Abstract
Myocardial infarction (MI) and its associated complications are one of the largest contributors to mortality and morbidity. Paradoxically, coronary reperfusion can cause further myocardial damage through processes such as generation of reactive oxygen species, accumulation of intracellular calcium, and abrupt pH change [ [1] Yellon D.M. Hausenloy D.J. Myocardial reperfusion injury. N Engl J Med. 2007; 357: 1121-1135 Crossref PubMed Scopus (2784) Google Scholar ]. Within the infarcted region contractile muscle is progressively replaced with fibrotic tissue leading to structural remodelling to compensate for altered hemodynamic load. The infarcted left ventricular (LV) wall undergoes thinning and expansion, leading to eventual heart failure [ [2] Hochman J.S. Choo H. Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage. Circulation. 1987; 75: 299-306 Crossref PubMed Scopus (406) Google Scholar ]. Activated protein C (APC) is an endogenous anticoagulant with powerful cytoprotective properties that make it an attractive therapeutic for treatment of IR injury. While short term benefit in rat myocardial IR injury has been shown with recombinant human APC (rhAPC) [ [3] Wang J. Yang L. Rezaie A.R. Li J. Activated protein C protects against myocardial ischemic/reperfusion injury through AMP-activated protein kinase signaling. J Thromb Haemost. 2011; 9: 1308-1317 Crossref PubMed Scopus (71) Google Scholar ], the translation of this action to long term remodelling remains to be demonstrated.
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