McNicol and Comcare [2003] AATA 559 (16 June 2003)

Last Updated: 1 July 2003

DECISION AND REASONS FOR DECISION [2003] AATA 559

ADMINISTRATIVE APPEALS TRIBUNAL )

) No A2002/237

GENERAL ADMINISTRATIVE DIVISION	)
	Re	BEATRICE MCNICOL

Applicant

And

COMCARE

Respondent

DECISION

Tribunal

Mr M J Sassella, Senior Member Dr M D Miller AO, Member

Date 16 June 2003

Place Canberra

Decision

The tribunal affirms the decision under review. The applicant qualifies for no costs associated with this application.

..............................................

Senior Member

CATCHWORDS

WORKERS' COMPENSATION - Death of employee - claim by spouse - spouse as dependant - employee died from myocardial infarction - whether death caused by compensable injury

Safety, Rehabilitation and Compensation Act 1988 ss 4(1) ("dependant", "dependent", "disease", "injury", "spouse"), 17(1), (2), (3), (4), (7), (9),

Casarotto v Australian Postal Commission (1989) 86 ALR 399

Lott and Comcare, Re (1996) 44 ALD 741

Nadge and Australian Postal Corporation, Re (1994) 33 ALD 710

Zickar v MGH Plastic Industries Pty Ltd (1996) 187 CLR 310

REASONS FOR DECISION

16 June 2003

Mr M J Sassella, Senior Member Dr M D Miller AO, Member

APPLICATION

1. This is an application by Beatrice McNicol ("the applicant") for review by the Administrative Appeals Tribunal ("the tribunal") of a decision of a delegate in Comcare ("the respondent") (T81) made on 29 June 2001. The decision was affirmed on 20 November 2001 by an independent review officer (T86) who rejected the applicant's claim for a death benefit under s 17 of the Safety, Rehabilitation and Compensation Act 1988 ("the Act")[1]. The applicant's husband, John McNicol ("the employee"), had died on a date between 25 and 28 May 2000 (T64), arguably as a result of a work-related injury.

HEARING

2. The tribunal convened a hearing in this matter in Canberra on 24 February 2003. Mr H Selby of counsel represented the applicant. Ms L Walker of counsel represented the respondent.

3. The tribunal heard oral evidence from Dr N G Ardlie, a physician, and from Professor M F O'Rourke, Professor of Medicine at the University of New South Wales, Head of the Vascular-Ventricular Interactions Program, Victor Chang Cardiac Research Institute at that university and a visiting medical officer in the Department of Cardiovascular Medicine and Hypertension at Sydney's St Vincent's Clinic.

4. The tribunal had access to the following documents which were admitted as exhibits:

Exhibit TD1 - Section 37 Statement and associated documents (exhibits T1 - T88) provided by the respondent.

Exhibit A1 - Applicant's statement of facts and contentions, 7 August 2002.

Exhibit A2 - Report by Dr Ardlie dated 13 June2002.

Exhibit A3 - Report by Dr D M Coles, a cardiologist, dated 13 September 1991.

Exhibit A4 - Report by Dr Coles dated 6 October 1998.

Exhibit R1 - Respondent's statement of facts and contentions, 16 May 2002.

Exhibit R2 - Report by Professor O'Rourke dated 22 April 2002.

Exhibit R3 - Report by Professor O'Rourke dated 26 August 2002.

LAW

5. At the date of death of Mr McNicol Comcare was liable to pay compensation to him under s 14 of the Act, his compensable condition being acute inferior-posterior myocardial infarction.

6. As noted earlier, liability to pay compensation to a dependant or dependants of a deceased employee is regulated by s 17 of the Act:

Compensation for injuries resulting in death

17. (1) This section applies where an injury to an employee results in death.

(2) Subject to this section and sections 16 and 18, if the employee dies without leaving dependants, compensation is not payable in respect of the injury.

(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 $120,000 and that compensation is payable to, or in accordance with the directions of, Comcare for the benefit of all of those dependants.

(4) If the employee dies without leaving dependants who were wholly dependent on the employee at the date of the employee's death but leaving dependants who were partly dependent on the employee at that date:

(a) subject to this section and to sections 16 and 18, Comcare is liable to pay compensation in respect of the injury of such amount, not exceeding $120,000, as Comcare determines, having regard to any losses suffered by those dependants as a result of the cessation of the employee's earnings; and

(b) that compensation is payable to, or in accordance with the directions of, Comcare for the benefit of those dependants.

...

(7) An amount of compensation paid or payable under this Act before the death of an employee:

(a) is not affected by subsection (2);

(b) shall not be deducted from the compensation payable under subsection (3); and

(c) shall not be taken into account in determining the compensation payable under subsection (4).

...

(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.

...

7. The fundamental requirement in s 17 is that the employee's "injury" resulted in his death. An injury is defined in s 4(1) of the Act. There was no dispute that the deceased Mr McNicol suffered an injury in accordance with the Act. The remaining issue arising in s 17(1) was whether that injury caused Mr McNicol's death.

8. The applicant must be a "dependant" in order to qualify for payment under s 17 of the Act. Section 4(1) of the Act defines dependent status via these definitions:

dependant, in relation to a deceased employee, means:

(a) the spouse, father, mother, step-father, step-mother, father-in-law, mother-in-law, grandfather, grandmother, son, daughter, step-son, step-daughter, grandson, grand-daughter, brother, sister, half-brother or half-sister of the employee; or

(b) a person in relation to whom the employee stood in the position of a parent or who stood in the position of a parent to the employee; being a person who was wholly or partly dependent on the employee at the date of the employee's death;

dependent means dependent for economic support;

9. The applicant was the spouse of the deceased employee. "Spouse" is defined in s 4(1) of the Act:

spouse includes:

(a) in relation to an employee or a deceased employee-a person of the opposite sex to the employee who lives with, or immediately before the date of the employee's death lived with, the employee as the spouse of the employee on a bona fide domestic basis although not legally married to the employee; and

(b) in relation to an employee or a deceased employee who is or was a member of the Aboriginal race of Australia or a descendant of indigenous inhabitants of the Torres Strait Islands-a person who is or was recognised as the employee's husband or wife by the custom prevailing in the tribe or group to which the employee belongs or belonged;

10. The applicant and the deceased employee were married (T66) and were living together at the time of his death (T68). There were no other dependants (T68).

11. As regards Mr McNicol's myocardial infarction as a cause of death the applicant bears an onus of persuasion, although she bears no fundamental onus of proof. Hill J in the Federal Court summarised the position in Casarotto v Australian Postal Commission (1989) 86 ALR 399, 412-413:

"In McDonald v. Director General of Social Security (1984) 1 FCR 354 Woodward J. in the context of social security legislation counselled against using the expression `onus of proof' where an application comes to the Administrative Appeals Tribunal for review. Of course, where a statutory provision such as s.190(b) of the Income Tax Assessment Act 1936 deals with the matter specifically there is no difficulty. The Administrative Appeals Tribunal is bound by s.43 of the Administrative Appeals Tribunal Act 1975 to carry out the review by placing itself in the shoes of the administrator, although it considers the matter having regard to the material before it rather than the material that was originally before the administrator. Since the tribunal is obliged to inform itself on any matter in such manner as it thinks appropriate (s.33(1)(c)) and is not bound as such by the rules of evidence, it is obvious that there may be difficulties if principles such as onus of proof applicable in proceedings before courts are strictly adopted.

