Multifactorial causation of stroke in Australia: a comparison
Daniel James Dascombe BPharm* |

*Medical Student, The Australian National University

Abstract

Stroke is a major source of morbidity and mortality globally. In Australia, stroke was projected to be the fifth leading contributor to the overall burden of disease in 2010, with a prevalence of 1.7% in females and 1.8% in males. However, there are undeniable disparities in the distribution of this burden. Australia’s Indigenous population experiences stroke prevalence twice that of the non-Indigenous population, with a corresponding discrepancy in overall burden of disease. There has been a steady decline in the prevalence of all cardiovascular disease, including stroke, over the last four decades but targeted measures are required to address these inequalities. Stroke causation is multifactorial; a complex interaction of broad community-based and specific biomedical and behavioural risk factors. In the Indigenous population, socioeconomic, environmental and psychological factors are especially pertinent to stroke causation. This report discusses these risk factors in the context of a proximal to distal causal pathway.

Introduction

S

troke is a significant contributor to the global disease burden; it is second only to coronary heart disease as a cause of death and is a major source of disability (1). In the Australian community there are an estimated 350,000 people living with the deleterious effects of stroke, with 11,220 deaths attributed to it in 2009 (2). Stroke can be broadly defined as an acute loss of brain function resulting from a disturbance in blood supply (3). There are two distinct disease processes implicated in this definition; ischaemic stroke results from the blockage of a blood vessel supplying the brain whilst haemorrhagic stroke results from the rupture and subsequent bleeding of a blood vessel (3). Ischaemic stroke represents approximately 80% of cases (3,4).

Compounding the burden of stroke mortality, this direct effect on the central nervous system leads to a wide spectrum of disability in stroke survivors, with rehabilitation representing a major cost to the healthcare system (5). Causation of stroke is complex and multifactorial, with independent risk factors largely common to coronary heart disease as well (2,4) adding to the importance of identification and management of these factors. 

Pattern of disease

In 2003, according to the Survey of Disability, Ageing and Carers (SDAC), approximately 346,700 Australians had suffered a stroke during their lifetime, corresponding to a prevalence of 1.7% for females and 1.8% for males (2,6). However prevalence increased significantly with age, with a concurrent increase in disparity between sexes: in the 65-74 years age group 8.1% of men and 5.3% of women had experienced a stroke (6). An analysis of data from the NEMESIS study by Thrift et al. (7) reflects these trends, showing the median age of patients having a stroke to be 75 years, with males tending to be affected at slightly younger ages than females.

The age-standardised rate of hospitalisation for stroke declined 12% in the period 1998-99 to 2007-08 to a rate of 176 per 100,000 for males and 131 per 100,000 in females (6). Similarly information from the Australian Institute of Health and Welfare (AIHW) (2,6) shows, in broad terms, a steady decline in age-standardised stroke mortality rates over the last four decades punctuated by an acceleration in the rate of decline over the period 1997-2006, as illustrated in figure 1. These declines have been greatest in ischaemic stroke with an average rate of approximately 8% per year, compared to 2% per year in haemorrhagic stroke (2).

Stroke death rates by sex, 1987-2007. Sourced from AIHW (6, p. 81.)

In Australia, stroke disproportionately affects disadvantaged sections of the community, representing a major challenge for health authorities. According to the 2007-08 National Health Survey (NHS), “those in the lowest socioeconomic group are 1.8 times as likely to have had a stroke as those in the highest.” (6). This trend is magnified in Indigenous Australians. The AIHW reports that overall stroke prevalence is almost twice as high in Indigenous Australians compared to their non-Indigenous counterparts (4,6). Furthermore Katzenellenbogen et al., in a study conducted in Western Australia, reported that the incidence rate of stroke was 2.6-fold greater in Indigenous men and 3.0-fold greater in Indigenous women compared to the non-Indigenous population (8). 

Burden of disease

According to the AIHW stroke was projected to be the fifth leading cause of burden of disease in 2010, contributing 117,000 disability adjusted life years (DALYs), 4.1% of the total national burden of disease (4). The findings of Cadilhac et al. (5) expand on this, showing that haemorrhagic stroke was associated with greater loss of health compared to ischaemic, largely due to a greater case fatality rate at a younger age. In 2003, 75% of the stroke burden for females and 68% of the male burden was due to years of life lost prematurely (4, 6), therefore it can be inferred that despite being much less common than ischaemic events, haemorrhagic events contribute more to the overall stroke disease burden.

