Socioeconomic status as a determinant of cardiovascular disease

The health and economic burden of cardiovascular disease (CVD) is greater than that of any other disease, and it remains the leading cause of death globally. Socioeconomic inequalities in CVD are apparent in most countries of the world, and it is well-established that people from lower socioeconomic groups have higher rates of premature death and suffer greater morbidity from the disease than do those from higher socioeconomic groups. This association occurs as a gradient that runs across the entire socioeconomic spectrum, so that the lower an individual’s social and economic position, the greater their risk of developing CVD. However, while there is an extensive body of work documenting this gradient, less is known about the mechanisms and pathways by which it occurs. A more complete understanding of these pathways is of paramount importance if we are to intervene effectively to reduce the burden of CVD among lower socioeconomic groups. This thesis aims to explore mechanisms and pathways between socioeconomic status (SES) and CVD and to describe the extent to which health care systems and targeting risk factors for the disease might potentially modify health inequalities. First, epidemiological methods are used to describe and explore pathways using data from two prospective Australian studies, the Melbourne Collaborative Cohort Study (MCCS) and the AusDiab Study. The MCCS is a large study of 41 514 men and women, the majority of whom were aged 40-69 years at baseline (1990-1994). AusDiab is a national population-based study of 11 247 adults enrolled in 1999-2000, with 6 400 participants returning for a 5-year follow up in 2004-2005. Using education level as a SES indicator, analyses are undertaken to firstly describe the socioeconomic gradient in CVD mortality in the MCCS and then quantify how much of this gradient can be explained by traditional risk factors for the disease, particularly smoking. Second, because cigarette smoking and abnormal lipids are known to be the two most important risk factors leading to CVD, an analysis of whether smoking-related changes in lipoprotein subclasses occur independently of other lifestyle risk factors for CVD is also undertaken. Third, the existence of socioeconomic gradients in most major risk factors for CVD is well-established, and using longitudinal data from AusDiab, this thesis explores the onset and development of these gradients over a 5-year time period. Longitudinal cohort studies such as the MCCS offer the ability to follow-up individuals over time, allowing for exploration of the pathways between SES and the development of CVD, and providing evidence for cause and effect relationships. Two methods by which existing cohort studies can be utilised more effectively for health inequalities research are described, including a method for record linkage between the MCCS and a state-wide hospital admissions dataset, and a method for retrospective geocoding of participant baseline addresses in the MCCS. Record linkage provides a means of passive follow-up of lower SES participants who may be more likely to drop out from a longitudinal study, while geocoding allows for use of geographic information systems (GIS) technology. GIS can be used in analysis of the relationships between environmental exposures and subsequent health outcomes, and an example of such analysis is provided using data from the MCCS to describe the association between neighbourhood disadvantage at baseline and subsequent fatal CVD events occurring in the cohort. Finally, this thesis explores interventions to reduce socioeconomic inequalities both in cardiovascular risk factors and in CVD itself. Broad public health measures to reduce risk factors such as smoking may have potential to reach lower socioeconomic groups, and this is illustrated using the example of legislation to reduce the effects of second-hand cigarette smoke. Current ‘best-practice’ recommendations for CVD prevention and treatment are also examined for their potential impact upon the SES-CVD gradient. Findings from this thesis demonstrate that strong SES gradients in fatal CVD and in major risk factors for the disease still exist in contemporary Australian adults. They provide supporting evidence that these gradients in risk factors contribute significantly towards gradients in CVD, and also reinforce that SES is a predictor both of incident CVD and of incident risk factors, and temporally precedes the onset of risk. Individual risk factors of greatest importance include smoking, which among women, may lead to CVD partially through its independent action on lipoproteins. Two methods by which existing cohort studies, clinical registries and other datasets can be adapted for use in health inequalities research are described in detail, thus increasing Australia’s research capacity in this area of vital importance. Finally, this thesis also identified that, despite the greater burden of CVD among lower SES groups, little is known about the impact of best-practice preventive and treatment interventions upon the SES-CVD gradient, or about barriers to their uptake and effectiveness. As such, these best-practice interventions themselves may be contributing to inequalities in CVD These findings have implications for health inequalities research, health policy and clinical practice and contribute significantly towards increasing our understanding of socioeconomic inequalities in CVD.