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However, concern has arisen about sport-related deaths among Indigenous people. In the early 1990s, an Indigenous footballer died during a game in a remote community. Despite subsequent mass screening of players and diagnosis of several cases of occult ischaemic and rheumatic heart disease, another football-related death occurred. The local football league president informed one of us (M C Y) that there was significant concern among the players about heart disease in sport.

In view of this concern and anecdotal reports of sporting deaths in other Indigenous communities, this study aimed:

• To estimate the incidence of sport-related sudden cardiac death related to ischaemic heart disease (IHD) among young Aboriginal sportsmen in the Northern Territory;

• To compare this with the incidence among the general population of sportsmen in Victoria; and

• To identify possible risk factors for myocardial infarction and sudden cardiac death which could provide valuable information for Indigenous sporting competitions.

A young competitive sportsman was defined as a male aged 15-37 years who participated in an organised team or individual sport in which regular competition is a component and in which a premium is placed on achievement.

Secondly, a computer search was undertaken of NT forensic pathology records for the period 1991-1996 to cross-check ABS figures and provide information for 1996. Search terms were "football", "footy", "sport", "exertion", "rugby", "basketball", "athletics", "running" and "swimming".

All deaths were confirmed as being caused by IHD from the autopsy findings. The Aboriginality of the deceased was also determined from the autopsy records, as the NT death registration system has provided for Aboriginal identification only since 1988.

The incidence of sudden cardiac deaths among NT Aboriginal Australian footballers was compared with that of Australian footballers in Victoria. The ABS provided Victorian participation rates for the two-year period July 1995 to June 1997, and the Victorian State Coroners Office provided information on sudden deaths in Australian football in Victoria from a computer search of forensic autopsies from 1990 to 1997 inclusive.

Mean age at death was 29.4 years (range, 21-36 years). All deaths occurred in coastal communities in the Top End of the NT (see Figure) between mid-September and early April (wet season), and all but one occurred in remote Aboriginal communities. Six of the eight deaths were associated with Australian football (which is played only in the wet season in the Top End) and one each was associated with soccer and touch football. All deaths occurred at or after half-time in the game or within an hour of its ending.

Autopsy findings are summarised in the Box. All eight players had evidence of coronary artery disease and four had myocardial abnormalities -- either hypertrophy or old infarcts.

According to the autopsy reports, two of the players had recently developed chest pain: one had been prescribed anti-inflammatory drugs the week before the game, and the other was under medical investigation for exercise-induced chest pain. A third player had experienced epigastric burning and possible chest pain before his death.¹ Four of the men were reported to have drunk large amounts of alcohol (one), kava (one) or both (two) on the evening before the game.

The NT Football Development Foundation reported that 110 Australian rules football teams played in the 1996-1997 season, giving an estimated 2750 players -- 2095 Aboriginal and 655 non-Aboriginal. Of the Aboriginal players, 578 played in an urban competition and 1421 (74%) played in a community league, with a small percentage participating in both. Based on the two methods of estimation, Aboriginal Australian footballers had between 25 050 and 31 425 player-years in the period 1982-1996 (inclusive). From these data, the incidence of sudden cardiac death due to IHD in young NT Aboriginal Australian footballers was 1 per 4175-5240 player-years (19-24 per 100 000 player-years). The incidence of sudden cardiac death in soccer and touch football games could not be calculated because of lack of data about participation in these games in remote communities.

According to the ABS, there were a total of 139 700 player-years in Australian football for males aged over 15 years in Victoria between July 1995 and June 1997. For the period 1990-1997, the Victorian State Coroner reported five sudden deaths in that State among Australian rules footballers aged under 38 years. Three of these deaths were attributed to IHD (mean age, 31.7 years), and the other two to trauma. Based on these data, the incidence of IHD-related sudden cardiac death in Australian football in Victoria was 1 per 186 000 player-years (0.54 per 100 000 player-years).

The estimated incidence of these deaths (19-24 per 100 000 player-years) was two to 12 times the reported total incidence of sudden cardiac death in sport³ (which includes all causes and all ages). It was also around 40 times the incidence of IHD-related sudden cardiac death among young Australian footballers in Victoria. These incidence data do not include sporting deaths due to other causes such as hypertrophic cardiomyopathy and rheumatic fever.

There is clearly some doubt about the precise incidence of these deaths among Aboriginal footballers. Firstly, the number of cases might have been underestimated if deaths were not reported to the Coroner or if relevant cases were missed because files could not be located. Secondly, calculation of the total number of player-years was based on estimated participation rates, and no specific information was available before 1996. However, there can be little doubt that the incidence of IHD-related sudden cardiac death among Australian footballers is very much greater for Aboriginal players in the NT than for players in Victoria.

