Background and aims: Inflammation appears to be pivotal in all phases of atherosclerosis from the fatty streak lesion to acute coronary syndromes. An important marker of inflammation is C-reactive protein. We thought to test the hypothesis that CRP measured at admission with acute coronary syndrome and at regular follow up durations is predictive of future cardiovascular events and to assess the relation of CRP levels to the complexity of coronary stenoses and to the coronary score as a surrogate of the total atherosclerotic burden. Methods:We prospectively recruited 91 patients presenting with acute coronary syndromes including those with ST elevation, clinical examination excludes those with evidence of infection or inflammation. All patients underwent coronary angiography (lesions were classified according to complexity into type A, B and C and coronary score was calculated by summing percent stenosis score times extent score over 15 coronary segments).Serum samples for measuring CRP level was withdrawn then patients was followed at 1, 4, 8 and 12 months and assessed for the occurrence of composite end points of nonfatal MI, UA or cardiac death. Samples for CRP were withdrawn in the 1st three follow up visits.Results:Admission CRP level could not predict future cardiovascular events (P=0.9) and did not correlate with complexity of coronary stenoses (P=0.42), meanwhile CRP at all follow up visits (1m,4m and 8m) correlated with both events (P=0.001,0.004and 0.01 respectively) and lesion complexity (P=0.001,0.01and<0.001respectively), CRP that preceded the event "pre-event CRP" was significantly higher than samples not followed by events. A cutoff value of 7.3 mg/l or 4.3 fold rise in CRP level had the highest sensitivity and specificity in detecting events. Despite being higher in patients developing events, coronary score did not correlate with any of the CRP samples.Conclusions: CRP done at admission is likely to be confounded by the inflammatory outburst that occur secondary to the occurrence of myocardial necrosis but it could be useful in following patients after acute coronary syndromes; its rise prior to the event may also indicate that CRP may not be a mere marker of plaque instability but also act as a mediator through its pro-inflammatory and pro-atherogenic effects. CRP is not a mere marker of the angiographic atherosclerotic burden but instead, a marker of coronary artery disease activity.