Epidemiology of Atherosclerotic Vascular Disease

Abstract

Prevention is now recognized as a first-line approach in the management of atherosclerotic cardiovascular disease (CVD), in both the Western World (Lloyd-Jones et al. (Circulation 121:586–613, 2010), Goff et al. (Circulation, 2013a), Perk et al. (Eur Heart J 33:1635–1701, 2012)) and internationally (Sacco et al. (Lancet 382:e4–e5, 2013)). Over the past six decades, epidemiologic investigation, the science most relevant to establishing means of prevention, has identified the major “risk factors” that contribute to the development of atherosclerotic CVD and its components: coronary heart disease, stroke, and peripheral artery disease (Kannel (J Am Coll Cardiol 15:206–211, 1990)). Because the major “risk factors” are modifiable, and their treatment reduces the likelihood of developing vascular disease, risk factor assessment has become an important feature of primary and secondary prevention of CVD.

The major modifiable cardiovascular risk factors with evidence for a strong independent relationship to CVD can be readily ascertained by ordinary office procedures (Kannel (J Am Coll Cardiol 15:206–211, 1990)). Prospective community-based studies like the Framingham Heart Study have documented the relevance of systolic blood pressure, blood lipids, glucose intolerance and adult-onset diabetes mellitus, and cigarette smoking to assess the propensity for a first atherosclerotic CVD event. Using these risk factors, which are common to all major atherosclerotic cardiovascular events, and a number of other predisposing factors specific to stroke and peripheral arterial disease, multivariate risk formulations have been produced for estimating the global risk of events as a function of the burden of coexisting risk factors (Wilson et al. (Circulation 97:1837–1847, 1998), Wolf et al. (Stroke 22:312–318, 1991), Murabito et al. (Circulation 96:44–49, 1997), D’Agostino et al. (Circulation 117:743–753, 2008)). Recent epidemiological research has brought attention to the potential role of newer risk markers measured in circulating blood, high-resolution subclinical vascular disease imaging modalities, and genetic and genomic factors underlying CVD. However, as of yet, there is insufficient evidence to recommend most of these newer measures in clinical practice (Goff et al. (J Am Coll Cardiol, 2013b)).