteriography was performed on the basis of the patient having suffered myocardial infarction some days before with possible continuation of anginal pain. Only one coronary artery was affected and collateral vessel supply to this artery was excellent. There was no need for angioplasty or surgery. Subsequent treatment was standard. In view of the very small infarct and excellent angiographic features, it is surprising that convalescence was so long and return to work so late with continuation of light duties. I am surprised that more than twelve months after this minor infarction, Mr Scanes described to me that he was still on “return to work program”. This man had a tiny myocardial infarction and suffers from non-threatening residual coronary disease, which was known at the time of his hospital admission in March 1993.
…
Mr Scanes has suffered a small inferior myocardial infarction. Infarction is so small that left ventricular ejection fraction at coronary arteriography three days after onset of symptoms was within the normal range. In terms of myocardial damage, Mr Scanes has probably suffered infarction to 5% of his left ventricle.
…
I believe there is a tenuous link between Mr Scanes’ employment and his smoking habit…I believe that there was no relationship between his occupation and his heart attack. I believe that the smoking was a bad habit which he has subsequently been able to control, and that the heart attack would have occurred whether or not he was a member of the ACT Police Force.
Professor O’Rourke did not give evidence in this proceeding.
Dr Graeme Griffith – Consultant Surgeon
On 18 June 2012, Dr Griffith provided a report regarding a separate condition suffered by Mr Scanes, but relevantly stated that:[43]
In 1991 [sic] he suffered a myocardial infarction for which he was an inpatient for a week. He was found to have a 5% arterial block with coronary angiography. At the time, he was a heavy smoker, which he immediately ceased completely. He takes aspirin 100mg as a prophylactic, and is currently not under any medical supervision from this point of view – not a position I would advise for an individual his age group. Her [sic] requires at least an annual assessment by a cardiologist and a regular ECG at least.
[43] Exhibit 1, pages 393-402.
Dr Griffith did not give evidence in this proceeding.
Dr Wai Meng Voon – Respiratory Physician
On 23 January 2018, Dr Voon reported to Mr Scanes’ general practitioner that ‘of concern is his complaint of near-constant central chest tightness, especially given his background history of ischaemic heart disease. He does not have any cardiology follow-up in place…There were no signs of right heart failure’.[44]
[44] Ibid., page 700.
On 7 February 2018, Dr Voon provided a report to Mr Scanes’ general practitioner following lung function tests performed two days earlier.[45] Dr Voon relevantly opined that ‘it would be also be worthwhile referring Warren to a cardiologist for investigation of possible underlying coronary artery disease in view of the chest tightness’.[46]
[45] Ibid., page 702.
[46] Ibid.
On 28 February 2018, Dr Voon provided a report to Mr Scanes in relation to his workers’ compensation claim for emphysema and agreed with Dr Coles’ report from 1993, which ‘also concluded that the amount of cigarette smoke is the sole contributing factor to his emphysema as well as his myocardial infarction’.[47]
[47] Ibid., page 41.
In August 2019, following a consultation with Mr Scanes after ‘a screening CT chest done in May this year’, Dr Voon reported to Mr Scanes’ general practitioner that there ‘were no signs of right heart failure’.[48] In February 2020, Dr Voon again stated that ‘there were no signs of right heart failure’.[49]
[48] Ibid., page 497.
[49] Ibid., page 494.
Dr Voon did not give evidence in this proceeding.
Associate Professor Gutman – Cardiologist
On 23 March 2021, Associate Professor Gutman provided a report to Ms Scanes’ solicitors in this proceeding, which relevantly stated that:[50]
I have been asked to assume that Mr Scanes did not suffer from any significant cardiac symptoms after 1993 and certainly did not suffer any further myocardial infarction. The most likely cause of sudden cardiac death in ischaemic heart disease is a cardiac arrhythmia. This is due to previous myocardial infarction which causes scarring of the left ventricular myocardium and at a much later date that the myocardial infarction patients can experience sudden cardiac death as it related to the scar/fibrosis of the left ventricular myocardium.
I have taken into account the medical history and the medical material supplied. It is my opinion that the accepted condition described was more likely to be the cause of the death suffered by Mr Scanes in 2020. It was more likely than not to be a cause of death due to the scarring of his left ventricle related to the myocardial infarction which occurred prior to 3 March 1993. The myocardial infarction occurred on 1 March 1993.
[50] Ibid., pages 129-131.
Associate Professor Gutman made a supplementary report dated 12 April 2022, which relevantly stated that:[51]
[51] Exhibit 2, pages 317-319.
I have now received additional information including the ambulance record and the emergency department notes from Calvary Hospital which lead me to change my opinion as to the cause of death.
…
The ambulance record noted that he had chest pain, a heart rate between 130 bpm and 150 bpm with an ECG demonstrating sinus tachycardia and inferior ST elevation.
Whilst the ambulance crew was in attendance, he deteriorated. He had no pulse and the ECG demonstrated a bradycardia and junctional rhythm. Initial record when the ambulance arrived indicated that at 8:33 am his heart rate was 138 bpm, sinus tachycardia, blood pressure 85/58 mmHg and he was cold, grey and clammy.
At 8:43 am, his pulse was 52 bpm with a blood pressure 65/33 mmHg. 12-lead ECG demonstrated sinus bradycardia.
At 8:52 am, his heart rate was 27 bpm with a junctional rhythm.
At 8:55 am, he had pulseless electrical activity and at 9:07 am he had ventricular fibrillation.
Atropine was administered when he had bradycardia with no effect.
Multiple defibrillator shocks were administered with no improvement in his rhythm or clinical status.
At Calvary Hospital, it was noted that his status had not improved. A transthoracic echocardiogram in ED demonstrated no pericardial effusion and the aorta was not dilated.
I am now of the opinion that he had an inferior myocardial infarction as the most likely cause of his death. He had a cardiac arrhythmia secondary to this acute myocardial infarction which occurred on 12 October 2020.
The reasons I now give for changing my opinion is that I have now been provided with full documentation of the course of events.
He had chest pain. His ECG demonstrated inferior ST elevation. He also did not have a primary cardiac arrhythmia when the ambulance arrived.
Associate Professor Gutman made a further supplementary report dated 23 May 2022, which responded to questions from Ms Scanes’ solicitor as follows:[52]
[52] Ibid., pages 325-326.
In your opinion, on the balance of probabilities, was Mr Scanes’ myocardial infarction in 1993 an effective or operative causal factor in his death on 12 October 2020, whether alone or in combination with other identified causes?
On the balance of probabilities, Mr Scanes’ myocardial infarction in 1993 was an effective or operative causal factor in his death on 12 October 2020.
2. If your answer to Q1 is “yes”, please explain the reasons for your conclusion.
When Mr Scanes was assessed by the ambulance crew on the day of his death, it was noted that he had a very low blood pressure. This is considered to be consistent with cardiogenic shock. The leading cause of cardiogenic shock is acute myocardial infarction due to left ventricular dysfunction. One of the significant predisposing factors for cardiogenic shock is previous infarction (A review of cardiogenic shock in acute myocardial infarction, L Khalid and SH Dhakam. Curr Cardiol Rev. 2008 February; 4(1):34-40).
Mr Scanes had a previous history of myocardial infarction in 1993 which contributed significantly to his episode of cardiogenic shock which caused his death in 2020. Cardiogenic shock continues to be the most common cause of death in patients hospitalised with acute myocardial infarction. (L Khalid and SH Dhakam, reference above). [emphasis in original]
Associate Professor Gutman gave concurrent evidence at the hearing of this proceeding, which is discussed further below in these reasons.
Associate Professor Colquhoun – Cardiologist
On 3 June 2021, Associate Professor Colquhoun provided a report to Comcare for the purpose of its assessment of Ms Scanes’ compensation claim, which ultimately became the subject of this proceeding, which report relevantly stated that:[53]
[53] Exhibit 1, pages 137-140.
The specific question you ask is: "In your opinion, was Mr Scanes' death on 12 October 2020, the result of his compensable myocardial infarction of June 1993? Please provide reasons for your opinion, noting Mr Scanes did not seek medical opinion for his condition after April 1997".
ANSWER
The short answer is "Yes". It has been clear in the medical literature for more than 50 years that if a patient survives a myocardial infarction (approximately 30% die from the initial event) they have an increased risk of suffering CHD death, an increased risk compared to age-matched control. Of patients who survive their myocardial infarction and are discharged, risk varies considerably from about 2% per year over the next 5 years of having a major coronary event or death, up to more than 25%. This was seen in our Australian LIPID Trial of which I was an investigator and I was one of the authors who published on prognosis post-infarction. This risk can be decreased considerably by lowering LDL cholesterol with modern therapy.
The LIPID Trial of which I was an investigator, 9,400 patients who survived an acute coronary syndrome were followed-up for 6.1 years, half on Pravastatin 40 mg and half on placebo. This 1 mmol/L reduction of LDL was associated with a relative reduction of coronary heart disease events of 24%.
Mr Warren Scanes suffered from stress (perceived stress) at work and this stress continued after his heart attack.
Psychosocial risk factors and heart disease were reviewed by the Heart Foundation (I was a member of the committee) approximately 20 years ago. We published in the Medical Journal of Australia "Stress and Cardiovascular Disease". In 2013, we published an update and I was Chair of the Expert Working Group. The title was "Psychosocial Risk Factors for a Coronary Heart Disease". Our group concluded "perceived chronic job strain and shift work are associated with a small absolute increase in the risk of developing coronary heart disease. But there is limited evidence regarding their effect on prognosis of CHD". Further evidence of long terms prognosis was obtained from the abovementioned Australian and New Zealand LIPID Trial. Professor Ralph Stewart was the lead author and our long-term data showed that perceived persistent stress over time after a myocardial infarction was associated with greater than 200% increase in sudden cardiac death. This was independent of any other risk factors, including vigorous lipid lowering. Important: it was perceived moderate to severe ongoing stress. Perceived stress was measured frequently during the 6-year period and then death rates were followed-up for more than a decade. These 3 papers are specifically relevant to the question you have asked me.
To answer your question again, perceived stress as well as measurable depression independent of classic risk factors, increases risk of first and recurrent cardiovascular events - unstable angina, myocardial infarction and sudden cardiac death. Vigorous lowering of LDL cholesterol decreases risk but does not abolish the risk.
