Acute Myocardial Infarction: Perspectives on Physiopathology of Myocardial Injury and Protective Interventions

Abstract

Diffuse coronary artery injury produces a host of physiopathological, structural and metabolic changes in cardiocytes that, if not rectified, result in significant loss of functional myocardium to cause cardiac contractile dysfunction. Restoration of blood perfusion to the infarct-related artery helps to limit the acute effects of myocardial infarction; however, cardiocyte injury may be exacerbated because of the restoration of blood perfusion to the ischemic zone (i.e. reperfusion injury). Various manifestations of reperfusion injury include no-reflow, myocardial stunning or hibernation and ventricular arrhythmias. Consequently, reperfusion of an infarct related artery is often viewed in the context of being a “double-edged sword.” Pharmacologic and non-pharmacologic interventions have been investigated in pre-clinical and clinical studies in the hunt to develop strategies to protect cardiomyocytes against the long-term effects of ischemia, or delay development of necrosis (resulting from ischemia or reperfusion). This book chapter will update current thinking on cardioprotective strategies to improve clinical outcomes in patients with coronary artery disease.