Mansfield and Repatriation Commission - [2002] AATA 1180

DECISION AND REASONS FOR DECISION [2002] AATA 1180

ADMINISTRATIVE APPEALS TRIBUNAL )

) No V2001/404

VETERANS' APPEALS DIVISION       )
           Re      YVONNE EVELYN MANSFIELD
  Applicant
           And    REPATRIATION COMMISSION
  Respondent

DECISION

Tribunal Mr J Handley, Senior Member

Date1 November 2002
PlaceMelbourne

Decision      The decision under review is affirmed.
  .........Sgd. Mr J. Handley.........
  Senior Member
CATCHWORDS
Veterans' Entitlements - Eligible service - connection between service and smoking conceded - diagnosis of atrial fibrillation conceded - whether applicant suffered ischaemic heart disease, being a 'cardiac disease' at clinical onset of atrial fibrillation - decision affirmed.
McKenna v Repatriation Commission [1999] FCA 323
Benjamin v Repatriation Commission [1999] FCA 1879

REASONS FOR DECISION

1 November 2002 Mr J Handley, Senior Member

The applicant applies to review a decision made by the Veterans' Review Board ("VRB") on 18 April 2002.
The VRB initially decided on 8 November 1999 to affirm a decision made by the respondent with respect to deep vein thrombosis and diabetes. It then varied a decision under review with respect to a condition described as "atrial fibrillation with transient ischaemic attack and retinal artery embolism". The VRB decided to vary that diagnosis and decided that the diagnosis of the condition then under review was "atrial fibrillation and cerebro-vascular accident with retinal artery occlusion". It adjourned the hearing with respect to that condition as diagnosed and on 18 April 2000 decided that the decision under review with respect to "atrial fibrillation" was affirmed.
The hearing of the application commenced in Albury on 29 January 2002. Evidence was heard only in Albury from Mrs Mansfield. Mr O'Riain appeared as solicitor agent on behalf of the applicant's solicitors. Mr Douglass appeared on behalf of the respondent. The hearing in Albury was adjourned for resumption in Melbourne to hear from local witnesses.
The applicant's Statement of Facts and Contentions do not specifically plead a review of the condition of atrial fibrillation, however the decision under review identified in the application to the Tribunal is the decision of 18 April 2000 only. An application made to extend time to lodge these proceedings pleaded the decision of 18 April 2000. Mr O'Riain in Albury confirmed that he was instructed only to pursue review with respect to atrial fibrillation.
The service of Mrs Mansfield was entirely within Australia and accordingly her entitlement is to be determined upon the balance of probabilities. The applicable Statement of Principle was Instrument No 10 of 1996 entitled "Atrial Fibrillation". The only applicable factor connecting service with atrial fibrillation was factor 5(a) which provides:
"suffering from cardiac disease at the time of the clinical onset of atrial fibrillation".
The "sub-hypothesis" advanced by the applicant, was that the applicant smoked cigarettes for a duration and in a quantity sufficient to satisfy the Statement of Principles with respect to ischaemic heart disease. This condition is the subject of Statement of Principle 81 of 1998 and 39 of 1999. In both instruments, ischaemic heart disease is defined as-
"For the purposes of this Statement of Principles, "ischaemic heart disease" means a cardiac disability, acute or chronic, arising from an imbalance between the supply and myocardial demand for oxygen which results from coronary atheroma or coronary vasospasm. Ischaemic heart disease may be evidenced by:
(i)        myocardial infarction (old or new); or
(ii)       angina; or
(iii)      arrhythmia with ECG evidence of myocardial ischaemia; or
(iv)      cardiac failure,"
The Full Federal Court in Benjamin v Repatriation Commission [2001] FCA 1879 ("Benjamin") decided (paragraph 41) that Statements of Principles were "not relevant to the question of diagnosis". However, all the medical witnesses agreed that the above definition adequately described ischaemic heart disease and was consistent with their understanding of that disease.