The myocardial infarction back in 1993, increased Mr Scanes' risk of sudden cardiac death, which finally did occur on 12 October 2020. [emphasis in original, footnotes omitted]
On 15 July 2021, Associate Professor Colquhoun provided a supplementary report to Comcare, which relevantly stated that:[54]
[54] Ibid., pages 144-147.
You have noted on the first page of your letter of 10 June 2021, that Mr Scanes had his myocardial infarction in June 1993 and he died in October 2020, “which is 27 years after the initial myocardial infarction and 23 years after he obtained any medical treatment in relation to this event”.
Having a heart attack (myocardial infarction) has been known since the early-1950s in the medical literature to have an effect on survival for the rest of an individual’s life. In 1951, Louis Sigler published “Prognosis of Angina Pectoris and Coronary Occlusion: Follow-up of 1,700 Cases”. In this study, he noted that others had reported the average survival after a heart attack was 3.4 years. In the early 50’s others had noted that 50% were dead at either 3 years or 5 years.
In 1962 Sigler reported on a 34-year follow-up of the 1,700 cases and noted that 68.4% of males and 89.6% of females were still living between 10 and 14 years. This decreased over time and, of the 43 males, he noted further that 31% of males were alive at 15 years or longer, but only 2.3% for 22 years or longer.
In our Australian LIPID trial where 9,014 patients following a heart attack or unstable angina were randomised a pravastatin or placebo. The trial was stopped at 6 years due to the clear decrease in death with pravastatin therapy. This was published in the New England Journal. Relevant to your question, we published a 16-year follow-up of the LIPID trial. I was an author of this study. It was noted “in LIPID, the absolute benefit from 6 years of pravastatin treatment appeared to be maintained for the next 10 years, with a similar risk of death amongst survivors in both groups after initial treatment”. In short, treatment with pravastatin, which led to a 1 mmol/L reduction, led to a 3% decreased in mortality at the 6-year mark. The natural death rate could be modified with lowering cholesterol.
A contemporary huge follow-up of patient in general who have sustained a myocardial infarction compared to aged matched controls was published in the British Medical Journal in 2017. It is a study of greater than 200,000 patients, half of whom had a myocardial infarction half were controls.
There were 4 cohorts at various ages, and they were followed-up for 24 years. It was noted “After 7 years, people with a first or recurrent AMI had double or triple the risk of mortality compared to the general population of equivalent sex and age”.
The authors noted “The adjusted hazard of all causal mortality for AMI patients was constant during the follow-up of 24 years; it did not matter how many years the cases had already survived they were still at high risk of dying than controls”. This study that encompassed approximately 75% of all heart attacks in England provides very robust data to answer your question. I quote further “Compared with no history of AMI by age 60, 65, 70 or 75, having a myocardial infarction was associated with … this translates into a decreased life expectancy of 5.9, 5.4, 4.1 and 3.7 years respectively.
In answer to your questions:
1. In your report you state that in 1993 Mr Scanes had an inferior myocardial infarction and angiography revealed an occluded right coronary artery. You state that Mr Scanes was treated with Aspirin and Metoprolol and that the Metoprolol was stopped on review by Dr Coles the following year on follow-up.
1(a) Did Mr Scanes suffer from any cardiovascular disease prior to the myocardial infarction in 1993? Please detail.
Not that I am aware of.
1(b) Did Mr Scanes suffer permanent damage or changes to his cardiac function as a direct result of myocardial infarction in 1993? Please detail.
Yes. A heart attack leaves permanent scarring of the heart muscle or myocardium. This is by definition as there is death to heart muscle.
1(c) Noting that Mr Scanes has made a full return to work, ceasing metoprolol and he did not require medical treatment from 1997 onwards and thus he has not required treatment for 23 years until the time of his death, had Mr Scanes’ acute myocardial infarction episode in 1993 resolved? Please provide your clinical justification to support your conclusion.
A myocardial infarction does not resolve. There is permanent scar to the heart muscle and, unless there is vigorous lowering of LDL – cholesterol, there will be progression of the underlying atherosclerosis, which results in further cardiovascular events. The scar per se can be a site for ventricular arrythmias, such as ventricular tachycardia or for ventricular fibrillation, which leads to death. It is clear in patients with coronary disease for every 1 mmol/L reduction of LDL there is 25% less heart attacks, 20% less strokes and 10% lower death rates over subsequent years. In addition, regression of the atherosclerosis in the coronary arteries has been demonstrated by intravascular ultrasound. I have been an investigator in a number of these important trials that have shown regression of plaque. When on-treatment LDL is approximately 1.8 mmol/L, 60% of patients show measurable regression of plaque in coronary arteries. When the LDL is approximately 0.8 mmol/L, up to 90% of patients show regression of plaque.
2. You have stated that ongoing stress after a myocardial infarction significantly increases a person’s chances of a sudden cardiac death. Mr Scanes left his AFP employment two years after his myocardial infarction, being 25 years prior to his death. Is any perceived stress in the 25 year period beyond 30 June 1995 when he left the AFP attributed to his employment with AFP? If so, please provide your clinical justification and detail if there is a relationship with his death in October 2020? Please provide relevant medical literature to support your conclusion where applicable.
Perceived stress in an important predictor of first and recurrent myocardial infarction and death and is well documented in the literature. In the INTER-HEART study which was a multicentre international trial comparing patients that had had a heart attack to age-matched controls, demonstrated clearly that perceived stress was one of the most important risk factors for explaining myocardial infarction across all patient groups in all countries as important as elevated cholesterol in diabetes. Specifically, perceived stress was measured in our Australian Lipid Trial (which I have mentioned above).
I was an author with Dr Ralph Stewart and perceived stress, which was persistent, was associated with a 285% greater death rate over the following 12 years. Our paper was published in the British Medical Journal and when it was presented at the European Society of Cardiology the research received a commendation as one of the best abstracts presented at the meeting.
3. You ask specifically “At the time of Mr Scanes’ cardiac arrest in October 2020, please comment on Mr Scanes’ absolute cardiovascular risk and detail his relevant modifiable and non-modifiable risk factors which were present. In addition to outlining these factors, please specifically address the below co-morbidities and lifestyle factors by providing your opinion on whether there is a contribution to his ischaemic heart disease that resulted in a cardiac arrest in 2020 and summarise the relationships between the below factors and what is reported in the medical literature.”
a. Smoking. It is well documented that Mr Scanes was a heavy smoker
b. COPD. Mr Scanes was diagnosed with emphysema
c. High levels of low-density lipoprotein (LDL) cholesterol. In your report you state that Mr Scanes had a LDL cholesterol level of greater than 2 when it was measured.
d. Hypertension. In your report you note that in 1984 hypertension was noted.
The concept of “absolute cardiovascular risk” relates to patients who have not had a cardiovascular event and predication of first event. In terms of secondary prevention, it relates to risk of further heart attacks and strokes related to what is called “secondary prevention”. Probably the best data on this comes from our Australian Lipid Trial of which I was a second author of the subsequent study on “Long-term risk stratification for survivors of acute coronary syndrome: results of the Lipid Study”. In this paper, we noted that with multiple risk factors such as high cholesterol, smoking and diabetes the risk of a further heart attack, stroke or death in the next 5 years was as high as 25% versus patients on statin with none of the above risk factors who survived a heart attack as low as 5%. There is no huge difference in absolute risk depending classic risk factors. When it comes to risk of dying in the first few months, this relates to impairment of heart function mainly, and the data on this is not relevant to the case at hand.
Considering all the contributing or risk factors you have identified above, and given the time which elapsed between Mr Scanes’ initial myocardial infarction in 1993 and his death in October 2020, with a 23 year period of no ongoing medical treatment, on the balance of medical probabilities, was Mr Scanes’ cardiac arrest caused by ischaemic heart disease a direct result of his myocardial infarction in 1993? Please explain your reasoning for your opinion, particularly addressing the timeframes involved in this matter
As explained above, having a heart attack is associated with increased risk of dying over a lifetime and has been documented over at least 24 years. This has been explained above. His cardiac arrest relates to his ischemic heart disease – both atherosclerosis in his coronary arteries and the scar left from his myocardial infarction. A scar can be irritable and can lead to sudden cardiac death, unrelated to acute ischaemia per se. [emphasis in original, footnotes omitted]

On 8 March 2023, Associate Professor Colquhoun provided a further supplementary report, following a request from Ms Scanes’ solicitor for his further opinion, which report relevantly stated that:[55]
[55] Exhibit 7.
A previous index myocardial infarction, which causes scar tissue, does not cause further heart attacks. Further heart attacks are due to ruptured or eroded atherosclerotic plaques in an artery, which has nothing to do with scar in muscle. Whether a patient has good functional capacity following infarction, is irrelevant as to whether or not a patient ruptures a plaque in the future inside an artery, which leads to an acute coronary syndrome, either sudden cardiac death, heart attack or heart failure.
…
In 1993, with the further evidence supplied to me with the recent letter, it is clear that on the day of death, he had a new acute inferior myocardial infarction, which is in the reports from Professor Jack Gutman and Dr Ken Hossack. It is this new myocardial infarction, which led to severe slowing of the heart rate and low blood pressure.
This is seen in many patients who have an inferior myocardial infarction and is due to excessive vagal activity (Bezold-Jarisch reflex) or it is due to severe acute impairment of right ventricular function, which leads to underfilling of the left ventricle and there is severe hypotension. The slow heart rate is vagal stimulation, and this is why Atropine was given for resuscitation. The first inferior myocardial infarction, due to the blocked right coronary artery, would have led to some permanent damage in the right ventricle and inferior wall of the left ventricle and, therefore, a further infarction in the same territory is likely to have been more haemodynamically significant as there was previous damage in the previous area.
In short, the previous infarction would have contributed to the poorer functional reserve during the acute event, which was fatal.
…
Dr Ken Hossack correctly agrees with me on the partial treatment of the number one cause for atherosclerosis — an elevated LDL cholesterol. At no stage was he in the target ranges at the time for a patient who has had an acute coronary syndrome or myocardial infarction. For the last 30 years or so, the target level of LDL in a patient who had had a heart attack, is less than 1.8 mmol/L. On 12 June 2020, his LDL was 2.7.
I note that Dr Hossack has stated “I disagree with Dr Colquhoun’s assertion that stress was a contributor to the death of Mr Scanes”. He goes on to quote an article in the Medical Journal of Australia, of which I was an author! He quotes the 2003 article out of context and, at the time, he said there was no strong or consistent evidence of a causal relationship.
