Abstract
Even though coronary artery disease (CAD) event rates have decreased by 50% in the US over the past 30 years, CAD still is #1 killer in both developed and developing world [1]. Moreover, CAD is a complex, multi-factorial disease. It involves multiple pathophysiologic processes including inflammation, cellular proliferation, lipid metabolism, hypertension, hyperglycemia, coagulation, and oxidation, all of which interact and each of which involves multiple genetic and environmental factors. Epidemiologic studies of ethnic minorities in general and South Asian immigrants (SAIs) in particular in developed countries have documented markedly increased rates of CAD and CAD mortality compared to whites [2]. South Asians residing in urban environments in the Indian subcontinent also show increased CAD prevalence [3,4]. Compared to Caucasians and other ethnic groups, CAD presents at younger ages in SAIs, with more diffuse and aggressive disease, and more deaths [5]. Other groups that migrate to developed areas also show increased rates of CAD and CAD mortality but the increases in SAIs exceed them in both prevalence and severity [3]. Differences in CAD outcomes between SAIs in the US and South Asians in India show that migration adversely affects established CAD risk factors and may even reveal new ones [6]. For example, the prevalence of dyslipidemia and type 2 diabetes (T2D) among SAIs has been increasing over the past decade [7].
Highlights
Division of cardiology, Department of Internal Medicine, University of Florida, College of Medicine, Jacksonville, Florida, USA
Epidemiologic studies of ethnic minorities in lowering LDL levels has been the major target in cardiovascular general and South Asian immigrants (SAIs) in particular in developed protection strategies, and clinical trials have clearly established that countries have documented markedly increased rates of coronary artery disease (CAD) and reductions in LDL are associated with a 30-45% reduction in clinical
high density lipoprotein (HDL) protects against CAD via several mechanisms, including its involvement in (a) the reverse cholesterol transport process, (b) protection of LDL from oxidation, and (c) selective reduction of endothelial cell adhesion molecules, which increases the release of nitric oxide (NO) and prostacyclin, and maintains endothelial function Epidemiological studies suggest that a 1 mg/dL increase in HDL is associated with a 2% to 4% reduction in CAD risk [11]
Summary
Among the many factors contributing to excess CAD risk in SAIs, dyslipidemias appear to play major roles. Epidemiologic studies of ethnic minorities in lowering LDL levels has been the major target in cardiovascular general and South Asian immigrants (SAIs) in particular in developed protection strategies, and clinical trials have clearly established that countries have documented markedly increased rates of CAD and reductions in LDL are associated with a 30-45% reduction in clinical
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