Raw mortality data emphasises this burden. In 2007, stroke claimed 8,623 lives, 6% of all deaths, while the 12 month mortality rate for patients experiencing their first ever stroke was one in three (2). It is projected however that over the next decade the burden of disease attributable to stroke will decline in line with continuing declines in mortality (4). This can be linked to better management of risk factors such as tobacco smoking and blood pressure (4). 

In keeping with the previously identified pattern of disease in the Indigenous population, the burden of stroke is similarly more pronounced in this group. According to Katzenellengogen et al. (8), Indigenous age-standardized DALY rates were approximately three times higher for both sexes when compared to non-Indigenous rates. Compounding this, they also found that over 60% of the nonfatal stroke burden in the Indigenous population occurred in the 15-54 year age group, compared to 24% in the same non-Indigenous population (8). This implies that Indigenous people are more likely to experience a stroke at a younger age, highlighting the health gap that currently exists in Australia.

Identification of Risk factors

Causation of stroke is complex; an interaction between risk factors, both modifiable and non-modifiable, across a wide spectrum from individual behavioural and biomedical factors to broader community-based socioeconomic factors (1,3,9). A number of risk factors, such as hypertension and tobacco smoking, have traditionally been considered synonymous with disease of the cardiovascular system however the INTERSTROKE study (1) has sought to identify and quantify the contribution of specific factors across 22 countries. Initial findings of the study suggest that ten modifiable risk factors are associated with 90% of the risk of stroke (1), highlighting the immense potential for targeted stroke prevention measures. These findings are summarised in table 1.

Stroke death rates by sex, 1987-2007. Sourced from AIHW (6, p. 81.)
Table 1. All stroke risk factors and population attributable risk as identified in phase 1 of the INTERSTROKE study. Adapted from O’Donnell et al. (1).

As can be seen in table 1, hypertension is the greatest contributor to stroke risk whilst the top five risk factors; hypertension, current smoker, abdominal obesity, diet and physical activity, constitute approximately 80% of the global risk for both stroke aetiologies (1). There are small, but significant, differences evident in these findings between ischaemic haemorrhagic events; for example, hypertension is a more potent risk factor for haemorrhagic than ischaemic stroke, with a reported population attributable risk (PAR) of 73.6% and 45.2% respectively, whilst increased alcohol intake showed a much larger correlation with haemorrhagic also (1). Atrial fibrillation (AF) is the predominant cardiac cause of stroke, with various studies estimating the increased risk of stroke in people with AF to be between two-and-seven fold (1,10). Increased psychosocial stress and depression were also associated with an increased stroke risk (1).

As has already been shown in pattern of disease a number of non-modifiable risk factors are clearly implicated in stroke causation. Increased age and male sex are both associated with increased risk (1,6).  Further to this there is strong evidence for a genetic basis to stroke in certain members of the population; data from the Framingham study shows that a parental history of stroke before the age of 65 increases the risk of stroke in offspring 2.79-fold (11).

Multifactorial model of stroke causation

Development of any model for stroke causation must consider the aforementioned biomedical and behavioural risk factors in the context of the overarching environmental and social influences applicable to different sections of the community (1,9). Whilst not directly implicated in stroke causation, these more distal factors influence prevalence of proximal risk factors. The AIHW (6) reports that stroke death rates in 2007 were highest for those in the lowest socioeconomic groups. This is supported by Heeley et al. (12) who found a higher prevalence of risk factors such as hypertension and smoking among those in the most deprived socioeconomic group, whilst those in this group were also more likely to be blue collar workers or unemployed, implying an association with level of education. Similarly environmental factors such as community remoteness and living conditions can influence a person’s ongoing access to healthcare (9). Thrift et al. (9) contend that the rate of stroke in Aboriginal people may in fact be underestimated in epidemiological studies because distance may impede hospital attendance in remote communities, potentially resulting in nonattendance for relatively minor events and thus underreporting of stroke.