This high incidence is a reflection of the poor state of Indigenous health in Australia. Generally, death rates among young and middle-aged adults are much higher for Indigenous than non-Indigenous Australians for most causes of death.^4,5 Young Indigenous adults have very high levels of rheumatic fever,⁶ type 2 diabetes mellitus,⁷ and IHD.⁸ After direct standardisation, the rate of sudden death (non-sporting) due to IHD in the NT is 5.5 times higher for Indigenous than non-Indigenous people.⁸ Risk factors for IHD are twice as prevalent among community-based Indigenous footballers than non-Indigenous controls.¹ All the deaths occurred either late in, or within an hour of, a football game played during the wet season in the Top End of the NT, when high humidity may have placed added strain on the exercising heart. This added strain further raises myocardial oxygen consumption, and can increase ischaemia, especially in those with a fixed coronary artery stenosis. This may lead to angina, myocardial infarction or sudden death. The American College of Sports Medicine recommends that consideration be given to cancelling sporting events when the wet bulb globe temperature (WBGT; a measure of heat stress during exercise) is in the extreme range (> 28 degrees C), because of the risk of thermal illness.⁹ The WBGT often exceeds 32 degrees C in mid-afternoon in Darwin, which has led to games often being held at night under floodlights. The stress of heat and humidity on the cardiovascular system during sport may also be reduced by maintaining hydration, improving fitness, changing rules to allow more interchange players and moving games to the dry season.

Four of the players had drunk large amounts of alcohol or kava the evening before the game. Both these drinks have diuretic properties, which may contribute to dehydration and haemoconcentration, thus increasing the cardiovascular stress of exercise. Kava, an intoxicating drink used widely in the South Pacific region, has been imported into northern Australian communities (especially East Arnhem) since the early 1980s, probably as an alcohol substitute.¹⁰ It has sedative, psychotropic, anaesthetic, diuretic and hepatotoxic effects. An NT study found that, while it did not significantly alter blood lipid levels or blood pressure, it significantly raised resting pulse rate.¹⁰ An association between kava use and sudden cardiac death has been suggested previously,^10,11 and is supported by our study. Research is needed urgently to clarify this issue and investigate other possible health consequences of kava usage.

Six of the eight players had generalised coronary abnormalities typical of middle-aged victims of sudden cardiac death.¹² As these abnormalities are likely to be associated with IHD risk factors, prodromal symptoms, an abnormal resting electrocardiogram or a positive exercise stress test, there is scope for prevention through screening. Indeed, four of the players had macroscopic myocardial abnormalities, which would be expected to produce changes on a resting electrocardiogram, and three had a history of chest pain. Pre-participation screening for occult IHD by exercise electrocardiography is usually only recommended for male athletes aged 40 years or older with multiple risk factors or a single, markedly abnormal risk factor.¹³ However, this screening may be warranted in Indigenous players younger than 40 years if they have significant risk factors for IHD.

Exercise is a double-edged sword in IHD: during exercise, risk of myocardial infarction and sudden death is increased, but, in the long-term, exercise reduces the incidence of IHD.¹⁴ Safe exercise should be encouraged among Indigenous people by identifying risk factors for sudden cardiac death. These may include reduced levels of aerobic fitness, smoking, dehydration due to consumption of diuretics such as alcohol and kava or insufficient fluid replacement, and heat and humidity stress. Educational messages for sportsmen can be positive (eg, sporting performance is enhanced, and health is promoted, by reducing smoking, remaining well hydrated and avoiding pre-game diuretic drinks such as alcohol and kava) and should include the advice not to play with recent chest pain until assessed by health staff.¹ Funding is needed for such educational and screening programs for "at risk" sportsmen.

Our study highlights the disturbing incidence of premature IHD in young Indigenous men and its effect on sport. Ultimately, the incidence will be reduced only by culturally appropriate long-term strategies which take a holistic view of this complex problem. In the short and medium term, programs with education of athletes, heat-stress reduction strategies, and cardiovascular screening should reduce the incidence of sudden cardiac death in sport. However, for any intervention to be successful, it is essential that it is initiated, owned and controlled by the communities themselves rather than imposed in a well-meaning fashion from the outside.⁷

Addendum: The results of this research have been of use already to one football league to support applications for funding for mass screening and an education program for footballers, and for a set of floodlights to enable play at night and thus reduce heat and humidity stress.

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Reprints will not be available from the authors.
Correspondence: Dr M C Young, Sports Medicine, Australian Institute of Sport, Leverrier Crescent, Bruce, ACT 2617.
Email: youngmATausport.gov.au

©MJA 1999
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