The claim of Mrs Mansfield comprised a number of links in a chain of connection with service. This review is concerned with whether the applicant suffered from cardiac disease at the time of the clinical onset of atrial fibrillation. In order to establish "cardiac disease", the applicant needs to demonstrate that she suffered "ischaemic heart disease". Ischaemic heart disease was said to be related to cigarette smoking, which was submitted as having a connection with service. The respondent conceded that the applicant satisfied the requisite quantity of cigarettes smoked and duration of smoking, and also conceded the diagnosis of atrial fibrillation. The "sub-hypothesis" between ischaemic heart disease and cardiac disease was crucial to the claim advanced by Mrs Mansfield (refer McKenna v Repatriation Commission [1999] FCA 323).
Yvonne Evelyn Mansfield
Mrs Mansfield is presently 75 years of age, having been born on 1 April 1927. She was a member of the Women's Royal Australian Navy between 7 June 1945 and 27 September 1946. Mrs Mansfield said she commenced smoking cigarettes after she enlisted, initially of two cigarettes per day, however at the completion of her service, she was then smoking twenty cigarettes per day. She ceased smoking in 1986.
Mrs Mansfied was educated to form 4 level at secondary school. After her children completed their secondary education, she commenced an accounting course by distance from the Gippsland Institute of Tafe and obtained a certificate in 1979. She worked between 1980 and 1994 with a firm of accountants in Myrtleford.
In 1985, Mrs Mansfield was widowed, but remarried in 1991. She and her husband travelled to France and Spain for their honeymoon, but whilst travelling on a train to Barcelona she became ill and said that she felt "uncomfortable" in her chest. She recalled pain in her chest and throat and was breathing deeply. She said the symptoms lasted for approximately 30 minutes. She described the pain as not being intense, but "very uncomfortable". That episode occurred in June 1991, but she did not then seek treatment. She returned to Australia in July 1991 and thereafter has been treated by Dr Perriment in Wangaratta. Dr Perriment has prescribed medication and later referred her to Dr Bolitho, a consultant physician in Wangaratta.
Mrs Mansfied said that she can recall occasions where her heart was "pounding" and on occasions that sensation was accompanied by chest pain. Dr Bolitho arranged a number of tests where she became short of breath and was also prescribed medication. On one occasion, he arranged for Mrs Mansfield to wear a Holter monitor, which recorded cardiac rhythm for a 24 hour period. She understood the analysis of that 24 hour period showed her heart to have steady rhythm on occasions and on other occasions to be in extreme of rhythm.
In cross-examination, Mrs Mansfield was referred to a number of entries within the T documents and medical records of Dr Bolitho, Dr Perriment, Dr Rosenbaum and Professor Myers. It was put to Mrs Mansfield that the histories taken by the doctors did not reveal any complaint of chest pain. Mrs Mansfield said that she has not ever used the word "pain" when describing her symptoms because she understood that word to mean "acute". She said that she would have described the sensation in her chest as being "tightness" or "discomfort". She said the pain was not "acute" and on a scale of 1-5 she would rate it (the pain) at 2. She also noted that the doctors had used the word "vague" when referring to her chest discomfort, but she said that was a word used by the doctors and not a word used by her.
Mrs Mansfield agreed that so far as she is aware, she had not ever been prescribed medication for cardiac disease and the medication that had been prescribed was only with respect to the abnormal rhythm of her heart.
When the hearing resumed in Melbourne, Mr DeMarchi appeared on behalf of Mrs Mansfield. Mr Douglas again appeared on behalf of the respondent.
Kenneth Arthur Myers
Professor Myers is the clinical Associate Professor of surgery at Monash University and is a consultant general surgeon at the Epworth and Monash Medical Centres. He has practised as a vascular surgeon since 1967 and provided a report to the applicant's solicitors dated 11 October 2001, following a consultation with Mrs Mansfield on 28 September 2001.
