Effect of therapy time from myocardial infarction onset to percutaneous coronary intervention on matrix metalloproteinases level and left ventricular remodeling in patients with acute anterior wall myocardial infarction

Objective To investigate the effect of time from myocardial infarction (MI) onset to percutaneous coronary intervention (PCI) on plasma matrix metalloproteinases (MMPs) level and left ventricle (LV) remodeling in patients with acute ST-segment elevation myocardial infarction of anterior wall, and the relationship between MMPs and left ventricular remodeling. Methods All patients with anterior wall STEMI undergoing PCI were divided into early PCI group (PCI within 18 h after MI onset) and delayed PCI group (PCI between 2 and 3 weeks after MI onset). Plasma MMP-2 and MMP-9 activities were assayed on admission, and at 2 days, 1 week after admission. One-year follow-up was finished after PCI. Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and left ventricle ejection fraction (LVEF) were measured by echocardiography at baseline and one year later to elucidate the effects of time from onset to PCI on LV remodeling and the relationship between MMP-2, -9 levels and LV remodeling. Results The MMP-9 activity at 2 days after myocardial infarction was lower in early PCI group than in delayed PCI group〔(46±26)μg/L vs. (66±40) μg/L, P=0.000〕. The changes in LVEDV and LVESV (ΔLVEDV and ΔLVESV) were lower and the change in LVEF (ΔLVEF) was higher in early PCI group than in delayed PCI group〔(10.9±6.2) ml vs. (15.0±6.0) ml, (–1.1±5.7) ml vs. (2.9±4.6) ml, (5.5±4.0) % vs. (3.8±3.4) %, P=0.000, 0.000 and 0.015〕. MMP-9 had positive correlations with ΔLVEDV and ΔLVESV, and a negative correlation with ΔLVEF at admission and after 1-year follow-up (r=0.32, 0.36 and–0.29, respectively, P=0.000, 0.000 and 0.001). Conclusions MMP-9 activity at admission is correlated with LV remodeling and LV function. Early PCI can reduce MMP-9 activity and improve LV remodeling after myocardial infarction. Key words: Myocardial infarction; Ventricle remodeling; Matrix metalloproteinases