C-reactive protein (CRP) is an acute phase reactant pro¬duced by the liver in response to inflammatory cytokines (1L-1, 1L-6) and tumor necrosis factor-a (TNF-a). C-reactive protein has been identified as a marker of risk for coronary events independent of other factors.
Although CRP has been found in atheromatous plaques and is suspected to enhance rupture of the plaque by both activating complement and impairing endothelial cell function, the exact source of elevated CRP levels among patients with acute coronary syndromes remains unclear. The suspicion is difficult to prove, and it is not well established if CRP is a marker of risk, a risk factor, or both.
In some studies CRP has been found to have prog¬nostic value among patients without evidence of myo-cardial necrosis. In patients with acute coronary syndromes and negative troponin-T, elevated CRP appears to be predictive of future adverse events. In addition it has been observed that CRP is a strong independent predictor of short- and long-term mortality among patients treated with early revascularization.
Many workers in the field agree high levels of CRP are associated with an increased risk of cardiovascular diseases, but the predictive power of this association is markedly diminished when adjusted for the risk factors. The clinical significance of the added value of CRP over conventional markers of coronary artery disease remains debatable.

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