In the updated Heart Foundation articles on psychosocial factors of heart disease, of which I was the chairman of the Special Advisory Group, we published two articles in 2013, which explained psychosocial risk factors in detail and recommended screening and treating for depression in patients with known coronary heart disease and/or risk factor for coronary heart disease.
From our Australian Lipid Trial, which was published in the New England Journal of Medicine in 1998, we screened for perceived stress on multiple occasions and then with long-term follow-up and published our findings in the British Medical Journal in 2017. Patients in whom there is moderate to severe perceived distress in their life, on multiple occasions during a 6-year follow-up, had a 250% greater chance of all-cause mortality during long-term follow-up.
In the letter from Dr William Knox, Psychiatrist, on 24 April 2019, Dr Knox states: “Mr Scanes told me of various incidents at work, which he believes account for his ongoing stress condition”. In the second last paragraph, Dr Knox states: “I would expect, however, that his high level of tension, frustration and anger, will continue until there is a working-through of his claim with Comcare. He certainly feels very bitter and hurt by how matters unfolded”.
In 2019, Dr David Coles in his letter, 20 April 1993, noted in his report, last paragraph: “In summary, this man’s chest pain presented at work, where he claims he is under stress. He supports his claim by giving evidence of his cigarette consumption when at work, compared to at home. Whilst this connection is valid, I do not think stress has definitely been shown to play a role in the development of coronary heart disease”. Dr David Coles admits that he’s under stress at work — “perceived stress”, but then does not know of the relationship between stress and coronary heart disease. There is an independent relationship between perceived stress, coronary disease, depression and a link to all-cause mortality, driven by coronary heart disease.
In 2017, his GP, Dr Bczynski [sic], from the ACT, states in the last paragraph: “I believe that Mr Scanes’ heavy smoking was related to significant stress at work whilst he was working for the AFP. It is not clear whether he actually suffered from post-traumatic stress disorder. I was a co-author of a 2017 paper published in the Medical Journal of Australia, which clearly showed multiple comorbidities with post-traumatic stress disorder and the higher rates of coronary heart disease. This area of psychosocial factors and heart disease is not an area of expertise of many cardiologists, and I can understand why Dr Hossack did not think that this was important.
…
In fact, the death of Mr Scanes, now with further information, clearly was related to an acute inferior myocardial infarction associated with severe hypotension and bradycardia, related to either Bezold-Jarisch reflex or right heart failure from underfilling of the right ventricle, this then led to later ventricular fibrillation — sudden cardiac death. It was due to the acute event and the decompensation, and the acute inferior myocardial infarction was almost certainly made worse by previous myocardial infarction in the same territory of the heart.
…
By definition, Mr Scanes had cardiogenic shock. The heart was the cause of low blood pressure. The slow heart rate and low blood pressure is in the context of inferior myocardial infarction. It is not due to a severe large heart attack, per se. In many patients, Atropine, which was given to him, reverses the problem almost immediately. Atropine does not improve heart function. Atropine does not relieve ischaemia; it simply breaks the vagal reflex from inferior ischaemia. It is not due to left ventricular dysfunction.
…
The death of Mr Scanes in 2020 was due to a new acute inferior myocardial infarction of previous myocardial infarction. His presentation of bradycardia with low blood pressure is consistent with a primary immediate vagal stimulation (Bezold-Jarisch reflex). Cardiogenic shock, per se, from a large damaged heart, is associated with tachycardia not bradycardia. The previous myocardial infarction in 1993 caused damage to the inferior wall of the left ventricle and probably the right ventricle and predisposed him to the haemodynamic compromise with further inferior myocardial infarction.
…
The 1993 infarction was an inferior myocardial infarction and from which Mr Scanes made a good recovery, regarding his ability to do physical activity.
However, as I pointed out in my earlier reports and in Dr Hossack’s report, his cholesterol was not adequately treated, in terms of the guidelines at the time and certainly by 2020, the gap from recommendations, such as the American Heart Association and the ESC, had widened further. In 2019, the European Societies of Cardiology recommended that in a patient who has had a myocardial infarction, that the on-treatment LDL should be less than 1.4 mmol/L.
Also, it would appear that he had significant ongoing perceived stress, a powerful independent, psychosocial risk factor for recurrent cardiovascular events and death. Almost certainly, he had depression, if it was screened, according to 2013 recommendations of the expert committee of the Heart Foundation, but this is nowhere seen in any of the correspondence that I have seen.
Resolution of depression either through placebo or any treatment, is associated with at least a 50% reduction of cardiovascular death, as seen in the long-term follow-up of patients in the Sad Heart and Enriched Trials. Adequate screening in treating a patient for psychosocial factors and particularly depression, in patients with coronary heart disease, is suboptimal in Australia and indeed throughout the world.
In patients who have had a heart attack, up to 30% have major/minor depression secondary to the myocardial infarction, although patients who have pre-existing depression have a greater risk of developing a heart attack. The damage from his first myocardial infarction in 1993 would have made him more susceptible to the haemodynamic problems he had with his index, fatal, inferior myocardial infarction in 2020.
Associate Professor Colquhoun gave concurrent evidence at the hearing of this proceeding, which is discussed further below in these reasons.
Dr Kenneth Hossack – Cardiologist
On 15 March 2022, Dr Hossack provided a report in this proceeding, which relevantly stated that:[56]
[56] Exhibit 6.
In my opinion, Mr Scanes did not have any ongoing effects as a result of the 1993 cardiac event. In particular at the time of the myocardial infarction, ventricular function was assessed in the normal range. Over the subsequent years Mr Scanes did not demonstrate any evidence of heart failure. Mr Scanes, after a period of time, was able to return to the work force. Mr Scanes had no history of cardiac arrhythmias following the event in 1993.
…
It would be my opinion that Mr Scanes sustained an acute coronary event that was complicated by a cardiac arrest. In providing this opinion I take into account that there is a history that Mr Scanes experienced chest pain before he had the syncopal episode. The laboratory tests indicate an elevated troponin. On the basis of ischaemic chest pain and an elevated troponin level a diagnosis of acute coronary syndrome is made. The cardiac arrest was a complication of the acute coronary syndrome. In my opinion, the acute coronary syndrome was due to plaque rupture.
I have listed LDL cholesterol values for Mr Scanes over the period 1997 to June 2020.[57]
LIPID VALUES
[57] See also Exhibit 3.
DATE  LDL mmol/L
02.04.1997                3.3
25.05.1998                3.1
22.11.2003                2.8
02.12.200[5]               1.8
22.09.2006                2.1
23.12.2008                2.3
21.0[5].2010               2.4
[12].01.2018               2.1
12.0[5].2020               2.7
In patients suffering a myocardial infarction due to coronary artery disease it is recommended that the target for LDL cholesterol is 1.5mmol/L or less. Over a 23 year period Mr Scanes had suboptimal lipid values. I am of the opinion that this was the major factor (>50% probability) that contributed to the progression of coronary artery disease in Mr Scanes. I am of the opinion that as a result of elevated cholesterol values Mr Scanes developed further plaque in the coronary arteries and part of the plaque ruptured to cause an acute coronary event in October 2020.
Treatment of elevated cholesterol with certain drugs results in stabilisation of plaque within the coronary arteries and minimizes the risk of plaque rupture leading to an acute coronary syndrome. I am of the opinion that Mr Scanes having ceased smoking in 1993, that smoking did not contribute to the event in October 2020.
I am of the opinion that the cardiac episode in 2020 was not a primary rhythm problem of the heart but was an acute coronary event complicated by a rhythm problem. The acute coronary event was due to progression of coronary artery disease due to elevated cholesterol.
…
I am of the opinion that on the balance of probabilities the major contributing factor to Mr Scanes death was hyperlipidaemia. It is possible that hypoxia as a result of severe lung disease could predispose Mr Scanes to a cardiac arrhythmia complicating an acute coronary syndrome.
I disagree with the opinion expressed by Associate Professor Gutman that the cause of death was due to an arrythmia caused by the myocardial infarction that occurred in 1993. It is my opinion that Associate Professor Gutman has ignored the significant contribution that untreated elevated cholesterol over a 23 year period makes to the progression of coronary artery disease. In providing his opinion, Associate Professor Gutman ignored the history that Mr Scanes had chest pain prior to the cardiac arrest and that laboratory tests indicated an elevated troponin at the time of the cardiac arrest. It is my opinion that the history of chest pain indicates that Mr Scanes was having an acute coronary syndrome. I am of the opinion that the acute coronary syndrome is due to plaque rupture that was associated with progressive coronary artery disease and was unrelated to the remote myocardial infarction that occurred in 1993.
…
I disagree with Dr Colquhoun’s opinion that the death on 12.10.2020 was a result of the myocardial infarction in 1993.
In my opinion, Dr Colquhoun has not taken into account the circumstances of the death. Specifically, Dr Colquhoun does not take into account that Mr Scanes was experiencing chest pain prior to the syncopal episode. I am of the opinion that the presence of chest pain was indicative of an acute coronary syndrome and not a primary arrhythmia as Dr Colquhoun opines.
I agree with Dr Colquhoun that the LDL cholesterol was abnormally elevated and my report indicates that it was abnormally elevated for a 23 year period following the myocardial infarction. Dr Colquhoun emphasises the importance of cholesterol lowering treatment in the improved survival of patients following an acute myocardial infarction. However, the studies that report an improved survival with the use of cholesterol lowering treatment do not suggest that the mechanism for the improved survival is an anti-arrhythmic effect. The studies indicate lipid lowering therapy slows or prevents progression of atherosclerotic disease and in some cases can cause reversal of plaque accumulation.
Stabilisation of plaque that prevents plaque ulceration or rupture is a major mechanism for the improved survival of patients with coronary artery disease who are prescribed cholesterol lowering therapy.
I disagree with Dr Colquhoun’s assertion that stress was a contributor to the death of Mr Scanes. In particular, I note in the article referenced by Dr Colquhoun (Medical Journal of Australia 2003, 178:272-276) stated: “The expert group concluded that (ii) there is no strong or consistent evidence for a causal association between chronic life events, work-related stressors, (job control, demands and strain), Type A behaviour patterns, hostility, anxiety disorders or panic disorders and CHD”.
This article does not support the contention of Dr Colquhoun that stress contributed to the death of Mr Scanes. [emphasis in original]
On 15 March 2023, Dr Hossack provided a supplementary report, which relevantly stated that:[58]
[58] Exhibit 8.