"It may be that what was said by Woodward J. in McDonald should be confined to the context of social security legislation. Thus in Minister for Health v. Thomson (1985) 60 ALR 701 at 712 Beaumont J, referring to proceedings before the Medical Services Committee established under the Health Insurance Act 1973 (Cth) said:

`Generally speaking, concepts of onus of proof used in adversary proceedings are inapplicable in administrative proceedings in the social security area: see McDonald v. Director-General of Social Security (1984) 1 FCR 354. However, where, as here, a breach of discipline, or something analogous, is alleged, the onus of proving such a breach lies upon the accuser. The general position is explained by Professor Enid Campbell in Principles of Evidence and Administrative Tribunals, published in Campbell and Waller (ed) "Well and Truly Tried", Monash Studies in Law (1982) p 53:

"There may be legal burdens of proof to be discharged in administrative proceedings just as much as there are legal burdens of proof in purely judicial proceedings. Sometimes the incidence of the burden of proof is spelled out by legislation, but more often than not it is simply implied in the nature of the proceedings. If, for example, entitlement to grant of a licence or benefit depends on proof that certain qualifications have been met, the burden of proving the relevant facts going to qualifications must fall upon the applicant. Similarly, where the issue to be decided is whether circumstances have arisen which would justify cancellation or suspension of a licence, or a finding that a breach of discipline had occurred, the onus of proving that these circumstances have arisen would devolve on the accuser. This would be so, notwithstanding that the accuser was also, of necessity, the person or body having authority to adjudicate."'

"Nevertheless, as a practical matter, an applicant for review in the tribunal in a case such as the present is asserting a claim for a right to compensation (cf. Vulic v.Capital Territory Health Commission (1982) 5 ALD 35 at 38 per Morling J.) and ultimately the tribunal, in considering the claim, can only act on the evidence before it; to do otherwise would be to commit an error of law. Thus in a practical sense, if not in a strict legal sense, it will be the responsibility of an applicant for review to ensure that there is laid before the tribunal all material which it will be necessary for the tribunal to have before it to enable it to come to a decision. Where, as here, material necessary to an applicant's case is not laid before the tribunal (and the reason for it not being put before the tribunal was that to do so would have been inconsistent with the applicant's case that there had been no recovery and that compensation should continue indefinitely) the applicant will not be able to complain if the tribunal, doing the best it can with the evidence before it, reaches a conclusion which is adverse to the applicant."

CHRONOLOGY

12. The original injury occurred at about 9.30 am on 15 April 1977 (T10). On that day, Mr McNicol said (T14), he arrived at work at the Attorney-General's Department at 8.50 am. At about 9.15 am he was in the office of his director when his telephone rang. Mr McNicol hurried to answer it. It was two rooms away. He then became ill. He felt himself begin to sweat. He sought a glass of water. An ambulance arrived and took him to hospital.

13. On 24 August 1977 the problem was diagnosed as acute infero-posterior myocardial infarction/coronary artery disease (T16). A medical referee considered that Mr McNicol had an underlying coronary artery atherosclerosis that was "probably" the cause of the myocardial infarction (T16). He suffered also from obesity and elevated serum cholesterol. The referee appeared to think that the rushing to the telephone involved unusual physical exertion which contributed to an aggravation, acceleration or recurrence of underlying disease.

14. On 31 August 1977 Dr D M Coles, a cardiologist, noted that the applicant's convalescence had been good with only occasional angina remaining (T17).

15. On 14 December 1977 the respondent's predecessor, the Commissioner for Employees' Compensation, accepted liability (T20). The determination suggested that Mr McNicol had contracted a disease to which his employment was a contributing factor.

16. Later it was thought that Mr McNicol may have had further heart attacks on 18 January and 9 March 1978 (T31). Dr M Faunce, the deceased employee's physician, reported on 12 August 1978 (T32) that Mr McNicol's angina had greatly increased in frequency and severity between February and May 1978. He was referred to the Royal Prince Alfred Hospital where angiographic studies showed:

"a very dominant left system with a severe lesion in the circumflex branch of his left coronary which gave off three posterior descending coronary arteries. In addition he had at least 50-60% lesion of his L.A.D. There was also a smaller lesion on the right which was not a dominant vessel. Mr. Grant successfully performed coronary artery bypass grafting on 6/6/78. He subsequently returned to Canberra at the end of June, but had an attack of biliary colic due to gall stone. ...

"The first symptoms of Mr. McNicol's heart disorder came on as an acute myocardial infarction while he was very busy and stressed at work on 15/4/77. His subsequent angina pectoris was related and based on this disorder of severe myocardial infarction of 15/4/77 and its precipitation by stress at work.

"The necessary heart surgery was thus also related to the original myocardial infarction and the underlying coronary artery disease. ..."

17. Mr McNicol ceased work in 1978 (T70). Compensation liability continued.

18. On 8 July 1986 Mr McNicol was admitted to hospital with recurrent severe chest pain assessed as due to angina pectoris (T49). He was discharged on 14 July 1986. Dr Faunce regarded the cause of this admission as related to the acute myocardial infarction on 15 April 1977.

19. On 19 August 1991 Mr McNicol was admitted to hospital with unstable angina (T79/139). Dr Coles investigated in September 1991 and was unable to demonstrate any patent grafts. The right and circumflex coronary arteries were totally occluded. In addition there was critical narrowing and generalised diffuse disease of the left anterior descending artery. He was assessed by Dr A Gale for revascularisation surgery but that was delayed and seems never to have taken place. Left ventricular global function was still within normal limits despite the earlier inferior infarction in 1977.

20. He was then well until admitted to hospital in 1994 with unstable angina and in 1996 with congestive cardiac failure (T79/139). He was given Diltiazem and recovered with withdrawal of this therapy (ex R2/2).

21. When seen by Dr Coles in 1998 he was reported as having returned to normal physical activities such as walking regularly without breathlessness or chest pain. By this time he had developed diabetes mellitus and required insulin (ex R2/2).

22. A post-mortem report dated 30 May 2000 (T64) related to an autopsy carried out at Southport, Queensland, on that date. Time of death was between 25 and 28 May 2000. The cause of death was certified as myocardial infarction with coronary atherosclerosis an antecedent cause. A death certificate to like effect was issued (T66). Dr C M Downes was the certifying doctor.

MEDICAL EVIDENCE

23. The later medical evidence commenced on 27 June 2000 (T67) with general practitioner, Dr E Quay, stating that the deceased last saw him in March 2000 just prior to his departure to the Gold Coast where he then died. The deceased's clinical records showed "that he regularly attended between 22.7.91 and 9.3.2000. He had a prior history of myocardial infarction and Hypertension and he had previously undergone Coronary Bypass Surgery in 1978 and 1991..." Dr Quay was "of the strong medical opinion that there [was] a causal relationship between [Mr McNicol's] known compensable medical condition and his death ...".

24. On 9 October 2000 a Comcare delegate wrote to Dr Downes calling her attention to the fact that only the myocardial infarct of April 1977 and any complications or direct sequelae of that condition were accepted for compensation and that the underlying coronary artery disease was not accepted (T70). A series of questions was posed:

"1. What is the cause of death?

