Prognostic Role of Plasma High-Sensitivity C-Reactive Protein Levels in Acute Coronary Syndromes

Abstract

Prediction of future adverse cardiac events in patients with known coronary artery disease (CAD) remains extremely challenging for the clinical cardiologist. Patients presenting with acute coronary syndromes (ACS) have a relatively high risk of recurrent angina, acute myocardial infarction (AMI), and death during hospitalization and follow-up. Data from multicenter trials show mortality rates >5% during the intermediate term (1,2). Early assessment of left ventricular (LV) function at echocardiography and the extension of CAD (in terms of number of vessels affected at angiography) constitute the most important tools available to estimate cardiac risk. However, although age, depressed LV function, and multivessel CAD are considered high-risk features, prognosis in lowrisk subjects remains difficult to establish and therefore optimal management remains an issue. Earlier in the 1970s and 1980s, experimental data were produced supporting an active role of inflammatory reaction in promoting atherosclerotic plaque formation and complications (3,4), but only in the past few years has evidence of a prognostic role of systemic inflammatory markers in terms of prediction of short-and long-term risk been presented. This is particularly true for C-reactive protein (CRP), a prototypic acute phase protein. Its levels rapidly rise after an inflammatory stimulus and, depending on the intensity of the stimulus, even a several-hundred-fold increase in plasma levels may occur (5). CRP is not consumed to a significant extent in any process and its clearance is not influenced by any known condition; therefore, its concentration appears to be dependent only on the rates of production and excretion. The long half-life of CRP, approx 19 h, makes its detection in blood easy even several hours after the acute stimulus. Because of all these characteristics CRP can be considered an “ideal marker.”