Abstract
The treatment of acute myocardial infarction (AMI) has evolved substantially over the past 3 decades. After an initial improvement in the mortality rate of AMI due to thrombolytics for pharmacologic reperfusion [1], further clinical advances were made employing primary percutaneous intervention [2,3]. While major effort is expended on reducing door-to-balloon time, reperfusion is rarely achieved within the first ‘golden hour’ of symptoms so as to actually abort AMI. As a result, most patients are left with a burden of infarcted myocardium, and therefore the substrate for ventricular remodeling, heart failure and malignant arrhythmias. In addition, much of the current therapy for patients post-AMI, including antiplatelet therapy, statins, b-adrenergic antagonists and modulators of the renin–angiotensin axis, are aimed at the prevention of recurrent cardiovascular events and the amelioration of left ventricular remodeling. Until recently, a pathophysiologic paradigm held that necrotic myocardial tissue lacked any chance of functional recovery. This paradigm is currently undergoing revision with the advent of stem cell therapy, which holds the promise of r egeneration of viable myocardial tissue.
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