2. Please indicate the exact anatomical location of the new infarct and its anatomical relationship to the old infarct.

3. Please outline the interrelationship of these two areas of pathology (ie, Is there a common arterial blood supply to the two areas?).

4. Please outline any pathology or complications seen in the coronary arteries. In particular please outline any coronary artery pathology that is present in any blood vessels associated with the coronary bypass grafts.

5. In your opinion, is the development of any such lesions directly related to the myocardial infarct of 15/4/1977 or were they, on the balance of probability versus possibility, due to constitutional issues such as age, lifestyle, obesity etc.? Please elaborate.

6. In your opinion, would the pathology and any associated complications seen in these vessels ... adequately account for the recent myocardial infarct?

7. In your opinion, was the death of Mr McNicol related to any direct sequelae of his work related myocardial infarct of 15/04/1977 or was it ... related to complications arising from the development of atherosclerotic lesions in the vessels replaced during his coronary artery bypass grafts?

8. In your opinion, are the lesions seen in the coronary arteries, that are the likely cause of the recent myocardial infarction, directly related to his employment prior to 1978?

..."

25. On 24 November 2000 Dr Downes responded (T73). Her answers were:

"1. Myocardial Infarction secondary to Coronary Atherosclerosis.

2. Posterior Inferior Myocardial Infarct close to the previous infarct.

3. There is a common arterial blood supply to the two infarcts.

4. Moderate to severe Atherosclerosis of new vessels.

5. In my opinion the development of the subsequent lesion is not related to the myocardial infarct of 15^th April 1977.

6. Yes. The infarct was due to the fact that patient had generalized arterial disease.

7. Mr McNicol's death was the result of complications arising from generalised Atherosclerosis.

8. The lesions of the coronary artery vessels are not related to his employment prior to 1978."

This led to rejection of the applicant's claim on 13 December 2000 (T74).

26. Dr N G Ardlie reported on 12 April 2001 at the applicant's request (T79). Dr Ardlie is a consultant physician. Dr Ardlie considered that the deceased may have suffered a "silent infarction" with no symptoms, hence he did not seek help at the time of onset. He said that silent infarction occurs more frequently in patients with hypertension and diabetes, both of which Mr McNicol had. He considered also that "the coronary lesions which progressively developed during Mr. McNicol's years of employment directly contributed to his myocardial infarction in 1977 and his death in May 2000". Dr Ardlie mounted a lengthy clinical argument to justify this. It had the following constituents:

* Coronary artery atherosclerosis plaque formation begins in early life. It remains clinically silent for decades.

* A plaque may crack at sites of mechanical stress. This causes thrombosis that underlies myocardial infarction.

* Atherosclerotic plaques that undergo disruption tend to be soft and contain a high concentration of cholesterol in the central core.

* The development of plaques to a point where they cause infarction is dependent on lipids such as cholesterol and is influenced by cardiovascular risk factors such as hypertension, obesity, smoking and diabetes mellitus.

* The conversion of a person with atherosclerotic lesions but no clinical symptoms into a patient with symptoms such as unstable angina or myocardial infarction is determined by complications mostly involving thrombosis developing in association with ruptured atherosclerotic plaque.

* Thrombi can be small or large. If small they can become organised and contribute to the growth of the plaque. If large and occlusive they lead to acute coronary syndromes such as myocardial infarction.

* Thrombosis results from the clumping together of platelets. Platelet aggregation can be promoted by circulating catecholamines such as adrenaline. "This mechanism provides a link between physical activity, emotional stress, cigarette smoking, and circadian variation in cardiac events, and the development of arterial thrombosis."

* Plaques rupture because of triggers or external pressures such as increases in heart rate and blood pressure.

* Acute coronary syndromes such as unstable angina and myocardial infarction are not due to slowly progressing plaque. Acute events are precipitated by plaque rupture which stimulates the formation of thromboses. There are two distinct processes, the slowly progressing formation of atherosclerotic plaque and a faster process of plaque destabilisation and rupture.

* Risk factors contributing to coronary artery atherosclerosis plaque formation in the employee's case included hypertension, diabetes, obesity, raised cholesterol and stress. Workplace stress contributed by causing plaque rupture. The physical stress, that is the increased heart rate, associated with rushing to answer the telephone caused plaque rupture leading to thrombosis, coronary occlusion and myocardial infarction.

* The fissuring of coronary atherosclerotic plaques may be a recurrent event.

27. Dr Ardlie expressed the opinion that the coronary lesions which progressively developed during Mr McNicol's years of employment directly contributed to his myocardial infarction in 1977 and his death in May 2000. Dr Ardlie gave as the basis for his opinion that both infarcts were located in the posterior and inferior region of the left ventricle and the affected areas of myocardium had a common arterial blood supply. He said that the second infarct could not be attributed to events in the grafted vessels since these grafts were shown to be totally blocked in 1991, long before the second infarct. He further explained that the plaques that had developed in the employee's coronary vessels and subsequently ruptured causing his first myocardial infarction continued to rupture and cause thrombosis, accounting for his episodes of unstable angina and eventually his death.

28. In summary, said Dr Ardlie, the employee's coronary disease first presented as a myocardial infarction at work on 15 April 1977. His subsequent angina was related, based on the underlying coronary disease. The necessary coronary bypass surgery was related to the underlying coronary artery disease and the second myocardial infarction, and his death, were also related, based on the underlying coronary disease. Dr Ardlie considered that the first infarct made Mr McNicol more vulnerable to the effects of any further compromise in left ventricular function.

29. Dr Coles reported to Dr Quay on 6 October 1998 (ex A4). He summarised Mr McNicol's medical problems then as coronary artery disease, coronary bypass graft (6 June 1978), left ventricular dysfunction and diabetes mellitus.

30. On 22 April 2002 Professor M F O'Rourke, whose credentials were detailed above in paragraph 3, wrote a report at the respondent's request (ex R2). Professor O'Rourke is, with Dr Nicholls of the University of Florida, author of McDonald's Blood Flow in Arteries, a treatise in its fourth edition and the standard reference around the world in the field of blood flow in arteries (transcript, page 30). In his report he made the following points:

* He agreed that the employee's heart condition suffered on 15 April 1977 was acute inferior myocardial infarction, described by him as "irreversible damage to the heart muscle on the inferior wall of the heart, and caused by lack of blood supply". However, he had difficulty agreeing with the respondent's determination that the infarction had been aggravated to a material degree by Mr McNicol's employment. He referred to the risk factors present in Mr McNicol at the time.. These were hypercholesterolemia and obesity. Their presence meant that a myocardial infarction could have occurred at any time at work or at home and probably was not aggravated to any material degree by the exertion of rushing to the telephone. The tribunal comments at this point that the parties rightly agreed at the hearing that the myocardial infarct was an injury simpliciter and not an injury in the form of aggravation of an underlying disease. Earlier decisions in the tribunal (Re Lott and Comcare (1996) 44 ALD 741) and the High Court of Australia (Zickar v MGH Plastic Industries Pty Ltd (1996) 187 CLR 310) supported this characterisation of the injury.

