One of the most debated topics in cardiovascular medicine is whether C-reactive protein (CRP), a component of the acute-phase response, is a causal factor in the pathogenesis of atherosclerosis.1,2 If it is, the implications could be far-reaching and include new approaches for the prevention and treatment of myocardial infarction and stroke.3 Support for a role of CRP in the pathogenesis of atherosclerosis comes largely from epidemiologic studies that have consistently observed an association between elevated plasma CRP levels and cardiovascular events.1,4,5 The statistical strength of such associations is at least as robust as that of established risk . . .
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Schunkert et al. (2008) studied this question.
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