In his report Professor Myers concluded:
"I believe that any such past atrial fibrillation would be a marker of underlying coronary artery disease causing myocardial ischaemia. This would be by far and away the most common cause of the condition at her age".
In evidence, Professor Myers said that on the history taken by him, atrial fibrillation had occurred in the past, but did not exist at the present time. He assumed that it had "reverted" by reason of medical treatment and he regarded this as being a "not uncommon" occurrence. He said that a patient going into "atrial fibrillation and out of atrial fibrillation" was an indicator of the extent of heart muscle "damage". He thought that persons of the age of Mrs Mansfield would exhibit "varying manifestations" of coronary disease, that may or may not precipitate a myocardial infarction or heart failure. He said it was impossible to determine the cause of the fluctuation or the degree of atrial fibrillation, but said that it was probably because of lack of circulation. It was his opinion that the most likely cause of atrial fibrillation in the case of Mrs Mansfield was coronary artery disease. He thought that she had classic risk factors by reason of previously being a smoker of cigarettes and by reason of her age. He said that if it was "accepted," that coronary heart disease was the "cause" of atrial fibrillation, it then would have been present for many years (transcript page 4).
Professor Myers disagreed with parts of the report of Dr Hammond, a medico-legal consultant, who was engaged by the respondent. In his report, Dr Hammond concluded that exercise stress tests did not evidence myocardial ischaemia. He then concluded that myocardial ischaemia would not be the cause of atrial fibrillation. Professor Myers said that the result of a stress test does not "exclude more subtle degrees of myocardial ischaemia" from coronary heart disease. Additionally, Professor Myers understood that Dr Hammond reported that there were other alternative causes for atrial fibrillation, namely mitral valve disease, toxicosis or idiopathic causes. Professor Myers understood that Dr Hammond was reporting that these factors may have been a cause of atrial fibrillation to the exclusion of ischaemic heart disease. Professor Myers said that in his opinion, the reverse was the true position namely, the most likely cause of the applicant's atrial fibrillation was ischaemic heart disease.
In cross-examination, Professor Myers was asked to consider the definition of "cardiac disease" as it appears in Statement of Principle No 10 of 1996. That definition reads:
"`cardiac disease' means any disease affecting the function and structure of the epicardium, myocardium or endocardium including myocardial infarction, cardiomyopathy from any cause, cardiac valvular lesions or acute trauma to the myocardium."
Professor Myers said that he did not locate any indication from the records of the treating doctors that Mrs Mansfield had suffered cardiac disease within the meaning of the above definition, save that the presence of atrial fibrillation was an indicator of the pre-existence of cardiac disease.
The following passage from the transcript records the position on this issue taken by Professor Myers:
"Do you have any - were you able to find any test results to indicate that Ms Mansfield had suffered any cardiac disease within that definition? --No, no. No. Myocardial infarction is a term - no, this is the simplistic nature of the statement of principles, obviously. That myocardial infarction means that an area of the myocardium has been damaged. Or frequently, the endocardium as well. Now, that may be massive, it may be minor, it may be clinically apparent, it may not. It may be seen on an ECG. It may become apparent as atrial fibrillation.
So, were you able to find any reference in the clinical material that suggested that that damage had taken place? ---Yes. The development of atrial fibrillation.
So, in effect, you are arguing backwards. You are saying the atrial fibrillation is evidence of cardiac damage, and therefore, the cardiac - - - ? ---How else can you argue it?
Well, did you find any evidence, any test results, any clinical evidence, that, in this case, Ms Mansfield had suffered from a myocardial infarction? ---Yes. I repeat myself. The presence of atrial fibrillation.
In terms of the definition of ischaemic heart disease, again, I take it, as you probably would be aware, ischaemic heart disease is defined and a number of - has a number of elements to it. One of them is myocardial infarction, old or new? --Mm.