* On the assumption that the 1977 infarction was caused to some degree by Mr McNicol's work, Professor O'Rourke considered that the effects of any work-related condition ceased with Mr McNicol's successful treatment of acute inferior myocardial infarction in April 1977 and by the time he returned to work in June 1977.

* The cause of Mr McNicol's death was myocardial infarction and coronary atherosclerosis, described as disease of the coronary arteries where the arteries are narrowed by the accumulation of fatty material in the wall of the artery. There was no disagreement with Dr Downes' diagnosis or autopsy findings. Under the circumstances of Mr McNicol's death, that is that he was found sitting in a chair, the terminal event was probably cardiac arrest from ventricular fibrillation, a chaotic rhythm of the heart which is often terminal in persons with coronary artery disease but which can often be corrected if the person is near a defibrillator which can be used. This is the most common mode of death in patients with long-standing ischaemic heart disease.

* His belief was that there was no relationship between Mr McNicol's terminal condition and his myocardial infarction or his former employment with the department, or his work generally. The death was attributable to the relentless progression of atherosclerotic disease in the coronary vessels and in the bypass grafts, and which occurred over 20 years after terminating his employment with the department, and in the presence of uncontrolled constitutional risk factors of obesity, hyperlipidemia and diabetes mellitus.

* Neither the compensable injury nor any subsequent medical treatment obtained by Mr McNicol in relation to that injury caused or contributed to the heart condition from which he died. Mr McNicol made a complete recovery from his myocardial infarction of 1977. Death was attributable to the progression of coronary atherosclerotic disease after he left his employment with the Attorney-General's Department in 1978.

31. Dr Ardlie provided comments on Professor O'Rourke's report (ex A2). On 13 June 2002 he wrote that his reading of Professor O'Rourke's report in no way altered his view. He said the following:

"Indeed, his report may be construed to be perpetuating a long-held conception of how atherosclerosis develops, and which now turns out to be wrong. He refers to relentless progression of atherosclerotic disease and risk factors. In a beautifully illustrated article in Scientific American (May 2002), a US expert Peter Libby, states that blood vessels do not occlude by gradually building up fatty plaques. Plaques grow in fits and starts as clots emerge.

"It is now established that fissuring is a common event in subjects with atherosclerosis and that it is an integral part of plaque progression. Incorporation of thrombus contributes to intermittent growth of plaques. Indeed, this process accounts for most of the growth of atheromatous coronary stenosis. In relentless progression is not caused by risk factors.

"Fissuring and thrombosis is also a recurrent event. A study in patients with unstable angina leading to infarction revealed revealed layered thrombi overlying fissured plaques. When thrombi resolve the cells breaking down release lipid or fat which forms an unstable plaque prone to fissuring. Recurrent episodes of mural thrombosis lead to coronary artery occlusion.

"In summary, plaque rupture caused Mr. McNicol's first myocardial infarct, and recurrent plaque and thrombosis caused episodes of unstable angina and eventually his death."

32. Professor O'Rourke in turn responded to Dr Ardlie on 26 August 2002 (ex R3). The professor commented that he knew Dr Libby personally and was familiar with his work. He said he had worked in Dr Libby's department at the Brigham & Women's Hospital on sabbatical leave some 20 years ago. He said that his research on arterial function and that of Dr Libby was complementary. He wrote:

"Dr. Ardlie has completely misrepresented Dr. Libby's point of view. Dr Libby in his reports concentrates on inflammation as a process which occurred in arteries following entry of low density lipoprotein cholesterol (LDL) into arterial walls. The inflammatory process can weaken the arterial wall and cause fissuring and rupture with development of thrombus and acute occlusion of the coronary artery. The progressive process of atherosclerosis is due to LDL entry into the wall and the inflammatory process which results. Dr. Ardlie appears to have misunderstood this and attributes atherosclerosis to recurrent fissuring and thrombosis. This is incorrect."

33. Mr Selby explained the medical basis of the applicant's case at page 9 of the transcript:

"The evidence that we believe will elicit from Dr Ardlie says that, but for the 1977 injury simpliciter, it does not follow that the late [Mr] McNicol would necessarily have died from the 2000 event. And what is central to this is, so there is no taking by surprise, that it was the left ventricle myocardium that was injured in both the '77 and 2000 attack, and it was the blood supply to the left ventricle which was compromised on both occasions.

"So it is the additive effect of the '77 incident and the 2000 incident which kills him, and to put it quite starkly, suppose that the terminal event had been to one of the other three sectors of the heart, if that had been the case, it is our view it would have been a waste of time for the applicant to come here, given the medical knowledge expressed by the competing experts.

"And, within that, we should probably also make quite clear, we accept that the late John McNicol had high risk factors for heart problems. He had them in '77. He had them until he died and we do not say that work per se did anything else to his blood vessel supply to his heart in between the event in '77 and when he died. It is the injury to the heart muscle that we are concentrating on."

34. Dr Ardlie gave oral evidence by telephone. He was asked which blood vessels were implicated in Mr McNicol's death. He answered at pages 12-13 of the transcript:

"... Dr Downes and her report, if I can call it a report, I can't remember what shape it was in at this stage, anyhow she implied that the grafted vessels - occlusion of the grafted vessels was implicated in the second infarct, the heart attack associated with his death. Well, in fact, that cannot be correct because those grafted vessels, if you read the details of all the information provided, provided to me, and presumably provided to everyone else, those grafted vessels had been blocked about 10 years previously. So it's impossible to implicate them in the events that occurred leading up to his death. You cannot reconcile the two. In fact, it's pathology in the native vessels, the very same vessels that were involved in the first infarct that were involved in the blockage, or further blockage, of those vessels was involved in the second infarct.

"I would now like to move to the condition of those native vessels to which you have just referred. The one, or ones, that blocked. Would you please describe the nature of the plaque build up and fissure or rupturing process which you contend is an explanation for the occlusion that leads to the attack?---It was the original belief up until - I'm not quite sure how many years ago now, perhaps 10 or 15 years ago, that the lipid or cholesterol related lesions gradually built up in vessel and led to blockage of that vessel, and if you block off a blood vessel, coronary artery in this instance, it will result in loss of blood supply to the heart muscle and that heart muscle will die and that's what we call a myocardial infarct, or heart attack. In fact that gradual build up of the fatty lesion in the vessel is not the process that occurs that causes a heart attack. What happens is, and this can be a very slow process because the first lesions have been detected in the first 10 years of life but they don't manifest usually until the third, fourth or fifth decade of life, so the process can be very slow. What happens is that the various risk factors, cholesterol, etcetera, lead to the development of a fatty lesion in the vessel wall - in the wall of the coronary artery and this fatty lesion if it is a so called `vulnerable plaque', and a vulnerable plaque is a lesion in which there is a central core of fat contained particularly over its [intraluminal] surface there is a thin capsule, and that is - those are the features of a so called `vulnerable plaque' and under certain circumstances those vulnerable plaques will rupture, crack, fissure, whatever you want to call it. And the circumstances that are associated with fissuring or rupturing of a plaque are increases in heart rate and blood pressure, and these impose increased physical forces on the plaque. The plaques in coronary arteries in fact are situated - they are in a terrible situation because they are in a - in contrast to other blood vessels the poor old coronary arteries lie on the surface of the heart in their initial course and with every beat of the heart they bend and twist and this imposes remarkable physical forces on the blood vessel and in particular of so-called vulnerable plaque, and this leads to a rupture of the plaque, and this exposes the contents of the plaque. And the contents of the plaque are thrombogenic. They lead to the immediate formation of a blood clot, or coronary thrombis. It's the build up of that thrombis, or clot, on the ruptured plaque, which in turn leads to inhibition of - prevention blood supply to the heart muscle, or myocardium. As a result of that deprivation of blood supply to the myocardium, the heart muscle dies, and that is what a myocardial infarct is. So, in summary, we don't have a gradual build up of fatty lesion. The initial phase in the pathology is the development of a fatty lesion, which is cholesterol dependent, and dependant on other risk factors, and then eventually physical forces - increase in heart rate, blood pressure - lead to a rupture of that plaque, and the ruptured plaque causes clotting or thrombosis, and it's the thrombotic event that occludes the coronary artery and causes a heart attack."

