Change in growth differentiation factor 15, but not C-reactive protein, independently predicts major cardiac events in patients with non-ST elevation acute coronary syndrome.

Among the numerous emerging biomarkers, high-sensitivity C-reactive protein (hsCRP) and growth-differentiation factor-15 (GDF-15) have received widespread interest, with their potential role as predictors of cardiovascular risk. The concentrations of inflammatory biomarkers, however, are influenced, among others, by physiological variations, which are the natural, within-individual variation occurring over time. The aims of our study are: (a) to describe the changes in hsCRP and GDF-15 levels over a period of time and after an episode of non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and (b) to examine whether the rate of change in hsCRP and GDF-15 after the acute event is associated with long-term major cardiovascular adverse events (MACE). Two hundred and Fifty five NSTE-ACS patients were included in the study. We measured hsCRP and GDF-15 concentrations, at admission and again 36 months after admission (end of the follow-up period). The present study shows that the change of hsCRP levels, measured after 36 months, does not predict MACE in NSTEACS-patients. However, the level of GDF-15 measured, after 36 months, was a stronger predictor of MACE, in comparison to the acute unstable phase.

Role of myeloperoxidase as predictor of systemic inflammatory response syndrome in patients with ST-segment elevation myocardial infarction after primary percutaneous coronary intervention.

Elevated cytokine levels have been reported after ischemia/reperfusion injury and might cause a systemic inflammatory response syndrome (SIRS) after primary percutaneous coronary intervention (PPCI). High myeloperoxidase (MPO) levels are reported to be a risk factor for early cardiac events in patients with acute coronary syndrome. Its role as a predictor of SIRS in patients with ST-segment elevation myocardial infarction treated with PPCI is unclear. Therefore, the aim of the present study was to investigate the role of MPO as a predictor of SIRS in patients with ST-segment elevation myocardial infarction treated with PPCI. A total of 250 patients with ST-segment elevation myocardial infarction treated with PPCI were admitted to our coronary care unit. The serum MPO levels were measured at admission using a commercially available enzyme-linked immunosorbent assay. Of the 250 patients, 47 developed SIRS within 48 hours after their admission to the coronary care unit; 10 of these patients were excluded from analysis because of the suspicion of sepsis. The remaining 203 patients had no SIRS during their coronary care unit stay. Compared to patients without SIRS, those with SIRS had greater serum MPO values (81.35 +/- 18.07 vs 67.03 +/- 16.98 ng/ml, p <0.0001) after PPCI. After controlling for different baseline clinical, laboratory, and angiographic variables, the baseline serum MPO levels were an independent predictor of SIRS (odds ratio 4.2, 95% confidence interval 1.9 to 8.4, p <0.001). In conclusion, our results have demonstrated that MPO is an independent predictor of SIRS after PPCI, suggesting a new clue for the interpretation of this phenomenon.