Human C-reactive protein (CRP) is an acute phase reactant. Its concentration, in trace amounts (usually 0.2 to 0.8 mg/dl) in normal individuals, can increase to levels of >40 mg/dl in patients with severe inflammation and infection. The function of CRP in inflammatory disease is not known with certainty, although a number of activities have been described. Elevated plasma levels of CRP can be detected as early as 4 to 6 hours after tissue injury, and peak levels are found after 24 to 72-hours. In recent years, CRP has been studied and found an independent predictor of cardiovascular disease (CVD) events, conferring up to a three-fold greater risk of future myocardial infarction in apparently healthy men with high baseline levels of CRP. Additionally, CRP seems to be a risk factor that is independent of other traditional cardiovascular disease risk factors such as smoking and hyperlipidemia. The purpose of this study is to determine the time frame in which CRP is in fact an independent predictor of the risk of future CVD events, this marker of inflammation may ultimately be added to the list of CVD factors commonly used to assess risk in otherwise healthy men. If CRP is proven an independent risk factor for CAD, then studies determining how CRP modification alters outcome in patients with an acute coronary event will be of particular interest. Data regarding the rapidity of response of CRP to this class of drugs will therefore be potentially useful in knowing how best to use HMG Co-A reductase inhibitors in both primary and secondary prevention of CVD, as well as in intervention during acute events.
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