I have reviewed the material provided including the reports of Associate Professor Gutman dated 12.4.22 and 23.5.22 and the report of Dr Colquhoun dated 8.3.23.
None of the material provided causes me to change my opinion. My opinion is that Mr Scanes died as a result of an acute myocardial infarction. The underlying factor that caused to the myocardial infarction was the rupture of atherosclerotic plaque as a result of poorly controlled cholesterol. In my opinion the myocardial infarction that occurred in 1993 did not contribute to the outcome of the myocardial infarction that occurred on 12.10.2020.
…
I agree with Associate Professor Gutman's opinion in his report dated 12.4.22 that Mr Scanes died as a result of a myocardial infarction.
I disagree with Associate Professor Gutman's opinion that the location of the myocardial infarction was an inferior myocardial infarction. The material provided to the experts does not include a copy of the ECG that was performed when the Ambulance officers arrived. The description in the ambulance record is that there was ST elevation of less than 1mm in leads 3 and AVF. In my opinion this does not meet the criteria for diagnosing an inferior myocardial infarction.
Associate Professor Gutman has not taken into account that Mr Scanes had well developed collateral supply to the right coronary artery at the time of the angiogram following the myocardial infarction in 1993. The angiogram demonstrated that the occlusion in the right coronary artery was complete and was in the proximal portion of the right coronary artery. It would be my opinion that the coronary artery on the left side of the heart supplying collateral flow to the right coronary artery was the culprit vessel for the myocardial infarction that occurred on 12.10.2020.
With respect to the report by Associate Professor Gutman dated 23.5.22. I disagree with Associate Professor Gutman's opinion that the myocardial infarction in 1993 was an effective and operative causal factor in Mr Scanes death on the 12.10.2020. It would be my opinion that the myocardial infarction that occurred in 1993 resulted in minimal damage to the myocardium and there was no significant residual impairment of cardiac function as a result of the myocardial infarction in 1993. The evidence for this is provided by the fact that Mr Scanes did not have any evidence of heart failure following the myocardial infarction and that after a period of time he was able to return to gainful employment. I disagree with Associate Professor Gutman's opinion that the prior history of myocardial infarction contributed significantly to the episode of cardiogenic shock. It would be my opinion that Mr Scanes died as a result of cardiac arrhythmias including ventricular fibrillation which did not respond to electrical cardioversion.
…
Dr Colquhoun and I agree that the myocardial infarction in 12.10 2020 was related to poorly controlled cholesterol. I agree with Dr Colquhoun's statement that "previous index myocardial infarction which causes scar tissue does not cause further heart attacks. Further heart attacks are due to ruptured or eroded atherosclerotic plaque in an artery which has nothing to do with scar in muscle".
Dr Colquhoun and I disagree on the effect of stress on the development of the myocardial infarction on 12.10.2020. In considering my report of 15.3.2022 Dr Colquhoun did not taken into account the assumption Mr Scanes did not experience stress related to his AFP employment beyond 1995.
The coronary angiogram performed in 1993 following the myocardial infarction demonstrated that there was collateral blood flow from the left system to the distal right coronary artery. In my opinion this collateral blood flow was in existence prior to the myocardial infarction and developed as a result of the slowly progressive stenosis in the proximal right coronary artery. When the proximal right coronary artery occluded completely in 1993 the presence of collateral blood supply preserved myocardial function and resulted in minimal cardiac damage. The functional result of the myocardial infarction in 1993 was such that Mr Scanes was able to return to work.
There is a large body of scientific evidence that indicates that following a myocardial infarction there is a process of positive remodelling that can occur. There can be compensatory hypertrophy of muscles around the myocardial infarction and hypertrophy of surviving myocardial muscle within the area of myocardial infarction. Over time the area affected by the infarction reduces in size and negates the adverse haemodynamic effects of the myocardial infarction.
Dr Colquhoun suggests that I quoted the Medical Journal of Australia article out of context. The quotation that I provided is the exact quotation from the abstract that was provided with the Medical Journal of Australia article.
I disagree with Dr Colquhoun that the research article that he refers to in the British Medical Journal 2017 is applicable to Mr Scanes. The research article examined individuals who following a myocardial infarction had assessment of stress and other psychological symptoms on four occasions. The risk that Dr Colquhoun quotes of 250% greater chance of mortality during long term follow up was found in individuals who had three or more assessments indicating psychological stress. Dr Colquhoun ignores the assumption that Mr Scanes did not experience stress related to his AFP employment beyond 1995. There is no evidence that Mr Scanes was ever assessed using the General Health Questionnaires Instrument.
I disagree with Dr Colquhoun's characterisation that Mr Scanes had an acute inferior myocardial infarction. In my opinion there is no documentation that Mr Scanes had an inferior myocardial infarction. Dr Colquhoun attributes the rhythm disturbances to an inferior myocardial infarction. In my opinion the rhythm disturbances is due to the acute myocardial infarction and is unrelated to the prior inferior myocardial infarction.
With respect to Dr Colquhoun's response to Question 2.
"Dr Hossack notes at pp.5-7 of his report that Mr Scanes had sub-optimal lipid values over a period of 23 years and this was (in his view) the major factor that contributed to the progression of his coronary artery disease, and a subsequent plaque rupture, which presumably resulted in further damage to the heart muscle. On the balance of probabilities, in your view, would the damage to Mr Scanes’ heart muscle caused by the 1993 myocardial infarction, have been a material factor in causing Mr Scanes’ death, when combined with further damage?
Answer
In 1993 [sic], with the further evidence supplied to me with the recent letter, it is clear that on the day of death, he had a new acute inferior myocardial infarction, which is in the reports from Professor Jack Gutman and Dr Ken Hossack. It is this new myocardial infarction, which led to severe slowing of the heart rate and low blood pressure.
This is seen in many patients who have an inferior myocardial infarction and is due to excessive vagal activity (Bezold-Jarisch reflex) or it is due to severe acute impairment of right ventricular function, which leads to underfilling of the left ventricle and there is severe hypotension. The slow heart rate is vagal stimulation, and this is why Atropine was given for resuscitation. The first inferior myocardial infarction, due to the blocked right coronary artery, would have led to some permanent damage in the right ventricle and inferior wall of the left ventricle and, therefore, a further infarction in the same territory is likely to have been more haemodynamically significant as there was previous damage in the previous area.
In short, the previous infarction would have contributed to the poorer functional reserve during the acute event, which was fatal".
I agree with the first part of Dr Colquhoun's answer apart from the date "1993" and characterisation that the new infarct was an inferior infarction.
I disagree with the content of the second paragraph. In my opinion Mr Scanes had a cardiac arrhythmia because he had an acute myocardial infarction. The arrhythmia occurred as a result of the acute infarction not as a result of the infarction in 1993.
I disagree with the assumption that the first infarction contributed to a poorer functional reserve was responsible for the ventricular fibrillation that resulted in death. The ventricular fibrillation was due to the acute infarction in 2020 and not the prior infarction of 1993.

Dr Hossack gave concurrent evidence at the hearing of this proceeding.
CONCURRENT EXPERT EVIDENCE
The three cardiologists who had provided written reports in this proceeding, Associate Professor Gutman, Associate Professor Colquhoun and Dr Hossack, gave concurrent evidence at the Tribunal hearing. Before doing so, they had been provided with a document, prepared, and agreed to, by the parties, which set out the following information (including footnote):
Preliminary Guidance Notes
1.Compensation is payable under ss.17 and 18 of the Safety, Rehabilitation and Compensation Act 1988 (Cth) ("the SRC Act") "where an injury to an employee results in death".
2.The relevant injury to be considered in this application is an "aggravation of coronary artery disease and resultant myocardial infarction" which was suffered by the Applicant's husband in March 1993?
3.There may be more than one "injury" which "results in" the death of a worker like Mr Scanes. The class of relevant injuries is also not limited to only the immediate precipitant cause (or causes) of death, but could include any previous "injury", or sequence of injuries, provided that they remain at the time of Mr Scanes' death a "cause in fact" or "an effective or operative cause" of the death.
4.The term "results in" in s.17 and 18 does not require the "significant contribution" test in s.5B of the SRC Act to be applied to the earlier injury. In this case, it is sufficient that it was accepted by Comcare that the 1993 aggravation and myocardial infarction occurred while Mr Scanes was "in the course of his employment".
5.In Kooragang Cement Pty Ltd v Bates (1994) 35 NSWLR 452 the NSW Court of Appeal outlined at pp.463-464 the following statement of principles, which are relevant to this application:
The result of the cases is that each case where causation is in issue in a workers compensation claim, must be determined on its own facts. Whether death or incapacity results from a relevant work injury is a question of fact. The importation of notions of proximate cause by the use of the phrase ‘results from’, is not now accepted. By the same token, the mere proof that certain events occurred which predisposed a worker to subsequent injury or death, will not, of itself, be sufficient to establish that such incapacity or death ‘results from’ a work injury. What is required is a common sense evaluation of the causal chain. As the early cases demonstrate, the mere passage of time between a work incident and subsequent incapacity or death, is not determinative of the entitlement to compensation. In each case, the question whether the incapacity or death ‘results from’ the impugned work injury (or in the event of a disease, the relevant aggravation of the disease), is a question of fact to be determined on the basis of the evidence, including, where applicable, expert opinions. Applying the second principle which Hart and Honoré identify, a point will sometimes be reached where the link in the chain of causation becomes so attenuated that, for legal purposes, it will be held that the causative connection has been snapped. This may be explained in terms of the happening of a novus actus. Or it may be explained in terms of want of sufficient connection. But in each case, the judge deciding the matter, will do well to return, as McHugh JA advised, to the statutory formula and to ask the question whether the disputed incapacity or death ‘resulted from’ the work injury which is impugned.[59]
6. The decision in Kooragang Cement was subsequently approved by the Full Federal Court in Ilsley v Wattyl Australia Pty Ltd (1997) 75 FCR 1, where the Full Court said (in a case dealing with incapacity rather than death):
The only additional general comments we consider it necessary to make are these. First, where the causal chain reveals multiple and sequential (or cumulative) injuries that are alleged to provide causes for an incapacity, before an earlier stage injury can properly be said to be an injury for the purposes of [the legislation], it must be able to be said that it remained an effective or operative cause of the incapacity. Secondly, as is well recognised, the sustaining an injury and the onset of incapacity resulting from that injury need not, and commonly does not, occur simultaneously: Accident Compensation Commission v CE Heath Underwriting & Insurance (Aust) Pty Ltd at 526-527.