35. Dr Ardlie agreed that the 1977 infarct caused "the loss of some heart muscle in the left ventricle". He described the process leading to the infarct as Mr McNicol, over the course of decades, developing fatty, atherosclerotic lesions which were dependent on Mr McNicol's risk factors. Mr McNicol then rushed to take a telephone call, which would have resulted in a transient increase in his heart rate and blood pressure. These imposed additional physical stresses on the plaque, leading in turn to the rupture of a vulnerable plaque. That in turn caused clotting which, in turn, caused his myocardial infarct. In his first report Dr Ardlie had referred to the production of adrenaline as a factor associated with the rush to the telephone. He explained at the hearing that adrenaline has been associated with increased blood clotting, a part of the process of coronary occlusion. As is documented below in paragraph 40, Professor O'Rourke disagreed with Dr Ardlie on this point.

36. Dr Ardlie described the connection he saw between the 1977 infarct and the 2000 fatal infarct at page 15 of the transcript:

"Now, what happens is that when the plaque ruptures, as it did in Mr McNicol, the blood clot that developed from the surface initially deprived the heart muscle blood supply and caused a heart attack. But at the level of the blood vessel itself, that blood clot, several things can happen to it. One, it can completely disappear; or (b) it can partly disappear, in other words it decreases in size. But eventually what residual blood clot there is becomes incorporated into the vessel wall, into the plaque that has ruptured. And that process is also associated with incorporation. It's associated with the breakdown of all the blood cells that were in the blood clot. The red cells, the white cells, the blood platelets, etcetera, they all break down, and they form a fatty deposit, and this again we've established with some work of our own done in the 1970s. So, as a result of that incorporation and breakdown of blood cells in the lesion, you develop on top of the original lesion, another vulnerable lesion. It has a central core of fat covered by a capsule. So here we now have another lesion prone to rupture, and given the right circumstances increases in heart rate, in blood pressure, this vulnerable lesion can again rupture and as a result another blood clot forms and the same process goes on again. In pathology articles devoted to this process they have clearly shown several events that occurred. You can see beautiful lesions that have perhaps undergone three or four ruptures and the blood clot is incorporated into the vessel wall forms a vulnerable lesion which in turn ruptures again and the process can go on three or four times. This can go on - this recurrent event, we don't know how long it takes, but we are looking at many, many years, perhaps decades. And one possible explanation for what happened in Mr McNicol is that it could be the very same lesion that caused his first heart attack that led in turn to the final heart attack which took his life as a result of this recurrent process that I have referred to."

37. Ms Walker, for the respondent, in cross-examination established the following:

* Dr Ardlie read Dr Downes' report indicating the site on the heart of the fatal infarct in 2000 as a site that merged with the site of the 1977 infarct. Dr Downes in fact described the second site as "close to" the first (paragraph 25 above).

* If one blood vessel (or artery) completely blocks up another may take over and supply the blood not supplied through the original vessel. This meant that the vessel supplying blood to the relevant part of Mr McNicol's heart that experienced a rupture of an atherosclerotic plaque, as Dr Ardlie saw it, leading to the myocardial infarct could have been a different vessel from the 1977 vessel. The vessel affected in 1977 may have occluded long before 2000. Dr Ardlie had suggested that it was the same vessel that experienced a rupture of atherosclerotic plaque in both 1977 and 2000. He accepted that either explanation canvassed in this bullet point could have been applicable.

* Dr Ardlie was unable to say whether the artery affected by the rupture of atherosclerotic plaque in 1977 had been replaced in a cardiac artery bypass graft in 1978.

* The ongoing effect of the 1977 myocardial infarct was that part of the heart muscle was replaced by a scar. This reduced its capacity to contract. The size of the scar determined the amount of functioning heart muscle, or myocardium, that remained. The effectiveness of the left ventricular pump was reduced. Cardiac failure resulted. There was a back-up of fluid in the lungs. In such a case the patient becomes short of breath, or the legs may begin to swell. Much depends on the part of the heart affected.

* The subsequent ruptures of atherosclerotic plaque in the artery were not related to the scarring from the 1977 infarction. They result from the development of vulnerable fatty lesions that are prone to rupture when physical force is imposed on them.

* Dr Ardlie reasoned that Dr Downes saw the grafted blood vessels as implicated in the second myocardial infarction because she had referred to "atherosclerosis in new vessels" as a coronary artery pathology that was present in blood vessels associated with coronary artery bypass graft.

38. Professor O'Rourke also gave oral evidence by telephone. The following emerged from Ms Walker's examination in chief:

* The fact that in 1991 Mr McNicol's left ventricular global function was still within normal limits despite the earlier infarction inferred that the impact of the 1977 infarction was not so extensive as to cause any severity of impaired contraction of the ventricle of the heart. The heart was still able to cope, and cope well, despite any scar that might have resulted from the previous infarct. Professor O'Rourke considered that the treatment given Mr McNicol had been successful and he had recovered with appropriate medication, with rest and with the development of scar tissue in the ventricular wall replacing the dead myocardium, or dead heart muscle.

* The 1978 coronary artery bypass graft was not treatment for the myocardial infarction.

* Professor O'Rourke did not agree entirely with Dr Downes' assessment that Mr McNicol died from myocardial infarction and coronary atherosclerosis. He saw the terminal event as probably cardiac arrest from ventricular fibrillation. Ventricular fibrillation was said to be a common complication of diffuse coronary atherosclerosis and of an acute myocardial infarct.

* Professor O'Rourke had a great deal to say about the notion of the relentless progression of atherosclerotic disease. He said he agreed with the views of Dr Peter Libby in the Scientific American article that Dr Ardlie had referred to. He said that there is a deposition of lipid or fatty material within the wall of the artery so that the wall becomes progressively narrowed and subject to areas where inflammatory processes can occur which weaken the wall and can cause a rupture of the innermost lining of the wall. A clot can then form.