So, I take it you had no verification other than the presence of atrial fibrillation that - - - ? --- That is correct.
All right. Similarly, with arrhythmia with ECG evidence of myocardial ischaemia. There is none present - - - ?---Well, you see, you could argue that atrial fibrillation is ECG evidence of myocardial ischaemia. That is the basis of my argument.
Would it surprise you that in 10 years of clinical notes compiled by Dr Bolitho, the suggestion of ischaemic heart disease has never arisen once? ---I don't think he has to. He has got a diagnosis of atrial fibrillation. It is not going to influence his management as to how he determines that that arises. I mean, there is a specific regime of management for atrial fibrillation, whatever its cause. In this case, from myocardial damage."
Professor Myers said that it appears the questions being asked of him confused clinical presentation with pathology. He agreed that there was "no clear cut evidence" of myocardial infarct causing severe chest pain, angina or intermittent chest pain. He said that it might be argued that in the absence of those symptoms there was also an absence of myocardial ischaemia. However, because Mrs Mansfield, in his view, had a consistent history of atrial fibrillation, it followed, in his view, that coronary artery disease did exist and was the "most likely cause" of atrial fibrillation. He acknowledged that there was no material which pointed to myocardial ischaemia, but said that the "presence of atrial fibrillation … would satisfy the Statement of Principles".
When reminded that from the clinical data before the Tribunal, Mrs Mansfield had completed four ECG's, one stress test and one echo cardiogram all demonstrating negative results, Dr Myers said "so what". He said the value diagnostically of tests of this type is that a "positive" finding might be demonstrated. He said that a negative finding "cannot tell you that something is not there". When it was put to him that he was arguing "by reverse logic", that the presence of atrial fibrillation indicated the presence of myocardial ischaemia, Dr Myers said that he was adopting "reasonable logic" and said, on the probabilities that atrial fibrillation did exist by reason of the presence of myocardial ischaemia.
Maurice Rosenbaum
Dr Rosenbaum is a cardiologist having practised in that field for approximately 30 years. He examined Mrs Mansfied on 30 March 1999, initially for an advocate who appeared on behalf of Mrs Mansfield at the VRB. A report arising out of that consultation was dated 6 April 1999. Subsequently, he has provided two further reports for the applicant's solicitors, dated 28 September 2001 and 15 October 2001.
In his first report, Dr Rosenbaum found that the applicant did suffer from atrial fibrillation. He found also that the applicant did suffer coronary artery disease by reason of prior cigarette consumption. He found that the "major cause of the irregular heart (atrial fibrillation) is the presence of coronary heart disease". In his report of 28 September 2001, he found that atrial fibrillation was intermittent and "presumed due to coronary heart disease". His third report concerned the outcome of an echo cardiogram which he performed on 10 October 2001. He found that the applicant was not in atrial fibrillation at that time and relied on the opinions expressed in his earlier reports.
In evidence, Dr Rosenbaum adopted the conclusions in his report of 6 April 1999 and said the relevant Statement of Principles were met.
Dr Rosenbaum was confident of the diagnosis of atrial fibrillation because the symptoms described by Mrs Mansfield were consistent with that diagnosis. Additionally, the ECG results contained within the file of Dr Bolitho confirmed the diagnosis.
Dr Rosenbaum said that the arrhythmia (atrial fibrillation) was demonstrated upon the ECG, indicating (to him) the presence of myocardial ischaemia. It followed, he said, that the definition of "ischaemic heart disease" as found in the Statement of Principles was satisfied. Additionally, he said that the definition of "cardiac disease" as defined within the atrial fibrillation Statement of Principles was also satisfied.
In cross-examination, Dr Rosenbaum said that the presence of arrhythmia with the ECG evidence of myocardial ischaemia was determined by the presence itself of an arrhythmia and secondly, by non-specific changes evident by the electro cardiogram.
