FEATURES OF SHORT-TERM MYOCARDIAL HIBERNATION

When severe ischemia, such as that resulting from a sudden and complet e coronary artery occlusion, is prolonged for more than 20-40 min, myo cardial infarction develops, and there is irreversible loss of contrac tile function. When myocardial ischemia is less severe but nevertheles s prolonged, the myocardium is dysfunctional but can remain viable. In such ischemic and dysfunctional myocardium, contractile function is r educed in proportion to the reduction in regional myocardial blood flo w; i.e. a state of 'perfusion-contraction matching' exists. The metabo lic status of such myocardium improves over the first few hours, as my ocardial lactate production is attenuated and creatine phosphate, afte r an initial reduction, returns towards control values. Ischemic myoca rdium, characterized by perfusion-contraction matching, metabolic reco very and lack of necrosis, has been termed 'short-term hibernating myo cardium'. Short-term hibernating myocardium can respond to inotropic s timulation with increased contractile function, although at the expens e of renewed worsening of the metabolic status. This occurrence of inc reased regional contractile function at the expense of metabolic recov ery during inotropic stimulation can be used to identify short-term hi bernating myocardium. When inotropic stimulation is prolonged, short-t erm hibernation is impaired and myocardial infarction develops. The me chanisms responsible for the development of short-term myocardial hibe rnation remain unclear at present. Significant involvement of adenosin e and activation of ATP-dependent potassium channels have been exclude d. The role of triggering events and acidosis is controversial. Short- term hibernating myocardium is, however, characterized by reduced calc ium responsiveness.