* Professor O'Rourke highlighted the differences between his views and those of Dr Ardlie. One difference was that Dr Ardlie referred to physical forces in the arterial wall causing rupture of the plaque (see paragraph 26 above, bullet points 2 and 8). Professor O'Rourke said there was nothing in the Libby article referring to that. The thrust of the Libby article was to refer to inflammations within the artery wall which weaken the atherosclerotic plaque and lead to the development of a clot and total occlusion of an artery. Dr Ardlie had referred in no sense to inflammation. Dr Ardlie referred to the narrowing of the artery as not being due to a progressive deposition of lipids within the arterial wall from adhesion of the fat laden cells circulating in the blood. On the other hand, Dr Ardlie referred to the repetitive clotting in the wall which leads to an atherosclerotic process. Professor O'Rourke said that that was not what Dr Libby was referring to in his article. He suggested that Dr Ardlie had completely misunderstood Dr Libby's article. It was put to Professor O'Rourke that Dr Ardlie appeared to be saying that a myocardial infarction stemmed from a vulnerable plaque, that is a lesion with the central core of fat, rupturing, cracking or fissuring as a result of increased heart rate and blood pressure leading to a blood clot or thrombosis which cuts the supply of blood to the myocardium, leading to the death of the heart muscle. Professor O'Rourke did not agree with that proposition. Again he said that was not what Dr Libby accepted. He said that there is instead a process of gradual build up of fatty material on the wall and there were illustrations within the Scientific American article that showed exactly that. These illustrations did not show the process Dr Ardlie was referring to. Rather, they showed that the final event in blockage is an inflammatory process within part of the wall which leads to weakening of the wall and a rupture. This is not an exposure to mechanical forces in the wall, but rather the weakening from inflammatory process that leads to exposure of the material within the wall to the blood and the formation of a clot. That was described as the proposition put by Dr Libby and the common view of the development of atherosclerosis and of acute heart attacks.

* Professor O'Rourke reinforced that he agreed when Dr Libby said that there is a progressive disease in the presence of uncontrolled risk factors which causes the progression of atherosclerosis throughout the coronary arteries and that the terminal event can be a clot forming due to the inflammatory process within the arterial wall which is generated by the fatty material within the arterial wall.

* Professor O'Rourke did not accept Dr Ardlie's suggestion that the same blood vessel which experienced atherosclerotic plaque rupture leading to the 1977 myocardial infarct may have experienced a similar rupture again leading to the 2000 myocardial infarct. Professor O'Rourke said that the vessel would not have ruptured. It would have occluded rather than ruptured. He said that there is every evidence that in the 23 years following the occlusion of the first artery, adequate compensation was made and that he was certain that the further problem was in another blood vessel which was supplying another part of the heart muscle which caused that muscle to die.

* Professor O'Rourke was not impressed by Dr Ardlie's arguments based on the assumption that the myocardial infarcts experienced in 1977 and 2000 were adjacent, or close to each other. He did not go into this in-depth but noted that Dr Downes, who had seen the heart of the deceased, saw no connection between the two infarcts.

39. Mr Selby cross-examined Professor O'Rourke. From the cross-examination the following emerged:

* Professor O'Rourke did not agree that the occlusion of a blood vessel was necessarily an event which caused clotting inside the blood vessel. He said the process could occur from a clot forming in an already narrowed vessel or it could occur through the atherosclerotic process continuing and totally "gumming up" the vessel. This would be independent of any clotting.

* Professor O'Rourke was asked again about Dr Downes' finding that the two muscle losses affecting the left ventricle were "adjacent" and it was put that this was consistent with blood supplies to "native vessels" being involved in the 1977 and 2000 events. He was asked whether he agreed or opposed the statement that the physical co-relationship of the two heart muscle effects was consistent with the same blood supply vessels being involved. He answered in the negative.. He thought there were two different vessels involved to cause a fresh myocardial infarct 23 years after an initial infarct. In the interim period Mr McNicol had had an angiogram done in 1991 in Canberra which showed a total destruction of the right coronary artery, the normal artery of supply to the inferior surface of the left ventricle. He thought this was a totally new and different lesion. His view was that, on the basis of the occlusion found in 1991 in the right artery, therefore the 2000 events must be caused by a failure in a totally different blood supply vessel from that in 1977.

* Professor O'Rourke refused to accept that if a blood vessel had been compromised at one point in time and there was further damage to the inside of the blood vessel one would look at the vessel compromised earlier for further damage first rather than going to other vessels which had apparently been satisfactory in the past. Professor O'Rourke said that one would have to do both. Further, he said that this had been done in Mr McNicol's case and lesions had been found widely throughout the coronary system that were threatening other parts of the myocardium.

40. In answers to questions from tribunal member, Dr Miller, Professor O'Rourke rejected Dr Ardlie's suggestion that a thrombosis could result from platelet aggregation promoted by circulating catecholamines such as adrenaline (paragraph 26 above, bullet point 7). He did not see that as consistent with Dr Libby's views. He did not agree that emotional stress was necessarily a cause of coronary artery thrombosis. He said that the problem could occur with or without emotional stress. He recalled that Mr McNicol had died sitting in a chair.

41. In a response to the senior member Professor O'Rourke said the following at page 40 of the transcript about the currency of Dr Ardlie's views:

"Well, he's completely misrepresented an article in Scientific American. He's completely misrepresented the views of an expert in this field. What Dr Libby has said is really got nothing to do with the assertions in his first report or in his second report. I think it's way off mainstream his view.

"So the Libby views in the Scientific American are completely inconsistent with the sorts of views that Dr Miller has just taken you through?---Yes, there's no reference there to emotional stress or other activities like that. It really refers to the development of atherosclerosis with the types of risk factors that Mr McNicol had, and then the final development of a clot which occludes an artery because of inflammation in the damaged arterial wall. But it doesn't deal with the circadian variation, or the morning increase in myocardial infarction. This man's myocardial infarction, I think both of them, did not occur in the early morning."

SUBMISSIONS

MR SELBY

42. The link between 1977 and 2000 was described as follows:

"Now, the link that the applicant draws between '77 and 2000 is this: yes, Mr McNicol had generalised blood supply problems in '77. A work event coincides with, whether one calls it rupturing, fissuring, cracking, whatever else, it all seems to amount to the same, but in any event it causes an occlusion of the blood supply vessel which resulted in the muscle wall loss in the left ventricle. The left ventricle is thereafter compromised. There is a difference between the experts as to the extent of that damage to the pump, and that comes up in that the professor today, as I understood it, was saying that in 1991 the pump - the left ventricular pump was okay. Dr Ardlie at the fourth page of T79, final paragraph which begins:

`In October 1991 an echo cardiogram...'

"Says in the final sentence:

`The left ventricular pump was functioning poorly.'

"He then goes on to agree, or to be in agreement with the professor in that:

`An arrhythmia may have contributed to Mr McNicol's death.'

"That is the top of the following page. Now thereafter, as explained in today's spoken evidence, Dr Ardlie says, given the two bits of damage to the left ventricular muscle wall and given the fact that in 1991 the grafts were totally occluded it is his opinion that the event is consistent with the same blood supply vessels in 2000 being involved as those in '77. And there was an exchange between him and Mrs Walker on that point which led to him reminding us that he had used the words `consistent with'.

"He says given what the work event had done to the native vessels in '77, in terms of causing that occlusion in '77, and given the natural history, over the expected history over the next 20-odd years and given that the deterioration, or the gradual build up of tissue in those native vessels can be silent. You recall that he even said that after a clot has formed it can then actually disappear altogether, or parts of it can disappear. He said then it is open to find that those compromised 1977 vessels finally packed-it-in in 2000. That occlusion resulted in the injury to the muscle, the pump failure, the possible arrhythmia, death.