When he was asked to consider that a diagnosis of myocardial ischaemia and/or ischaemic heart disease had not ever been made by the doctors who had treated Mrs Mansfield, Dr Rosenbaum said that it need not have been made and its presence had no influence on treatment. He said the presence of ischaemic heart disease was relevant only to satisfaction of the Statement of Principles and was not relevant to the treatment of atrial fibrillation.
Dr Rosenbaum was then asked to comment on a number of ECG reports, commencing with the report found at page 23 of the notes of Dr Bolitho. The ECG was conducted during a stress test and is reported as "negative exercise test". Dr Rosenbaum said that the report does not support, but does not exclude, the presence of ischaemic heart disease. He said on the balance of probabilities he maintained his opinion that the condition existed. He said the report of an ECT of December 1997 completed whilst wearing a Holter monitor was not directed towards ischaemic changes. An echo cardiogram performed on 28 July 1999 showed a mild enlarged left atrium, which he said was a probable indication of the presence of ischaemic heart disease.
In re-examination, Dr Rosenbaum said that ischaemic heart disease was a slow progressive disease which would have been well and truly established before the diagnosis of atrial fibrillation in 1991. He said the presence of an enlargement of the left atrium and ECT evidence of myocardial ischaemia, in combination, confirmed his opinion that on the probabilities that ischaemic heart disease has been and continues to be present.
Jeremy Hammond
Dr Hammond is a cardiologist who examined Mrs Mansfield at the request of the respondent on 5 September 2001. He provided a report dated 30 October 2001.
In his report, Dr Hammond noted that the applicant has suffered intermittent atrial fibrillation since 1991. He noted that an exercise stress test in 1991 did not indicate evidence of myocardial ischaemia at that time and subsequently she had not suffered any symptoms, which he regarded as "being convincing symptoms of myocardial ischaemia". Dr Hammond noted that there was no evidence in the applicant of impaired left ventricular function nor any evidence of segmental systolic dysfunction and no evidence of any previous myocardial infarction.

Whilst recognising that coronary arthroscelrosis and the development of ischaemic heart disease is recognised as a mechanism causing atrial fibrillation, he reported that there were many other causes. He noted sinus node dysfunction is recognised as a major cause of atrial fibrillation in persons over the age of 50, and particularly is understood to be the basis for atrial fibrillation where no other cause can be identified.
Having been asked to consider the definition of "cardiac disease" within the Statement of Principles, Dr Hammond reported that there was no evidence of old or new myocardial infarction on ECG or echo cardiography, there was no evidence of angina, an exercise test in 1991 was negative for myocardial ischaemic and whilst there was evidence on an ECG of arrhythmia, there was no evidence, then, of myocardial ischaemia. He concluded that there was no evidence of myocardial ischaemia being present.
On the balance of probabilities, he concluded "I do not find there is enough evidence to relate the onset of atrial fibrillation in 1991 in Mrs Mansfield to the claimed conditions of coronary arthroscelrosis and ischaemic heart disease". Additionally, he reported, "although coronary arthroscelrosis is one of the possible causes of atrial fibrillation in Mrs Mansfield's case in particular noting her age at the time of onset of atrial fibrillation alternative likely explanations for the onset of atrial fibrillation do exist".
In evidence, Dr Hammond disagreed with the opinion expressed earlier by Professor Myers that the presence of atrial fibrillation of itself indicated the presence of an underlying ischaemic disease. He said there were many causes for atrial fibrillation comprising sinus node dysfunction, rheumatic heart disease, mitral stenosis, hypertension, diabetes or raised cholesterol. He said that atrial fibrillation would be unlikely to be the only manifestation of ischaemic disease because ischaemic disease, as a pre cursor to atrial fibrillation, acts in combination with myocardial infarction or cardiac failure. Additionally, ischaemic heart disease would occur in combination with inflammatory conditions of the heart, rheumatoid arthritis, auto immune diseases, thyrotoxicosis and tachycardia.
