Abstract
Therapeutic approaches to left ventricular dysfunction in ischemic heart disease are likely to be guided by the answers to 2 major questions: (1) which mechanisms account for the deterioration or loss of contractile function, and (2) can contractile function be improved or restored therapeutically? Both questions can face considerable diagnostic challenges. Two main mechanisms have been implicated in the pathophysiology of reversible dysfunction—myocardial hibernation and myocardial stunning. Both general concepts share a number of clinical features so that standard clinical approaches often fail to discriminate between them. The presence of regionally increased fibrosis in scar tissue formation associated with decreased blood flow further complicates the search for truly reversible dysfunction.
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