ABSTRACT
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.
KEYWORD
Acute-phase reactants - coronary heart disease risk - prospective epidemiological
studies - mechanisms - modulation of the inflammatory response