High sensitivity C-reactive protein is associated with worse infarct healing after revascularized ST-elevation myocardial infarction.

BACKGROUND

The inflammatory response due to myocardial tissue injury in the setting of acute ST-elevation myocardial infarction (STEMI) is essential for proper local infarct healing. However, an excessive inflammatory response may aggravate myocardial damage and hampers infarct healing processes. The present study aimed to investigate the association of systemic inflammatory biomarkers with infarct size (IS) dynamics post-STEMI, using cardiac magnetic resonance (CMR) imaging.

METHODS

This prospective observational study included 245 STEMI patients treated with primary percutaneous coronary intervention (pPCI). Peak values of high-sensitivity C-reactive protein (hs-CRP), white blood cell count (WBCc) and fibrinogen were determined serially until 96 h after pPCI. Infarct healing, defined as relative IS reduction from baseline to 4 months after STEMI, was assessed using late gadolinium enhanced CMR imaging.

RESULTS

IS significantly decreased from 16% of left ventricular mass (LVM) (Interquartile range [IQR]:8-24) at baseline to 10% (IQR:5-17) at 4 months (p < 0.001). Relative IS reduction was 35% (IQR:8-50). Whereas peak WBCc (p = 0.926) and peak fibrinogen (p = 0.161) were not significantly associated with relative IS reduction, peak hs-CRP showed a significant association with IS reduction (p = 0.003). In multivariable logistic regression analysis, the association between peak hs-CRP and relative IS reduction remained significant after adjustment for baseline IS, hypertension, hs-cardiac troponin T and N-terminal pro B-type natriuretic peptide (odds ratio:0.35 [95% confidence interval:0.19-0.63]; p = 0.001).

CONCLUSIONS

In STEMI patients treated with pPCI, hs-CRP was independently associated with 4 months IS reduction as determined by CMR, suggesting a pathophysiological interplay between inflammation and adverse infarct healing in survivors of acute STEMI.