7. The comments of the Full Court relating to "incapacity" apply equally to "death".
[59] In the SRC context, Re Kooragang Cement was applied by Drummond J in McAuliffe v Comcare [2002] FCA 769 at [11] and by DP Humphries and Member Fricker OAM in Connelly v MRCC [2021] AATA 702.
Questions
1. In light of the above, do you consider that the accepted "aggravation of coronary artery disease and resultant myocardial infarction" in March 1993 "resulted in" Mr Scanes' death in October 2020?
2. In this regard please consider the following aspects of Mr Scanes' medical history:
(a) the period before Mr Scanes' 1993 myocardial infarction;
(b) Mr Scanes' 1993 myocardial infarction;
(c) the period occurring between the 1993 myocardial infarction and the 2020 myocardial infarction;
(d) Mr Scanes 2020 myocardial infarction
[emphasis in original]
The Tribunal put the above agreed questions to the three expert witnesses at the hearing.[60]
[60] Transcript of Proceedings, pages 39 and 41.
Associate Professor Gutman opined that Mr Scanes’ myocardial infarction in 1993 ‘contributed to his death in 2020’ and the infarction he suffered at that later time.[61]
[61] Ibid., page 41.
Associate Professor Colquhoun told the Tribunal that ‘the risk factors that caused his heart attack in 1993 weren’t treated adequately and non-treatment of course contributed and caused’ his fatal myocardial infarction in 2020.[62] Associate Professor Colquhoun referred to there being ‘over 60 risk factors and risk markers that cause atherosclerosis’.[63] He stated that the ‘two key ones’ to ‘prevent further events’ are: ‘lowering the LDL cholesterol’ to ‘less than 1.4 in a person of very high risk’ and Mr Scanes ‘never had adequate treatment of his LDL’; and the second was ‘psychosocial risk factors’, which ‘as important as biological factors in causing heart disease’.[64] Associate Professor Colquhoun stated that Mr Scanes had ‘untreated risk factors’ that, after his 1993 heart attack, ‘caused his eventual death’.[65] Associate Professor Colquhoun further told the Tribunal that ‘having a heart attack doesn’t cause another heart attack’; it was ‘untreated risk factors that caused the original atherosclerosis in his arteries and it progresses, of course, unless you have treatment which was not adequately done’ and opined that they ‘all agree his LDLs certainly wasn’t adequately treated’.[66] Associate Professor Colquhoun also noted, in relation to Mr Scanes’ ‘continuing stress’, that ‘[n]o one measured it according to guidelines’, and referred to a report in 2019 by Dr William Knox, Psychiatrist, which purportedly stated that Mr Scanes had an ‘ongoing stress condition’.[67] Associate Professor Colquhoun said that, while the initial infarction was a long time ago and Mr Scanes was ‘very lucky to have survived as long as he did’ and the 1993 myocardial infarction ‘contributed’ to his eventual death in 2020.[68]
[62] Ibid.
[63] Ibid.
[64] Ibid.
[65] Ibid.
[66] Ibid.
[67] Ibid., page 42.
[68] Ibid.
Dr Hossack told the Tribunal that the accepted injury from 1993 did not result in Mr Scanes’ death in 2020.[69] He opined that there was ‘no contribution’ from the myocardial infarction in 1993, but rather that the factors between 1993 and 2020 ‘contributed’ to Mr Scanes’ myocardial infarction in 2020, which was the ‘sole cause’ of his death.[70] Dr Hossack said that he and Associate Professor Colquhoun agreed that Mr Scanes’ ‘high cholesterol values are a major factor in the development of the myocardial infarction that resulted in the death’ of Mr Scanes.[71] Dr Hossack also noted his instructions were that stress related to Mr Scanes’ employment with the AFP ceased when he stopped that work in 1995.
[69] Ibid.
[70] Ibid.
[71] Ibid.
Counsel for Ms Scanes asked the experts whether they agreed that the myocardial infarction in 1993 was associated with a total occlusion of the right coronary artery such that it completely stopped blood flow through that artery.[72]
[72] Ibid., page 43.
Dr Hossack told the Tribunal ‘that should be taken in the context that the distal right coronary artery was supplied by abundant collaterals from the left system’.[73] Associate Professor Colquhoun agreed that there was a complete occlusion of the right artery in 1993 and, referring to Dr Hossack’s evidence, said that ‘it can occlude an artery and it can get supplied backwards…from collaterals which open up – well, if you’re lucky, open up straight away, and it limits the size of the infarction’.[74] He further opined that ‘if you block an LAD later where the collaterals are coming from, well, then you’ll have further infarction’.[75] Associate Professor Gutman agreed with Associate Professor Colquhoun’s evidence and with what Dr Hossack wrote in his report of 15 March 2023, being that: ‘[i]t would be my opinion that the coronary artery on the left side of the heart supplying the collateral flow to the right coronary artery was the culprit vessel for the myocardial infarction that occurred on 12.10.20’.[76] Associate Professor Gutman opined that, ‘although the recent event in 2020 caused the – was a heart a[tt]ack – caused his death, it was contributed by the fact that he had an occluded right coronary artery as well’, which was ‘a major area of the heart that’s not pumping’ and ‘that would fit his clinical scenario’ of ‘chest pain, heart attack from the left-sided artery’ and ‘pump failure’.[77]
[73] Ibid.
[74] Ibid., pages 43-44.
[75] Ibid., page 44.
[76] Ibid and Exhibit 8.
[77] Transcript of Proceedings, page 44.
Dr Hossack said he disagreed with the proposition that there was no blood flow in the right coronary artery.[78] He told the Tribunal that ‘when the right coronary artery occluded completely’, there was still ‘blood taking oxygen to the heart muscle through the right coronary artery that had been blocked because it was being filled by collaterals’.[79] Dr Hossack further stated that this was important because Mr Scanes’ ‘ventricular function’, which was measured at the time of the coronary angiogram, was in the ‘normal range’ and it was recorded that the ‘wall of the left ventricle was hypokinetic, not akinetic’ and, in his experience, this factor combined with collateral blood supply to the area that is hypokinetic ‘in all probability, that area will become normal and there will be no residual findings of a myocardial infarction in that particular area’ and noted that was because the myocardial infarction in 1993 was ‘so small’, exemplified by the fact that he survived a number of years after that event ‘without any cardiac symptomatology’ or ‘evidence that he developed heart failure’, which would signify ‘impaired left ventricular function’.[80] Associate Professor Colquhoun told the Tribunal that Dr Hossack’s opinion was ‘correct’; ‘[c]ollaterals limited the infarction’ in 1993 and, while it ‘blocks an artery off’, ‘he had plenty of collateral flow and that’s why it was a small infarction’ and was one of the explanations for why he lived so long until his fatal recurrent infarction which killed him’.[81] Associate Professor Gutman told the Tribunal that ‘I think we all agree that he had a right coronary occlusion’ and there were ‘collaterals which limited the size of the myocardial infarction’, but said ‘there is some hesitation to admit that, because the collateral supply to that right coronary artery was now jeopardised because of the blockage of the left coronary artery, and that would result in a bigger heart attack than it would’ve been otherwise if the right coronary artery wasn’t blocked’.[82] In this regard, Associate Professor Gutman said if the right coronary artery was not blocked from the 1993 event, then ‘one could also suggest that now that the left coronary artery might get supply from the right coronary artery, in the opposite direction’, but irrespective of that, the fact that both right and left coronary arteries were blocked would result in a ‘huge heart attack’, because there would be no blood supply to the blocked right coronary artery.[83]
[78] Ibid., page 45.
[79] Ibid.
[80] Ibid., page 46.
[81] Ibid.
[82] Ibid.
[83] Ibid., pages 46-47.
Dr Hossack agreed with the proposition that Mr Scanes’ untreated LDL cholesterol worsened over time and produced increased atherosclerosis in the arteries and that this put him further at risk of another myocardial infarction.[84] Counsel for Ms Scanes then put to Dr Hossack that, if Mr Scanes had reasonably good function until the myocardial infarction in 2020, the collateral filling was working as well as expected between 1993 and 2020.[85] He agreed.[86] Dr Hossack told the Tribunal he agreed that Mr Scanes’ myocardial infarction in 2020 was due to the development of an atherosclerotic plaque that ‘ruptured or ulcerated in the left coronary system’.[87] He also agreed that there was an interruption to the blood supply on the left-hand side of the heart, which side was compensating for the fact that the right coronary artery had been occluded in 1993.[88] Dr Hossack was then asked whether, if that blood supply is compromised through another plaque rupture which causes an occlusion in the left-side blood supply, that built upon the original right-sided blood supply already being compromised.[89] Dr Hossack disagreed because, if the left anterior descending artery or the left main coronary artery was the ‘culprit’, the size of the myocardial infarction would be ‘so large’ that ‘the outcome would not be influenced by any prior myocardial infarction that occurred in 1993’, which was ‘small’ and ‘there’s a lot of scientific evidence to indicate that there can be remodelling of the left ventricle and that normal contracting heart muscle can regenerate within the area of the myocardial infarction and cause the left ventricle to function normally’.[90]
[84] Ibid., page 47.
[85] Ibid.
[86] Ibid.
[87] Ibid., page 48.
[88] Ibid.
[89] Ibid.
[90] Ibid.
In response to a request for any such evidence, Dr Hossack referred to the ventriculogram performed after the myocardial infarction in 1993, which noted that the function, or ‘ejection fraction’ was within the ‘normal range’ and the electrocardiogram performed in 2005, which found ‘no evidence of an inferior myocardial infarction’.[91] As a result of the ventriculogram, Dr Hossack opined that Mr Scanes had ‘normal left ventricular function following the myocardial infarction’ in 1993, because its size was ‘small’ and resulted in ‘no residual damage to the left ventricle’.[92] Dr Hossack agreed that his opinion was that Mr Scanes’ underlying stenosis in the right coronary artery had been present for some time because collateral filling of the right coronary artery had occurred and this usually happens over a long period of time.[93] He also agreed that the myocardial infarction in 1993 was not fatal because of the presence of blood supply from the left side had been present for some time.[94] It was put to Dr Hossack that this explained why the myocardial infarction in 1993 was small.[95] He told the Tribunal that its size was ‘due to a number of factors’, such as the ‘amount of myocardium that is subtended by the right coronary artery that was occluded’ and it was also ‘modified by the fact that collaterals were present’.[96] Dr Hossack further told the Tribunal his opinion regarding the cause of Mr Scanes’ death in 2020 was his ‘very large myocardial infarction due to the occlusion ‘of the left main or the left anterior descending coronary artery’ and additional ‘rhythm problems’ recorded by the ambulance officers, including a ‘junctional bradycardia’.[97] This meant there was ‘an interruption to the conduction system of the heart, and a part of heart where the electrical impulse is passed through and are distributed over the left ventricle was affected by the myocardial infarction; and that has a very adverse prognosis for a person developing that type of rhythm disturbance in the setting of an anterior myocardial infarction’.[98]
[91] Ibid., pages 48-49.
