Inflammation plays a critical role in the development of atherosclerosis as well as the acute onset of thrombotic complications such as myocardial infarction, a leading cause of death. Accumulation of macrophages expressing proteolytic and thrombogenic molecules may promote plaque disruption and thrombus formation. Clinical evidence suggests that hypercholesterolemia is a major coronary risk factor, further supported by pre-clinical observations that hypercholesterolemia induces oxidative stress in the arterial wall, promoting endothelial cell activation and leukocyte invasion. Recent advances in clinical and preclinical vascular medicine have established that lipid-lowering therapy prevents acute coronary complications by limiting inflammation in atheromata. Dyslipidemia and macrophage activation also promote other forms of cardiovascular problems such as metabolic syndrome and calcification. Further understanding of the mechanism for vascular inflammation will provide new insight into atherogenesis as well as preventive cardiovascular medicine. New approaches, including molecular imaging, may identify subclinical inflamed cardiovascular lesions and monitor effects of therapies such as lipid lowering. (154 words)
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