Acute-phase reactants and coronary heart disease.

Inflammation is considered to play an essential role in the initiation, progression, and the final pathophysiological steps of atherosclerosis, plaque erosion or fissure, and eventually plaque rupture. Prospective studies have identified several markers of systemic inflammation that are predictors of future cardiovascular events, not only in apparently healthy subjects, but also in patients with unstable angina and previous myocardial infarction. Measurement of inflammatory markers may add to the predictive value of total and high-density lipoprotein cholesterol in assessing coronary risk long-term. Various biological mechanisms exist that could explain the pathological effects of these inflammatory molecules. Finally, the results from recent clinical trials indicate that the net benefit of various compounds in primary and secondary prevention of coronary heart disease, like aspirin, statins, and ACE inhibitors, may be mediated, at least in part, by modifying the consequences of the inflammatory response on vascular risk. However, further studies are required to address these associations because the mechanisms that cause an inflammatory response are only incompletely understood and deserve further investigation.