[92] Ibid., page 49.
[93] Ibid., pages 49-50. See also Exhibit 8.
[94] Ibid., page 50.
[95] Ibid.
[96] Ibid.
[97] Ibid., pages 50-51.
[98] Ibid., page 51.
Associate Professor Colquhoun told the Tribunal that it was ‘clear’ that Mr Scanes had ‘collateral flow’ and that was why ‘he had a limited infarction’ in 1993.[99] That earlier heart attack caused ‘dead muscle’ and ‘he had collateral flow that kept his heart within the normal range, despite some dead heart muscle.[100] However, Associate Professor Colquhoun opined that Mr Scanes ‘died because of his second and fatal myocardial infarction’; it was ‘untreated risk factors as we said which led to progression of disease and his fatal event in the end’.[101] Associate Professor Gutman said, ‘Yes, I agree with that’ and further opined that the ‘damage done’ as a result of Mr Scanes’ myocardial infarction in 1993 ‘was small’ and ‘didn’t contribute significantly to his demise’ in 2020.[102] However, the ‘blocked right coronary artery’ was the ‘most important aspect of his demise, having had another heart attack, or another blocked artery, in 2020, blocking the left side’ and, if the right coronary artery was not blocked in 1993, the size of the myocardial infarction in 2020 ‘would’ve been less’.[103]
[99] Ibid.
[100] Ibid.
[101] Ibid.
[102] Ibid.
[103] Ibid. page 52.
Counsel for Comcare referred Associate Professor Gutman to his three reports in this proceeding.[104] He agreed that his first report was no longer relevant because he had subsequently received information regarding the ambulance call out and associated events in 2020.[105] Associate Professor Gutman also said that his second report, in which he stated that his opinion was that Mr Scanes’ ‘had an inferior myocardial infarction as the most likely cause of his death’, was ‘not relevant’ and he was ‘taking that back.[106] Counsel then referred Associate Professor Gutman to his third report and, most relevantly, the reference to Mr Scanes potentially suffering ‘cardiogenic shock’ and one of the ‘significant predisposing factors for cardiogenic shock is previous infarction’.[107] Associate Professor Gutman agreed with the proposition that cardiogenic shock is when the heart cannot pump enough blood and oxygen to the brain and other vital organs.[108] It was put to Associate Professor Gutman that none of his reports addressed the issue of whether there was a causal connection between the 1993 myocardial infarction and Mr Scanes’ death in 2020.[109] Associate Professor Gutman told the Tribunal that ‘it’s because he’s had a previous myocardial infarction in 1993, and the previous myocardial infarction is additive’ and ‘most likely’ to cause ‘cardiogenic shock with a new myocardial infarction’.[110] Furthermore, Associate Professor Gutman said that ‘I don’t think any of us dispute that his untreated cholesterol over many years contributed to his current myocardial infarction in 2020’, but that he was not asked to address this factor in his written reports.[111] To this end, Associate Professor Gutman told the Tribunal he agreed with Dr Hossack in relation to elevated LDL cholesterol levels and agreed with the importance Dr Hossack attached to these elevated cholesterol levels to the myocardial infarction that led to the death of Mr Scanes in 2020.[112] Associate Professor Gutman said he agreed and that Mr Scanes’ high cholesterol levels contributed to his myocardial infarction in 2020.[113]
[104] Exhibit 1, pages 129-131 and Exhibit 2, pages 317-320 and 325-326.
[105] Transcript of Proceedings, page 53.
[106] Ibid. See also Exhibit 2, page 319.
[107] Transcript of Proceedings, page 54. See also Exhibit 2, page 326.
[108] Transcript of Proceedings, page 54.
[109] Ibid.
[110] Ibid.
[111] Ibid., page 55.
[112] Ibid.
[113] Ibid.

By way of background, the contemporaneous medical reports of Dr Coles, Cardiologist, from shortly after Mr Scanes’ myocardial infarction in 1993 are instructive.[162] Dr Coles identified Mr Scanes’ occluded right coronary artery as the cause of his infarction in 1993, but also noted there was ‘good retrograde filling in the left system’, which ‘implied that the narrowing that precipitated the total occlusion had been present for some time’ and Mr Scanes ‘had well preserved left ventricular function so his outlook should be reasonable’.[163] Importantly, Dr Coles encouraged the checking of Mr Scanes’ ‘fasting cholesterol and triglyceride levels’ and ‘if appropriate use lipid lowering agents’.[164] On the available evidence, such medication to control cholesterol was not prescribed for Mr Scanes and he had consistently high cholesterol for decades in advance of his death in 2020. The Tribunal is satisfied that Mr Scanes’ untreated and abnormally elevated cholesterol led to the heart attack in October 2020 that resulted in his death and that this process was unrelated to his accepted injury in 1993.
[162] Exhibit 1, pages 201, 924-925 and 927.
[163] Ibid., pages 201 and 927.
[164] Ibid, page 924.
In addition, Professor O’Rourke, Cardiologist, also considered that a coronary angiogram performed shortly after the 1993 myocardial infarction demonstrated that ‘left ventricular ejection fraction was excellent’ and the occluded right coronary artery ‘filled promptly with abundant collaterals from the left injections’.[165] In this regard, Professor O’Rourke referred to Dr Coles being alert ‘to the possibility that high grade obstruction of the right coronary artery had been present for quite some time, allowing development of collateral vessels such that acute occlusion caused a very small myocardial infarction’.[166] Professor O’Rourke also noted that Mr Scanes’ infarction was ‘so small that left ventricular ejection fraction at coronary arteriography three days after onset of symptoms was within the normal range’ and he ‘suffers from non-threatening residual coronary disease, which was known at the time of his hospital admission in March 1993’.[167]
[165] Exhibit 5.
[166] Ibid.
[167] Ibid.
In 2012, Dr Griffith, Consultant Surgeon, relevantly noted that Mr Scanes was not under any medical supervision in relation to his heart, which was ‘not a position I would advise for an individual [in] his age group’ and recommended annual review by a cardiologist and a regular ECG.[168] In 2018, Dr Voon, Respiratory Physician, reported his concern about Mr Scanes’ ‘complaint of near-constant central chest tightness, especially given his background history of ischaemic heart disease’ and noted that he ‘does not have any cardiology follow-up in place’.[169] Later that year, Dr Voon opined that it would be ‘worthwhile referring Warren to a cardiologist for investigation of possible underlying coronary artery disease in view of chest tightness’.[170]
[168] Exhibit 1, page 394.
[169] Ibid., page 700.
[170] Ibid., page 702.
As set out above, Associate Professor Gutman provided three written reports in this proceeding and gave evidence at the Tribunal hearing. During cross-examination by Counsel for Comcare, Associate Professor Gutman confirmed that his first two reports were no longer relevant. In his third report, Associate Professor Gutman’s conclusion was that Mr Scanes died due to ‘cardiogenic shock’, the leading cause of cardiogenic shock is ‘acute myocardial infarction due to left ventricular dysfunction’ and that one of the ‘significant predisposing factors for cardiogenic shock is previous infarction’.[171] He agreed in cross-examination that cardiogenic shock is when the heart cannot pump enough blood and oxygen to the brain and other vital organs.[172] In this regard, Associate Professor Gutman’s reports did not adequately address the central issue in this proceeding of what, if any, causal link there was between Mr Scanes’ myocardial infarction in 1993 and his death in 2020. At its highest, Associate Professor Gutman identified the previous infarction as being a ‘significant predisposing factor’.[173] To this end, the question of what in the particular circumstances of Mr Scanes’ cardiac health caused the cardiogenic shock remained unanswered in written form by Associate Professor Gutman.
[171] Exhibit 2, page 326.
[172] Transcript of Proceedings, page 54.
[173] Exhibit 2, page 326.
At the hearing, Associate Professor Gutman told the Tribunal that ‘the previous myocardial infarction is additive’ and ‘most likely’ to cause ‘cardiogenic shock with a new myocardial infarction’.[174] Associate Professor Gutman also opined that, while the ‘recent event in 2020…caused his death’, it was ‘contributed to by the fact that he had an occluded right coronary artery’.[175] To this end, Ms Scanes relied on Associate Professor Gutman’s evidence at the hearing that ‘the fact that he had damage now not only to the left sided artery but also to the right coronary artery…the less likely you are to survive’.[176] While Associate Professor Gutman told the Tribunal that the right coronary occlusion from 1993 ‘contributed’ to Mr Scanes’ death, he then said it ‘wasn’t the damage; it was the blocked artery’ and that ‘risk modification would’ve made a difference’.[177] This latter evidence was a significant qualification. Ms Scanes acknowledged that the ‘collaterals’ process had commenced before the 1993 infarction as a result of her late husband’s underlying constitutional coronary heart disease, that is, the non-work related coronary disease process which predated his accepted workplace ‘injury’. The Tribunal considers that Associate Professor Gutman’s evidence, when taking into account the totality of the medical evidence before the Tribunal, goes no further than identifying a risk factor, but not the actual circumstances of Mr Scanes’ cardiac health that resulted in his death. In this regard, Associate Professor Gutman went on to note that all of the experts who gave evidence to the Tribunal agreed that Mr Scanes’ ‘untreated cholesterol over many years contributed to his current myocardial infarction in 2020’ and that, significantly, he was not asked to address this issue in his reports.[178] Associate Professor Gutman ultimately also accepted that this and other risk factors were very important in Mr Scanes’ subsequent myocardial infarction in 2020 and, when it was put to him that the starting point in relation to Mr Scanes’ death was his elevated cholesterol, which led to a piece of plaque displacing, he told the Tribunal that ‘yes, I agree that the heart attack in 2020 was due to a ruptured plaque in one of the left-sided vessels’.[179] While Ms Scanes did not resile from her contention that the accepted injury resulted in her late husband’s death, Ms Scanes accepted that his untreated high cholesterol contributed significantly to his myocardial infarction in 2020 and that both Associate Professors Gutman and Colquhoun accepted this position.
