Relation of inflammatory markers with myocardial and microvascular injury in patients with reperfused ST-elevation myocardial infarction

In patients with acute ST-elevation myocardial infarction (STEMI), elevated concentrations of inflammatory markers are correlated with worse clinical outcome. The aim of this study was comprehensively to investigate the relationship of circulating markers of inflammation with myocardial and microvascular damage after STEMI.

In 111 consecutive STEMI patients, blood samples were obtained on admission and from day 1 to day 4 after primary percutaneous coronary intervention and analysed for high-sensitivity C-reactive protein (hs-CRP), white blood cell count and fibrinogen. Cardiac magnetic resonance imaging was performed within the first week and 4 months after primary percutaneous coronary intervention.

Peak concentrations of hs-CRP (20.5 (9.6–44.4) mg/L), white blood cell count (12.4 (10.5–15.3) G/L) and fibrinogen (3640 (3150–4550) mg/L) showed significant correlations with both infarct size (r=0.31 to 0.41; P<0.01) and left ventricular ejection fraction (r=−0.29 to −0.39; P<0.01) assessed in the acute as well as chronic stage following STEMI. Furthermore, peak concentrations of these inflammatory markers were significantly higher in patients with microvascular obstruction compared to patients without microvascular obstruction (P⩽0.01). C-statistics revealed that the prognostic values of all three biomarkers for the prediction of large chronic infarct size (>8% of left ventricular myocardial mass) were moderate without significant differences (area under the curve: hs-CRP 0.73 (95% confidence interval (CI) 0.63–0.82), white blood cell count 0.67 (95% CI 0.56–0.78) and fibrinogen 0.69 (95% CI 0.59–0.79); all P>0.12). Combination of inflammatory markers did not significantly increase the area under the curve (P>0.05).

In reperfused STEMI patients, increased levels of hs-CRP, white blood cell count and fibrinogen are associated with decreased left ventricular function and more pronounced myocardial damage at baseline and 4 months after infarction.