"By contrast, Professor O'Rourke disputes the process of blood vessel compromise and he even wishes to dispute the, if I might put it as the relevance of the link between the work incident - relevance is not the right word. It is not that he said it wasn't relevant. He simply says; well, it could have happened anywhere. One can say with respect to the two learned experts that they hold, each of them, strongly to their respective views. Each of them appears to be well qualified, in terms of academic credentials and in terms of their peer recognition. They disagree as to which is to be the preferred medical science.

"In the end then, we come down to trying to apply the best legal principle solution to the disputed medical science, and with that we come back to a heart attack at work causing a clot, causing muscle wall damage, followed by another event in 2000, another occlusion, muscle wall damage in the same part of the heart leading to death. Dr Ardlie says it is consistent that the same compromised blood supply was involved. Dr O'Rourke says; no, it is not. But Dr O'Rourke cannot get over the two facts of muscle wall damage in the same part of the heart and the fact that the first attack occurred at work."

MS WALKER

43. Ms Walker commenced by paraphrasing the applicant's case:

"... that in 1977 a blood vessel was compromised which led to the myocardial infarct, and it packed-it-in again in the year 2000, and that is the link between the two events which makes the second of them compensable and therefore the death. If we were in a civil trial I would have made a no case to answer submission when that proposition became extant, because it is simply not consistent with the burden or the standard of satisfaction that the tribunal needs in order to find a compensable condition. Because when asked about that proposition Dr Ardlie said it was one possible explanation. It could have been the same lesion which recurred. He said there were other possible explanations.

"So even on Dr Ardlie's evidence at the highest it would not be enough, in our submission, to satisfy the Tribunal that compensation should be paid for Mr McNicol's death. However, if one wants to look a little further behind Dr Ardlie's rationale for that proposition it falls, in our submission, yet again because Dr Ardlie said he came to that conclusion because the second myocardial infarction scar was adjacent to the first. I asked him what he meant by `adjacent' and he was unable to say.

"He said it depended on what Dr Downes meant by adjacent. But he thought that of itself it was significant. Well, Dr Downes did not even use the word `adjacent'. She, in her report, used the word `close'."

44. Dr Ardlie, said Ms Walker, could not say which blood supply to the left ventricle was involved at the time of the second infarct. He had conceded that there were a number of arteries supplying the left ventricle.

45. Ms Walker observed that Professor O'Rourke considered that it was unlikely that in fact the same blood vessel was responsible for the second myocardial infarct because it had done its damage on the first occasion and had become occluded. It was unlikely that that blood vessel could do any further damage.

46. Ms Walker suggested that the evidence supported the proposition that the 1977 myocardial infarct had relatively short lived effects. The employee was hospitalised. He returned to work shortly after. It was not until 1978 that he began to have angina symptoms and he was investigated further for heart disease and a coronary artery bypass graft was done in 1978. The Commissioner for Employees' Compensation accepted liability for that procedure but, said Ms Walker, probably should not have. That surgery was not required to address the effects of myocardial infarct, but to address the underlying condition.

47. Dr Coles considered that Mr McNicol had effectively recovered in his report on 31 August 1977 (T17). Dr Coles was the treating practitioner. Ms Walker conceded that scarring of the ventricle remained. However, it was not bound to be symptomatic.

48. Ms Walker submitted that the tribunal should accept Professor O'Rourke's evidence in preference to Dr Ardlie's. She said he was the more eminent in the field. His evidence was said to be more logical. In that Dr Ardlie proposed that vessel rupture can be a silent event with no outward symptoms, there may have been a number of silent ruptures that could have occurred between 1977 and 2000, not when Mr McNicol was at work, and which explained the fatal event in 2000.

49. Ms Walker suggested that Dr Ardlie had developed a theory that a myocardial infarct results because of vulnerable plaque which ruptures as a result of an increased heart rate or blood pressure. This view is not accepted, she said, by physicians in this field generally and seemed based on a misreading of Dr Libby's article.

50. She concluded:

"Just in closing, in the respondent's submission, this is a relatively straight forward matter in that we have an underlying atherosclerotic process, it manifests in 1977 in the workplace, and on that basis liability was properly accepted. The effects of that first myocardial infarction are shortlived other than for scarring on the left ventricle. There is no evidence that that scarring of the left ventricle has had any significant ongoing impact. There is a further known myocardial infarction in 2000 which resulted in death. That is not linked, in our submission, with the earlier accepted condition and therefore liability for a death claim pursuant to section 17(3) ought not flow."

FINDINGS ON MATERIAL QUESTIONS OF FACT WITH REFERENCE TO THE EVIDENCE AND OTHER MATERIAL IN SUPPORT OF THOSE FINDINGS

51. The tribunal sees an apparent illogicality in the case advanced here for the applicant. An injury in the form of a myocardial infarct is accepted by all parties as an injury simpliciter. For such an injury to be an "injury", in accordance with the definition of "injury" in s 4(1) of the Act, it must have arisen out of, or in the course of, the employee's employment. The infarct in 1977 easily fulfilled that criterion as it occurred in working hours when Mr McNicol was at work. However, the infarct in 2000 occurred as an injury simpliciter 23 years after Mr McNicol ceased work. Thus, it did not occur in the course of Mr McNicol's work. Could it have arisen out of his work? This is not so great a problem in a case where an employee has an injury in the form of a disease. A disease can be precipitated through some material workplace contribution and later flare ups may be compensable. This flows from the definitions of "disease" and "injury" in s 4(1).

52. Ms Walker suggested somewhat facetiously that the applicant's arguments in paragraph 42 above amounted to a "Nadge case imposed on a Zickar case". The reference to "Nadge" was to Re Nadge and Australian Postal Corporation (1994) 33 ALD 710. Senior Member Barnett decided that case. The facts and holdings are set out below:

"...

the respondent denied liability to compensate the applicant for injury to his back which became painful after playing on the beach on 1 January 1993. The reason given for the determination was that the injury did not occur in compensatable circumstances. The applicant asserts however that the beach incident merely brought on a renewal of symptoms of a former injury for which the tribunal had previously determined that the respondent was liable.

...

(4) The tribunal makes the following finding of facts:

(a) The applicant was injured in the course of his employment with the respondent on 6 June 1988 and suffered an injury to his spine at the L4/L5 vertebrae.

(b) As a result of that injury he was incapacitated for work and the respondent accepted liability for that work-caused incapacity.

(c) In 1990 the applicant underwent a laminectomy operation performed by Dr David Wright, in which his L4/L5 vertebrae were fused.

(d) As a result of the operation the applicant's pain was considerably reduced and he was able to resume full time employment.

(e) On the medical evidence of Dr Wright, the tribunal finds, although the applicant had resumed full-time employment, that there was a continuing weakness at the L4/L5 level and the applicant's symptoms continued at a low level thereafter.

(f) In January 1993 the applicant was playing on the beach with his children with a ball and during that play he was involved in quite strenuous but normal family activities. These activities consisted of throwing a ball the size of a tennis ball with children and playing cricket. It included running, jumping to catch the ball, standing in water up to his waist, diving for the ball, and falling in the water. These activities, though quite strenuous, were no more than the normal activities of a family man of the applicant's age playing at the beach with his children.