With respect to an opinion expressed by Dr Rosenbaum, who detected an enlargement of the left atrium attributable to coronary artery disease precipitating atrial fibrillation, Dr Hammond thought that both clinical features were not necessarily significant. He said that an enlargement of the left atrium is a common finding in persons of the age group of Mrs Mansfield and he would not attribute it to ischaemic heart disease alone and/or in the absence of prior myocardial infarction.
With respect to an opinion expressed by Dr Rosenbaum, that an ECG of 6 April 1999 demonstrated minor non-specific changes which satisfied part of the ischaemic heart disease definition of ECG evidence of myocardial ischaemia, Dr Hammond thought that the printed report of the echo cardiogram as performed by Dr Rosenbaum was of "extremely poor quality". He said it was impossible to interpret any changes with any certainty.
Dr Hammond was impressed by the clinical data obtained by Dr Bolitho who in 1991 performed a number of tests. He observed from the findings obtained by Dr Bolitho that there was no evidence of myocardial ischaemia. He acknowledged that an exercise stress test does have limitations, sometimes referred to as a "false negative test", however any such uncertainty would be in the range of 5 to 10 percent of patients. On balance, he was satisfied there was no evidence of myocardial ischaemia then present.
When he reviewed clinical data of Dr Bolitho contained in his report of 1999, (refer T documents page 78) and the results of an echo cardiogram conducted by Dr Rosenbaum conducted in October 2001, Dr Hammond noted a consistency in the findings, namely the absence of any abnormality of the left ventricle and a consistency in the findings of the function of the left ventricle and wall thickness. He said these features were also indicative of the absence of ischaemic heart disease.
Dr Hammond also disagreed with an opinion expressed by Dr Rosenbaum, that an enlargement of left atrium was evidence of ischaemic cardiomyopathy being an indicator of ischaemic heart disease. Dr Hammond said for this proposition to be sound there would need to be evidence of a decrease in left ventricular function of a significant degree, which was not present in the case of Mrs Mansfield.
As to the evidence of Professor Myers, that the applicant may have suffered a myocardial infarction which would be "very minor" yet not be detected on clinical tests, Dr Hammond thought that this was a possibility, but not probable. He thought on balance the degeneration of the sino-atrial node was the most likely cause of the atrial fibrillation suffered by the applicant.
As to the non-specific changes reported by Dr Rosenbaum in an ECG that he performed, Dr Hammond said those features could have occurred by reason of medication then being consumed. He said the changes were of no diagnostic significance and from an ECG that he performed, there were no non-specific changes present at all.
With respect to opinions expressed by Professor Myers and Dr Rosenbaum that the presence of ischaemic heart disease was not clinically relevant to the treatment of atrial fibrillation and therefore not reported by Dr Bolitho, Dr Hammond said that Dr Bolitho was a well recognised cardiac specialist practising in Wangaratta, who is "universally agreed by everyone who knows him" as practising to a high level. He said that Dr Bolitho would have investigated the possibility of ischaemic heart disease being present and he would have thought Dr Bolitho regarded those investigations as being important. This was because of the history that he obtained of Mrs Mansfield having chest pain and by reason of her age. He said the clinical file of Dr Bolitho indicated that investigations were undertaken to determine whether ischaemic heart disease was present.
In cross-examination, Dr Hammond agreed with Mr DeMarchi that if an angiogram was performed it was likely that coronary arthrosclerosis would be present. However, he said ischaemic heart disease is different to coronary arthrosclerosis because the former condition describes a depletion or starving of blood flow to the heart, whereas coronary arthrosclerosis is a description of the presence of plaque which might progress to a state that may then be described as ischaemic heart disease. He, therefore, agreed with an opinion expressed by Dr Rosenbaum that coronary arthrosclerosis is likely to be present should an angiogram be performed. However, it would need to be determined whether the presence of coronary arthrosclerosis is causing any functional effect upon the coronary arteries to permit a diagnosis of myocardial ischaemia.