[174] Transcript of Proceedings, page 54.
[175] Ibid., page 44.
[176] Ibid., page 66.
[177] Ibid.
[178] Ibid., page 55.
[179] Ibid., pages 66-67.
Dr Hossack gave direct evidence to the Tribunal refuting Associate Professor Gutman’s opinion regarding the effect of Mr Scanes having occlusions to both the right and left sided arteries, as follows:[180]
MR GREY: You're saying, Dr Hossack, that the myocardial infarction in 2020 is a new event unrelated to past history? That's your position, correct?
DR HOSSACK: I think I qualified that; unrelated to the past myocardial infarction in 1993.
MR GREY: Yes, right. But if the past myocardial infarction in 1993 had resulted in - or if the result of the plaque that went with it had resulted in the occlusion of the right coronary artery to the extent that blood flow was severely attenuated in that artery except for the presence of collateral filling, then the position would be, wouldn't it, that, as long as that situation was maintained, you might say, 'Well, he can survive quite well.' But if there did - if something happened to compromise the collateral flow from the left side, then that could have the effect of triggering a myocardial infarction, and it would be wrong to say that's a completely new event because the vulnerability to that happening is a result of what happened in 1993. Isn't that right?
DR HOSSACK: I disagree with that proposition. I think if the left main coronary artery or the left anterior descending coronary artery occlude, then that is going to cause a major myocardial infarction, and, in my opinion, that was the reason why the deceased - well, for the outcome.
[180] Ibid., page 61.
The Tribunal has also set out above in detail the written reports provided by Associate Professor Colquhoun in relation to this proceeding. While Associate Professor Colquhoun’s first report answered in the affirmative to the question of whether Mr Scanes’ death in 2020 was the result of his 1993 infarction, his evidence in relation to that purported causation did not continue to be so emphatic. In this regard, Associate Professor Colquhoun referred generally to ‘an increased risk’ of subsequent death following survival of a myocardial infarction.[181] However, he also referred to the risk being reduced ‘considerably by lowering LDL cholesterol with modern therapy’ and to Mr Scanes suffering from ‘stress (perceived stress) at work’, although he continued to misunderstand that this latter condition was diagnosed by Dr Knox, Psychiatrist, in 1996, and not in 2019, some 24 years after Mr Scanes ceased employment with the AFP.[182] In his report of June 2021, Associate Professor Colquhoun also referred to psychosocial risk factors and considered that ‘perceived stress as well as measurable depression…increases risk of first and recurrent cardiovascular events’.[183] However, there was no evidence before the Tribunal that Mr Scanes’ stress, diagnosed in 1996, continued for over 20 years and that this had any bearing on his cardiac health in 2020 or that he was diagnosed with any psychosocial condition. In any event, based on the weight of evidence, the Tribunal is not satisfied that these possible factors were related to Mr Scanes’ death in 2020. At its highest, Associate Professor Colquhoun’s evidence was that Mr Scanes’ myocardial infarction in 1993 was a risk factor for a possible future infarction or increased his risk of sudden cardiac death.[184] This opinion was succinctly expressed by Associate Professor Colquhoun in his evidence to the Tribunal that ‘a heart attack does not directly cause another heart attack’ and ‘having a heart attack doesn’t cause another heart attack’.[185]
[181] Exhibit 1, page 139.
[182] Ibid.
[183] Ibid., page 140.
[184] Ibid., pages 140 and 144.
[185] Transcript of Proceedings, page 56.
Associate Professor Colquhoun plainly considered that untreated elevated cholesterol was an important risk factor. For example, in his supplementary report, Associate Professor Colquhoun opined that ‘unless there is vigorous lowering of LDL – cholesterol, there will be progression of the underlying atherosclerosis, which results in further cardiovascular events’.[186] Moreover, Associate Professor Colquhoun’s further supplementary report opined that a previous index myocardial infarction ‘does not cause further heart attacks’, which are ‘due to ruptured or eroded atherosclerotic plaques in an artery’.[187] He noted Dr Hossack’s evidence regarding ‘the number one cause for atherosclerosis – an elevated LDL cholesterol’ and that at ‘no stage’ was Mr Scanes ‘in the target ranges at the time for a patient who has had an acute coronary syndrome or myocardial infarction’.[188] To this end, Associate Professor Colquhoun stated that it was ‘this new myocardial infarction, which led to severe slowing of the heart rate and low blood pressure’.[189]
[186] Exhibit 1, page 145.
[187] Exhibit 7.
[188] Ibid.
[189] Ibid.
In his evidence at the Tribunal hearing, Associate Professor Colquhoun relevantly opined in relation to Mr Scanes that: ‘the risk factors that caused his heart attack in 1993 weren’t treated adequately and non-treatment of course contributed and caused’ his fatal myocardial infarction in 2020; Mr Scanes ‘never had adequate treatment of his LDL’; his untreated risk factors ‘caused his eventual death’; atherosclerosis in the arteries progresses ‘unless you have treatment which was not adequately done’; and all three experts ‘agree his LDLs certainly wasn’t’ adequately treated’.[190] In addition, Associate Professor Colquhoun opined that Mr Scanes’ untreated risk factors ‘led to the progression of disease and his fatal event’.[191] Associate Professor Gutman agreed with this evidence and that the ‘damage done’ as a result of Mr Scanes’ 1993 infarction ‘was small’ and ‘didn’t contribute significantly to his demise’ in 2020.[192]
[190] Transcript of Proceedings, page 41.
[191] Ibid., page 51.
[192] Ibid.
The written reports of Dr Hossack, set out above in detail in these reasons, disclose his careful and thorough analysis of the totality of the medical evidence regarding Mr Scanes and his cardiac health over a long period of time. In his first report, Dr Hossack identified that Mr Scanes’ ventricular function was assessed in the normal range shortly after his myocardial infarction in 1993, Mr Scanes did not demonstrate any evidence of heart failure in the following years and he was able to return to the work force. In his supplementary report, Dr Hossack opined that the 1993 myocardial infarction resulted in ‘minimal damage to the myocardium and there was no significant residual impairment of cardiac function’ and pointed to there being no evidence of Mr Scanes subsequently having heart failure and his return to gainful employment.[193]
[193] Exhibit 8.
Relatedly, Dr Hossack noted that Associate Professor Gutman had not accounted for Mr Scanes’ ‘well developed collateral supply to the right coronary artery at the time of the angiogram following the myocardial infarction in 1993’.[194] The angiogram demonstrated that the occlusion in the right coronary artery was ‘complete’ and, Dr Hossack opined, ‘the coronary artery on the left side of the heart supplying collateral flow to the right coronary artery was the culprit vessel for the myocardial infarction that occurred on 12.10.2020’.[195] Dr Hossack further opined that the collateral blood flow was occurring ‘prior to the myocardial infarction’ in 1993 and ‘developed as a result of the slowly progressive stenosis in the proximal right coronary artery’. When this right coronary artery occluded completely in 1993, ‘the presence of collateral blood supply preserved myocardial function and resulted in minimal cardiac damage’ at that time.[196] This accords with the aforementioned contemporaneous reports of Dr Coles and Professor O’Rourke from 1993 and 1994, respectively. In support of his opinion, Dr Hossack referred to:[197]
a large body of scientific evidence that indicates that following a myocardial infarction there is a process of positive remodelling that can occur. There can be compensatory hypertrophy of muscles around the myocardial infarction and hypertrophy of surviving myocardial muscle within the area of myocardial infarction. Over time the area affected by the infarction reduces in size and negates the adverse haemodynamic effects of the myocardial infarction.
[194] Ibid.
[195] Ibid.
[196] Ibid.
[197] Ibid.
At the Tribunal hearing, Dr Hossack referred to Mr Scanes’ ventricular function, which was measured at the time of the coronary angiogram in 1993, being in the ‘normal range’, and that the ‘wall of the left ventricle was hypokinetic, not akinetic’ which, combined with collateral blood supply, ‘in all probability’ leads to the area becoming ‘normal’ with ‘no residual findings of a myocardial infarction in that particular area’.[198] This was due to the 1993 infarction being ‘so small’, evidenced by the fact Mr Scanes survived many years afterwards without any cardiac symptomatology or heart failure, which would have signified ‘impaired left ventricular function’.[199] Associate Professor Colquhoun agreed with Dr Hossack’s opinion.[200]
[198] Transcript of Proceedings, page 46.
[199] Ibid.
[200] Ibid.
Counsel for Ms Scanes put to Dr Hossack the proposition that, if the blood supply is compromised through another plaque rupture which causes an occlusion of the left-hand side blood supply, this builds upon the fact that the original right-sided blood supply was already compromised.[201] Dr Hossack disagreed because if the left anterior descending artery or the left main coronary artery was the ‘culprit’ of Mr Scanes’ death, the size of the myocardial infarction would be ‘so large’ that ‘the outcome would not be influenced by any prior myocardial infarction that occurred in 1993’, which was ‘small’ and again noted that ‘there’s a lot of scientific evidence to indicate that there can be remodelling of the left ventricle and that normal contracting heart muscle can regenerate within the area of the myocardial infarction and cause the left ventricle to function normally’.[202] In response to a request for any such evidence, and demonstrating his command of that evidence, Dr Hossack referred to the specific measurements from the ventriculogram performed on Mr Scanes after the myocardial infarction in 1993, which noted that the function, or ‘ejection fraction’ was within the ‘normal range’ and to the electrocardiogram performed in 2005, which found ‘no evidence of an inferior myocardial infarction’.[203] Moreover, Dr Hossack referred to the angiogram performed in 1993 when ‘the arteries on the left side of the heart were all regarded as clear’, the significance of which was that ‘the myocardial infarction in 2020 is a completely new event, unrelated to the prior history’.[204] For the avoidance of doubt, and for the reasons set out in this decision, the Tribunal accepts Dr Hossack’s opinion in relation to this issue and finds that the existing occlusion of the right coronary artery did not result in Mr Scanes’ death in 2020. The Tribunal is satisfied that Mr Scanes’ death was due to a separate and distinct process.
[201] Ibid., page 48.
[202] Ibid.