(g) During the games the applicant noticed an increase in the severity of his lower back pain but continued with the games as it did not feel significantly more painful than the continuing pain which he had experienced in the lower back since the date of the operation.

(h) The pain got worse during the next few months. The applicant spent a considerable amount of time off work at various periods as the pain incapacitated him.

(i) The incident on 1 January 1993 apparently caused no new injury but did cause a worsening of the continuing pain at the L4/L5 level.

(5) The applicant claims that the increase in severity of his symptoms resulted from the 1988 injury. The respondent submits that the activities on the beach constituted in effect a new accident or injury which constitutes a break in causation between the 1988 injury and the more severe symptoms which occurred on 1 January 1993. Consequently, Mr Brooksby says the respondent is not liable to compensate the applicant for the incapacity which occurred during 1993.

The law

(6) If the 1993 incident is treated as a new injury the applicant's claim must fail because of the way `injury' and aggravation are defined in s 4 of the Safety Rehabilitation and Compensation Act 1988 (Cth) (the Act). There would be no liability because the injury or aggravation did not `arise out of or in the course of his employment'. If however, the increased pain suffered by the applicant is properly classed as a renewal of the symptoms caused by the 1988 injury the applicant's claim will succeed. Many authorities were cited by each counsel on this question of causation including the leading High Court case of Commonwealth v Butler (1958) 102 CLR 465 and the Western Australian Supreme Court case of; F & T Grassi Pty Ltd v Ellendale Estate Pty Ltd [1985] WAR 294 where philosophical questions of causation, as applicable to the Law, were fully discussed. In the end however it boils down to a question of common sense. Did the applicant's activities on the beach constitute a new injury or an aggravation of the 1988 injury, in either of which cases the respondent is not liable, or did the old injury re-occur `when it played up either spontaneously or because of the ordinary stresses and strains of living and working...?'; Canale v Commissioner of Main Roads (1982) WA WCB 163 approved by Burt CJ in; Grassi v Ellendale, supra, p 297.

(7) The tribunal finds that there was no new injury or accident in 1993 and that the pain was a direct result of the 1988 injury. It is significant that the applicant had undergone major surgery in 1990 and that although the resulting spinal fusion considerably reduced his pain and allowed him to resume a normal working life, it did not completely remove the symptoms at the level of the original injury, as the pain there continued at a lower level of severity. The activities which the applicant engaged in on 1 January 1993 were not excessive but really constituted part of the normal day to day living activities of a normal family man of his age. The symptoms had never completely resolved, and the more severe symptoms occurred in exactly the same position as the earlier and continuing symptoms at the point of fusion in his spine. This is not merely a case where the 1988 injury and subsequent operation were predisposing factors, but that injury and the operation and subsequent weakness were direct and proximate causes of the increase in symptoms which occurred on the beach and shortly afterwards in 1993. For this reason the respondent is liable to pay compensation for the resulting incapacity.

..."

53. This was effectively the argument put by Mr Selby in this case. The elements in Nadge (above) that brought about a favourable resolution in that case, and that found echoes in Mr Selby's submissions, were:

(a) What was looked for was a renewal of the symptoms caused by the 1988 injury rather than a new injury or an aggravation.

(b) What was looked for was also described as the old injury re-occurring either spontaneously or because of the ordinary stresses and strains of living and working.

(c) The pain in 1993 was a direct result of the 1988 injury.

(d) The pain from the 1988 injury had reduced through spinal fusion but had never entirely gone away. The more severe 1993 symptoms occurred in exactly the same place as those in 1988.

(e) Mr Nadge's activities in 1993 were not excessive but were part of day to day living activities of a normal family man of his age.

(f) The 1988 injury, the operation and the subsequent weakness were direct and proximate causes of the increase in symptoms which occurred on the beach and shortly afterwards in 1993.

54. Did this analysis apply in Mr McNicol's case? An immediate problem is the lack of certainty about the aetiology of the 2000 myocardial infarct as compared to the observable features of the orthopaedic aetiology in Nadge (above). The applicant's case requires acceptance of the proposition that the same blood vessels served Mr McNicol's left ventricle in 1977 and in 2000. This was based on Dr Ardlie's interpretation of Dr Downes' evidence that the two myocardial infarction scars were "close" as meaning that they were "adjacent". This was therefore not immediately convincing as evidence. Dr Ardlie thought that the vessels compromised in 1977 had continued functioning until 2000 when they had blocked. They had been adversely affected in the intervening years by the build up of fatty lesions on the vessel wall which fissured or ruptured because of such risk factors as diabetes, blood pressure, high cholesterol and heart rate increases and which then caused clots inhibiting the blood supply.

55. Professor O'Rourke was not attracted by this analysis. He saw the blood vessel involved in the 1977 infarct as most likely occluded early in the piece and replaced by other blood vessels which went on to supply blood to the left ventricle. Professor O'Rourke was impressed by the almost complete recovery Dr Coles recorded in August 1977. Professor O'Rourke was also critical of Dr Ardlie's understanding of the causes of atherosclerosis. Professor O'Rourke considered he was adopting Dr Libby's analysis that the rupturing of plaque in the vessel wall resulted from inflammation arising from build up of fatty material in the wall, not from physical force. Both experts saw clots emanating from plaque rupture as the problem, however Professor O'Rourke saw the plaque rupture as caused by inflammation rather than from physical force.

56. The tribunal appreciated the efforts of both experts to be of assistance and to share their respective views, providing detailed explanations with care and patience. However, where such a disagreement amongst experts exists it is necessary to identify who provides the more credible evidence. In the present case it was noted that Professor O'Rourke has quite extraordinary credentials. Not only is he a cardiac specialist, but he has written the world's leading text on blood flow in arteries, blood flow being the very issue at the core of the tribunal's deliberations.

57. Dr Ardlie, by comparison, is a consultant physician, a Doctor of Medicine, a Doctor of Philosophy and Fellow of the Royal Australian College of Physicians. While his attainments are considerable, they are less focussed on cardiology and blood flow. It appears also from Professor O'Rourke's evidence that Dr Ardlie's views on the causes of plaque rupture incline towards the unorthodox.

58. For these reasons the tribunal preferred Professor O'Rourke's analysis and found that it was not satisfied that Mr McNicol's death was caused by a myocardial infarct that was a recurrence or renewal of the compensable myocardial infarct that occurred in 1977.

CONCLUSION

59. The tribunal has found that Mr McNicol did not die as a result of the injury, in the form of a myocardial infarction, that he suffered in 1977 and for which he and the applicant could be compensated under the Act.

DECISION

60. The tribunal affirms the decision under review. The applicant qualifies for no costs associated with this application.

I certify that the 60 preceding paragraphs are a true copy of the reasons for the decision herein of Mr M J Sassella, Senior Member and Dr M D Miller AO, Member

Signed: .......................................................................................

Associate

Date of hearing 24 February 2003

Date of decision 16 June 2003

Counsel for the applicant Mr H Selby

Solicitor for the applicant Pamela Coward & Associates, Lawyers

Counsel for the respondent Ms L Walker

Solicitor for the respondent Sparke Helmore, Solicitors

[1] http://www.austlii.edu.au/au/legis/cth/consol_act/sraca1988368/.