As to the ECG performed by Dr Rosenbaum which he reported as demonstrating non-specific changes, Dr Hammond said that it was a "possibility" that the changes could be explained by the presence of ischaemia.
In re-examination, Dr Hammond was taken by Mr Douglass to the atrial fibrillation Statement of Principle. The witness agreed that the applicant did suffer from atrial fibrillation, but he was firm in his opinion that she did not suffer from cardiac disease at the time of clinical onset of atrial fibrillation. He said "if you want to say is there evidence of other disease present, myocardial infarction, myocardial ischaemia, cardiomyopathy, my opinion is that there is no evidence of disease of that type or evidence of any other cardiac disease at the time of onset of atrial fibrillation".
Dr Hammond acknowledged that there was a likelihood of the applicant, having smoked cigarettes for 40 years and by reason of her age, suffering from a cardiac disease, however in the absence of clinical data, the absence of chest pain on exertion and in the absence of a positive stress test he regarded the presence of cardiac disease as a "low probability". He acknowledged that before any investigations were undertaken there would be a "significant possibility" of the presence of ischaemic heart disease, however subsequent clinical tests and the data produced indicate - to him - that on the balance of probabilities cardiac disease is not and has not been present.
Conclusion and Reasons for Decision
By reason of the applicant's service being entirely within Australia, her rights are to be determined upon the balance of probabilities.
Additionally, the connection between service and injury has required examination of two Statements of Principles. By reason of the introduction of Statements of Principles into the regime of veterans' entitlements from 1994, the exercise of determining the rights of Mrs Mansfield has been necessarily complicated and, I doubt, intended. I agree with the sentiments expressed by Mr DeMarchi in his closing submissions, that were it not for Statements of Principles, the review would have been less onerous, because it would simply have involved an examination of whether on the balance of probabilities a connection existed between cigarette smoking and atrial fibrillation. The presence of Statement of Principles has imposed a much broader inquiry necessitating evidence being given by three prominent and able medical practitioners (which was also not intended by the introduction of Statement of Principles).
The case advanced by Mrs Mansfield was that by reason of her service, she developed a smoking habit which satisfied the ischaemic heart disease Statement of Principles as to quantity and duration. However, in order to satisfy the atrial fibrillation Statement of Principles, Mrs Mansfield needed to establish that she suffered cardiac disease.
There was no controversy that the clinical onset of atrial fibrillation was in 1991, when Mrs Mansfield presented to Dr Bolitho.
Ischaemic heart disease, is a "cardiac disease" as defined in the atrial fibrillation Statement of Principle. The issue that evolved by these proceedings was whether at the time of clinical onset, Mrs Mansfield suffered from cardiac disease. If she did, there must be a finding on the balance of probabilities that atrial fibrillation was connected with service.
Professor Myers agreed in part with Dr Hammond that there were potentially many causes for atrial fibrillation, however on balance, I thought that the evidence of Professor Myers was not credible and was speculative. In effect, it was his position that atrial fibrillation is explained by myocardial ischaemia, yet he acknowledged that there was no clinical data which pointed to the existence or presence of myocardial ischaemia. Additionally, it was his opinion that the atrial fibrillation suffered by Mrs Mansfield could be explained by a pre-existing myocardial infarction, thereby satisfying the definition of ischaemic heart disease within the applicable Instruments. However, there was no evidence that an infarct had ever occurred. The evidence of Professor Myers, no doubt well intentioned, did not approach or resemble a standard of credibility sufficient to permit any finding of the balance of probabilities that cardiac disease existed at clinical onset.
