C-reactive protein during and after myocardial infarction in relation to cardiac injury and left ventricular function at follow-up.

Background: Acute myocardial infarction (MI) invokes a large inflammatory response, which contributes to myocardial repair. Hypothesis: We investigated whether C-reactive protein (CRP) measured during MI vs at 1 month follow-up improves the prediction of left ventricular (LV) function. Methods: We prospectively enrolled 131 consecutive patients with acute MI and without non-cardiovascular causes of inflammation. We correlated admission and peak levels of CRP during hospitalization and high-sensitivity (hs) CRP at 1 month follow-up with markers of cardiac injury. Clinical follow-up and echocardiography for LV function were performed at a mean of 17 months. Results: Median CRP levels were 1.89 mg/L on admission with MI, peaked to 12.10 mg/L during hospitalization and dropped to 1.24 mg/L at 1 month. Although admission CRP levels only weakly correlated with ejection fraction in the acute phase of MI (coefficient -0.164, P = 0.094), peak CRP was significantly related to ejection fraction (coefficient -0.4, P < 0.001), hsTroponin T (0.389, P < 0.001), and white blood cell count (0.389, P < 0.001). hsCRP at 1 month was not related to the extent of acute cardiac injury. These findings were replicated in an independent cohort of 57 patients. Peak CRP predicted LV dysfunction at follow-up (OR 11.0, 3.1-39.5 per log CRP, P < 0.001), persisting after adjustment for infarct size (OR 5.1, 1.1-23.6, P = 0.037), while hsCRP at 1 month was unrelated to LV function at follow-up. Conclusions: hsCRP 1 month post-MI does not relate to acute cardiac injury or LV function at follow-up, but we confirm that peak CRP is an independent predictor of LV dysfunction at follow-up.