Obesity is associated with an increased risk of atherosclerotic coronary heart disease (CHD). This fact combined with the rapid increase in the prevalence of obesity in the United States population threatens to reverse many of the advances made in reducing CHD morbidity and mortality and drives major problems with morbidity, mortality, and health care costs (1). Uncertainty remains as to whether excess weight is independently associated with CHD, or whether the association between obesity and CHD is mediated through other risk factors linked to obesity such as physical inactivity, hypertension, dyslipidemia, and abnormal glucose metabolism. If obesity causes or accelerates atherogenesis, the responsible mechanisms remain largely unknown. Adiposity and obesity may exacerbate the development, progression, and destabilization of atherosclerotic heart disease via direct adverse effects on fat and glucose metabolism. Beyond the metabolic effects associated with obesity, adiposity may also contribute to CHD via inflammatory mechanisms mediated by adipocytokines, especially those mediators associated with visceral fat accumulation. All of these issues establish the need for a greater understanding of the complex biologic and clinical interplay between excess adiposity and cardiovascular disease (CVD).
|Original language||English (US)|
|Title of host publication||Obesity and Cardiovascular Disease|
|Number of pages||22|
|State||Published - Jan 1 2006|
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