Dr Rosenbaum was of the opinion that the applicant satisfied the definition of ischaemic heart disease, because he found evidence of arrhythmia with ECG evidence of myocardial ischaemia. It was not in dispute that the arrhythmia was in fact the atrial fibrillation, however the evidence of myocardial ischaemia, according to Dr Rosenbaum, was the presence of non-specific changes in an ECG which he conducted. I was also unimpressed by the evidence of Dr Rosenbaum. He justified an opinion of the existence of ischaemic heart disease because an ECG report, whilst not confirming the presence of the disease, did not exclude it. It is inconceivable that this opinion demonstrates the presence at clinical onset of ischaemic heart disease, on the balance of probabilities.
Dr Hammond thought that that ECG was of poor quality and subject to interpretation. Additionally, it was his opinion that the non-specific changes could be explained by the medication being prescribed for Mrs Mansfield. He was not of the opinion that the non-specific changes amounted to evidence of myocardial ischaemic, as was the opinion of Dr Rosenbaum. Additionally, an ECG conducted by Dr Hammond did not demonstrate non-specific changes.
With respect to the definition of "ischaemic heart disease" (para 6) there was no evidence that the applicant suffered angina, nor cardiac failure. For the reasons given above, I am not satisfied Mrs Mansfield has ever suffered a myocardial infarction. It was suggested that by the absence of Dr Bolitho recording a finding of ischaemic heart disease, that its presence could not be excluded because it was relevant only to satisfy the Statement of Principle and not by way of treatment. I thought that proposition was novel and probably is insulting the professional competence of Dr Bolitho. Whilst he did not give evidence in these proceedings, he is well known as a competent cardiac physician in north-eastern Victoria and it is inconceivable – as was the opinion of Dr Hammond – that he would not have investigated the possibility of the applicant having suffered from ischaemic heart disease. This would have been consistent of course with his duty as a competent cardiac physician. Dr Hammond was satisfied – having observed Dr Bolitho's file – that he had in fact investigated ischaemic heart disease, but determined that it did not exist. To complete the analysis therefore of the ischaemic heart disease definition, there is evidence of arrhythmia but no satisfactory evidence of the presence of myocardial ischaemia on ECG, on the balance of probabilities.
I thought the evidence of Dr Hammond was sound, balanced and well reasoned. Indeed, it appeared from his evidence that he was attempting to find a basis to recommend to the respondent that liability be found in favour of Mrs Mansfield (refer transcript page 47). This would be consistent with the beneficial interpretation to be given to the Veterans' Entitlements Act in its application to veterans. Nonetheless, he could not find from any clinical data that ischaemic heart disease was present. He agreed that should an angiogram be performed that coronary arthrosclerosis would probably be present, but this he said is a different clinical finding to that of ischaemic heart disease.
Dr Hammond acknowledged that ischaemic heart disease might be a cause of atrial fibrillation, but he identified many other potential causes. On balance, it was his opinion that atrial fibrillation can be explained by the degeneration of the sino atrial node. It followed that he was in disagreement with an opinion expressed by Dr Rosenbaum, that the major cause of the atrial fibrillation was the presence of coronary artery disease.
On balance, the evidence of Dr Hammond is sound and is to be preferred. The cause of the atrial fibrillation is not, on the balance of probabilities, "ischaemic heart disease" being "cardiac disease". For the reasons given above, I am not satisfied that Mrs Mansfield does suffer from that disease.
It follows, that by reason of being unable to establish on the balance of probabilities that cardiac disease did or continues to exist, that I cannot find on the probabilities that Mrs Mansfield suffered from cardiac disease at the time of the clinical onset of atrial fibrillation.
In the circumstances, I cannot find, on the balance of probabilities that factor 5(a) "exists".
The decision under review must, in the circumstances, be affirmed.
I certify that the 66 preceding paragraphs are a true copy of the reasons for the decision herein of Mr J. Handley, Senior Member.
Signed:         .....................................................................................
  Secretary
Date/s of Hearing  29 January 2002, 12 April 2002
Date of Decision  1 November 2002
Counsel for the Applicant        Mr D. DeMarchi
Solicitor for the Applicant
Counsel for the Respondent    Mr R. Douglass
Solicitor for the Respondent