Role of apoptosis in myocardial hibernation and myocardial stunning

Abstract

Clinicians have long recognized that left ventricular dysfunction in patients with coronary disease is a reversible condition [1,2]. In 1975 Vatner and associates first described post-ischemic myocardial dysfunction in conscious dogs produced by brief coronary occlusions followed by reperfusion [3]. In 1982, Braunwald and Kloner [4] coined the term ‘myocardial stunning’ to describe prolonged but reversible myocardial dysfunction following restoration of myocardial blood flow. In 1985, Rahimtoola observed progressive recovery of chronic left ventricular dysfunction following coronary artery bypass grafting in the absence of transmural necrosis [5]. He described these findings as ‘hibernating myocardium’ reflecting a state of persistently impaired myocardial function at rest due to reduced coronary blood flow that can be partially or completely restored to normal if the net balance between myocardial oxygen supply and demand is favorably altered [6]. The major difference between stunned and hibernating myocardium is the level of myocardial perfusion which is chronically reduced in hibernating myocardium but normal in stunned myocardium. Until recently, the observation of functional recovery was thought to imply that the structural morphology of stunned and hibernating myocardium must be essentially normal. However, increasing evidence from analysis of myocardial biopsy specimens obtained during coronary artery bypass surgery have revealed that stunned and hibernating myocardium are accompanied by several structural changes including apoptotic cell death.