Early measurements of plasma matrix metalloproteinase-2 predict infarct size and ventricular dysfunction in ST-elevation myocardial infarction.

Abstract

Immediate reopening of the acutely occluded infarct-related artery via primary PCI is the preferred treatment in ST-elevation myocardial infarction (STEMI). However, the sudden reinitiation of blood flow can lead to a local acute inflammatory response with further endothelial and myocardial damage, so-called reperfusion injury. The activation of matrix metalloproteinases (MMPs) is suggested to be a key event in this process. To investigate circulating MMPs, tissue inhibitors of metalloproteinases (TIMPs) and myeloperoxidase (MPO) in relation to infarct size, left ventricular dysfunction and remodelling in a STEMI population undergoing PCI. 58 Patients with STEMI undergoing primary PCI were included. Blood samples were collected at baseline before PCI and at 12, 24 and 48 h for later analysis of MMPs, TIMPs and MPO by ELISA. Infarct size, left ventricular (LV) dysfunction and remodelling were assessed by cardiac MRI at 5 days and 4 month after STEMI. Plasma MMP-2 at 0 and 12 h showed a consistent and significant correlation with infarct size and LV dysfunction measured both at 5 days and at 4 months and correlated well with troponin I measurements. For TIMP-1 and TIMP-2 some support was found for associations with infarct size and LV dysfunction, but these were not as consistent as for MMP-2. MMP-8, MMP-9 and MPO did not overall correlate with measures of infarct size, LV dysfunction or remodelling. In patients with STEMI, circulating levels of MMP-2, measured early and even before reperfusion therapy, are strongly associated with infarct size and LV dysfunction. This provides further evidence for the role of MMP-2 in ischaemia-reperfusion injury.