Stunning: Damaging or protective to the myocardium?

Abstract

There are several potential outcomes of myocardial ischemia. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. Interventions aimed at reducing mechanical activity and oxygen demand, either before ischemia or during reperfusion, have been shown to delay the onset of ischemic damage and to improve recovery on reperfusion. When myocardial ischemia is less severe but still prolonged, myocytes may remain viable but exhibit depressed contractile function. Under these conditions, reperfusion restores complete contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed hibernating myocardium. Depression of mechanical activity is, actually, a protective mechanism whereby the hibernating cells reduce their oxygen demands in the setting of reduced oxygen supply. A third possible outcome after a short period of myocardial ischemia is a transient postischemic ventricular dysfunction, a situation termed stunned myocardium. As in the case of hibernating myocardium, the depressed contractile function occurring during stunning could be a protective mechanism, allowing the reperfused cells to gradually recover their metabolism and function.

Depression in Coronary Heart Disease Patients: Etiological and Screening Issues

“…CHD represents one of the most significant causes of mortality in major developed countries [1]. Importantly, because of the manifestation of CHD as a purely physiological clinical presentation [2], many CHD patients experiencing significant psychological distress, in particular depression, fail to receive appropriate psychiatric assessment, support and intervention [3,4]. This is surprising because of clearly established links between CHD and depressive illness [5].…”

On some pathogenetic and adaptation mechanisms of acute coronary disease

“…Hence, this diagnosis is tentative and requires more precise definition after thorough instrumental and laboratory studies. Acute coronary failure with foci of degeneration is a focal ischemic myocardial injury without necrosis; it can be reversible ("hibernated myocardium") [2,8,9]. Coronary bloodflow deficit in hibernated myocardium is insufficient for necrosis development, but it can cause pH changes, which, in turn, impairs contractile function of cardiomyocytes [7].…”