Stroke death rates by sex, 1987-2007. Sourced from AIHW (6, p. 81.)
Figure 2. Multifactorial model for causation of stroke, showing distally to proximally socioeconomic and environmental factors, health behaviours, biomedical and genetic factors, as well as accounting for overarching non-modifiable and psychological factors. Adapted from AIHW (4, p. 65)

The multifactorial model in figure 2 presents a proximal to distal causal pathway, showing schematic links between different factors. Whilst proximal factors such as smoking and hypertension are inextricably linked to stroke pathology, a holistic perspective shows the fundamental path between distal and proximal factors; for example a person with a lower level of education is more inclined to be of a lower socioeconomic status, and thus more likely to smoke tobacco and have hypertension. Additional complexity arises from the multiplicative effect of certain risk factors in combination with others; for example abdominal obesity increases the risk of diabetes (13), and both are significant risk factors for stroke. The global impact of a person’s psychological wellbeing is also considered. This model of causation not only incorporates the stroke risk factors identified, but highlights the multifaceted nature of the stroke causal pathway, and the different levels at which disease prevention measures can be targeted.

Differences between Indigenous and non-Indigenous populations

Disparities in the burden of stroke between Australia’s Indigenous and non-Indigenous populations are predictably paralleled by disparities in risk factor prevalence at all points in the causal pathway. In terms of health behaviours the AIHW in collaboration with the Australian Bureau of Statistics (ABS) (14) reports that 45% of Indigenous people over the age of 15 are current daily smokers compared to 17% in the non-Indigenous population. Furthermore Vos et al. (15) report that tobacco smoking is the largest contributor to the overall Indigenous burden of disease and well documented health gap. Given the proximity of smoking to development of stroke, these statistics are clearly significant in explaining the gap in stroke burden. In terms of biomedical factors, the prevalence of diabetes in Indigenous Australians is approximately three times that in non-Indigenous (14), obviously contributing to increased stroke risk, whilst hypertension is slightly more prevalent also (14).

Stroke death rates by sex, 1987-2007. Sourced from AIHW (6, p. 81.)
Table 2. Health risk factors by selected socioeconomic indicators, Aboriginal and Torres Strait Islander people aged 15 years and over. Sourced from AIHW (14).

In seeking to explain the excess risk of stroke in Indigenous Australians Thrift et al. (9) cited more distal factors, including socioeconomic and educational disadvantage, and psychological factors. Education level is central to health literacy and socioeconomic status, and in 2008 the year 12 retention rate for Indigenous students was 47%, well below the national average of 75% (14). Table 2 lists some key risk factors in the context of key socioeconomic indicators in the Indigenous population. This table illustrates the effect of distal factors, employment and educational status, on proximal factors in the Indigenous population, confirming the link established in the multifactorial model.

The downstream effects of low socioeconomic status on stroke causation are clearly varied; however the AIHW (14) also reports a correlation with poor diet and low levels of exercise. Similarly the reported rate for episodes of high or very high levels of psychological distress in Indigenous adults was 32%, twice that of the non-Indigenous population (14). As well as being an independent risk factor for stroke, psychological stress is also linked with other factors, especially smoking and risky alcohol consumption (14). This again emphasises the significance of the interaction between factors, whilst undeniably implicating psychological factors in Indigenous stroke risk. Environmental factors also contribute to the gap; 20% of Indigenous households report that they cannot access emergency services, whilst in remote areas only 69% reported access to medical/health clinics (14). This not only has a severe impact on the capacity to seek acute medical treatment, but presents a barrier to the ongoing management of chronic conditions that contribute to stroke risk.

Conclusion

The risk factors for stroke are the same in Australia’s Indigenous and non-Indigenous populations, however the burden of stroke is not shouldered equally. This is symptomatic of a society in which Indigenous people continue to experience considerably worse health, social and economic outcomes than their non-Indigenous counterparts (9,15), a situation that has become entrenched since European colonisation over 220 years ago. In addressing this disparity, and in seeking to reduce the burden across the community, recognition of the multifactorial nature of stroke causation is vital. Targeting of the traditional proximal cardiovascular risk factors must continue to be a priority for health professionals involved in primary care; however there is scope for health and social policy to target the distal community-based factors clearly inherent in stroke causation in Australia. Socioeconomic, environmental and psychological factors are particularly pertinent in rectifying the Indigenous health gap. Additionally, in the context of an aging population a holistic approach to stroke prevention is imperative in continuing the declines in morbidity and mortality achieved over the last 40 years.  

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