[203] Ibid., pages 48-49.
[204] Ibid., page 60.
In this regard, Dr Hossack opined that ‘the acute coronary syndrome was due to plaque rupture’.[205] To this end, Dr Hossack identified and listed Mr Scanes’ nine cholesterol readings taken over a 23 year period from 1997 to 2020.[206] Dr Hossack relevantly opined that, in patients suffering a myocardial infarction due to coronary artery disease, ‘it is recommended that the target for LDL cholesterol is 1.5mmol/L or less’ and that, over a 23 year period, Mr Scanes ‘had suboptimal lipid values’.[207] These nine cholesterol level readings ranged from 1.8mmol/L to 3.3mmol/L, all being in excess of the aforementioned recommended target level.[208] The Tribunal again notes that, on the available medical evidence, Mr Scanes’ long history of elevated cholesterol was untreated up until his death in 2020.
[205] Exhibit 6.
[206] Ibid.
[207] Ibid.
[208] Ibid.
Dr Hossack referred to studies that indicate that ‘lipid lowering therapy slows or prevents progression of atherosclerotic disease and in some cases can cause reversal of plaque accumulation’.[209] In this regard, Dr Hossack opined, stabilisation of plaque that prevents plaque ulceration or rupture ‘is a major mechanism for the improved survival of patients with coronary artery disease who are prescribed cholesterol lowering therapy’.[210] Accordingly, Dr Hossack’s thesis in his first report was that Mr Scanes’ untreated elevated cholesterol was the ‘major factor’ contributing to the progression of coronary artery disease in Mr Scanes and that, as a result, he developed ‘further plaque in the coronary arteries and part of the plaque ruptured to cause an acute coronary event in October 2020’.[211] In his supplementary report, Dr Hossack opined that the ‘underlying factor that caused the myocardial infarction was the rupture of atherosclerotic plaque as a result of poorly controlled cholesterol’.[212] Dr Hossack’s evidence at the Tribunal hearing regarding his thesis of what caused Mr Scanes’ death was that when there is cholesterol and the subsequent build-up of plaque, the covering of the plaque is ‘soft and it allows that plaque to rupture’ and a blood clot then occurs in that region causing a heart attack.[213]
[209] Ibid.
[210] Ibid.
[211] Ibid.
[212] Exhibit 8.
[213] Transcript of Proceedings, page 60.

Dr Hossack noted that Associate Professor Gutman in his reports had ‘ignored the significant contribution that untreated elevated cholesterol over a 23 year period makes to the progression of coronary artery disease’, and ‘ignored the history that Mr Scanes had chest pain prior to the cardiac arrest and that laboratory tests indicated an elevated troponin at the time of the cardiac arrest’.[214] Additionally, Dr Hossack noted that Associate Professor Colquhoun had ‘not taken into account the circumstances of the death’, being Mr Scanes ‘experiencing chest pain prior to the syncopal episode’.[215] Dr Hossack opined that the presence of chest pain was ‘indicative of an acute coronary syndrome’.[216]
[214] Exhibit 6.
[215] Ibid.
[216] Ibid.
As set out above in these reasons, in cross-examination from Counsel for Comcare, it was put to Associate Professor Colquhoun that he did not disagree with Dr Hossack’s conclusions regarding the impact of Mr Scanes’ untreated and elevated cholesterol levels in relation to his death in 2020.[217] He replied, ‘Absolutely not’ and to do so ‘would be ridiculous’.[218]
[217] Transcript of Proceedings, page 57.
[218] Ibid.
In this regard, Counsel for Comcare also referred Associate Professor Gutman to the importance to which Dr Hossack ascribed to Mr Scanes’ elevated cholesterol levels; he told the Tribunal that ‘I agree with him’.[219] Furthermore, Associate Professor Gutman was asked whether he agreed with Dr Hossack ‘as to the importance which he attaches to that particular aspect of this man’s presentation, and the fact that they were untreated for so long in respect of what occurred in 2020?’[220] Associate Professor Gutman replied that, ‘I agree that, yes, the fact that he had high cholesterol for so long continued to his myocardial infarction in 2020’.[221] While Associate Professor Gutman said that the occlusion to the right coronary artery ‘contributed’ to Mr Scanes’ death, he also noted that ‘risk factor modification would’ve made a difference’.[222] Based on Associate Professor Gutman’s subsequent evidence, the Tribunal considers that this was primarily a reference to addressing Mr Scanes’ elevated cholesterol levels in relation to which Associate Professor Gutman had earlier agreed with Dr Hossack’s opinion regarding their importance to his death.[223] To this end, Associate Professor Gutman further agreed that Mr Scanes’ ‘risk factors’ were very important in his subsequent myocardial infarction in 2020.[224] As a result, Counsel for Comcare put to Associate Professor Gutman that ‘the starting point for all of this’ was the fact that Mr Scanes had elevated cholesterol which led to a piece of plaque displacing and then leading to his infarction in 2020.[225] Associate Professor Gutman initially agreed that this ‘would be a contributing factor’ and there were ‘multiple risk factors’, but when the point was pressed that this was the starting point in relation to what occurred to Mr Scanes in October 2020, Associate Professor Gutman ultimately conceded that, ‘yes, I agree that the heart attack in 2020 was due to a ruptured plaque in one of the left-sided vessels’.[226]
[219] Ibid., page 55.
[220] Ibid.
[221] Ibid.
[222] Ibid., pages 44 and 66.
[223] Ibid., page 55.
[224] Ibid., page 66.
[225] Ibid.
[226] Ibid., page 67.
The Tribunal has considered the statutory formula set out in section 17 of the SRC Act to determine whether the accepted injury from 1993 ‘results in’, or resulted in, Mr Scanes’ death.
Based on the weight of evidence, the Tribunal is not satisfied that Mr Scanes’ accepted injury from 1993 resulted in his death in 2020. As the NSW Court of Appeal said in Kooragang Cement Pty Ltd v Bates (1994) 35 NSWLR 452, (Kooragang Cement) ‘the mere proof that certain events occurred which predisposed a worker to subsequent injury or death, will not, of itself, be sufficient to establish that such incapacity or death ‘results from’ a work injury’. To this end, a common sense evaluation of the causal chain is required. Relevantly, Kooragang Cement held that ‘a point will sometimes be reached where the link in the chain of causation becomes so attenuated that, for legal purposes, it will be held that the causative connection has been snapped’. That is, in the form of a novus actus interveniens.
The decision of Kooragang Cement was approved by the Full Federal Court of Australia in Ilsley v Wattyl, although the latter case dealt with incapacity rather than death. In Ilsley v Wattyl, it was held that the injury upon which reliance is placed must remain ‘an effective and operative cause’. In this regard, based on the weight of evidence, the Tribunal finds that the injury suffered by Mr Scanes in 1993 was not an ‘effective or operative cause’ of his death in 2020.[227]
[227] Ilsley v Wattyl.
The Tribunal accepts the opinion of Dr Hossack regarding the history of Mr Scanes’ cardiac health and its role in his death in 2020. As outlined above in these reasons, it was evident that Dr Hossack had conducted a thorough and detailed analysis of Mr Scanes’ medical history and had a strong grasp of its affect on his health and the circumstances that led to his death in 2020. For the reasons set out above, Dr Hossack’s evidence is therefore given more weight than that of Associate Professors Colquhoun and Gutman in this proceeding. While it may be accepted that Mr Scanes’ injury predisposed him to another myocardial infarction, based on the medical evidence, the Tribunal does not accept that this increased risk is sufficient to find that the accepted injury resulted in his death some 27 years later. The existence of risk does not maintain any causal chain from the 1993 injury to Mr Scanes’ death in 2020.
The Tribunal accepts the research of Dr Hossack regarding Mr Scanes’ longstanding untreated and abnormally elevated cholesterol levels. As set out above in these reasons, under cross-examination at the hearing, both Associate Professor Colquhoun and Associate Professor Gutman ultimately agreed with Dr Hossack’s opinion regarding the important role Mr Scanes’ cholesterol played in his death and that it was due to ruptured plaque from atherosclerosis which led to the occlusion of his left-sided coronary artery. Based on the accepted evidence, this physiological process was separate and distinct from Mr Scanes’ 1993 infarction, or the accepted ‘injury’. In short, the Tribunal accepts Dr Hossack’s thesis regarding the singular role played by Mr Scanes’ untreated high cholesterol over many years which led to a portion of plaque shedding and resulted in the fatal occlusion of his left-sided coronary artery in 2020. Accordingly, on the balance of probabilities, the Tribunal finds that Mr Scanes’ history of untreated high cholesterol was a novus actus interveniens which, even if there was a causal chain from the 1993 injury, snapped that chain of causation.
Having regard to all of the evidence, the Tribunal is not satisfied that Mr Scanes’ 1993 injury remained an ‘effective or operative cause’ of his death in 2020.[228] The Tribunal finds, on the weight of medical evidence, that the effective or operative cause of Mr Scanes’ death was the occlusion of his left-sided artery in the heart due to atherosclerosis as a result of untreated high levels of cholesterol over a sustained period of time, which process was not related to the accepted injury in 1993. Accordingly, Comcare is not liable to pay compensation to Ms Scanes under sections 17 and 18 of the SRC Act.
[228] Ilsley v Wattyl.
DECISION
The Tribunal affirms the decision under review pursuant to subsection 43(1)(a) of the Administrative Appeals Tribunal Act 1975.

I certify that the preceding 124 (one hundred and twenty-four) paragraphs are a true copy of the reasons for the decision herein of Member W Frost.

.............................[sgd]...........................................
Associate
Dated: 31 October 2023

Date(s) of hearing: 23 November 2022 and 28 July 2023

Date final submissions received: 11 September 2023

Counsel for Applicant: Mr Leo Grey

Solicitors for Applicant:
Mr Richard Faulks, Sneddon, Hall & Gallop Lawyers

Counsel for Respondent: Mr Charles Clark

Solicitors for Respondent: Mr Luke Wooley, Sparke Helmore Lawyers

Date(s) of hearing:	23 November 2022 and 28 July 2023
Date final submissions received:	11 September 2023
Counsel for Applicant:	Mr Leo Grey
Solicitors for Applicant:	Mr Richard Faulks, Sneddon, Hall & Gallop Lawyers
Counsel for Respondent:	Mr Charles Clark
Solicitors for Respondent:	Mr Luke Wooley, Sparke Helmore Lawyers