Incomplete, delayed functional recovery late after reperfusion following acute myocardial infarction: "maimed myocardium".

The objective of the current editorial is to introduce a new concept ("maimed myocardium") that we believe describes more accurately the incomplete, delayed recovery of LV function that may occur late after reperfusion after AMI. It has been demonstrated previously that myocardium remains viable for a prolonged period in many patients with nonsustained coronary occlusion, despite the occurrence of myocardial necrosis; late reperfusion may result in myocardial salvage in reversibly ischemic (stunned) segments (complete recovery) and in intensely injured (maimed) segments that display partial return of LV function over time (incomplete recovery). Clinically, the basis for maimed myocardium is the observation that delayed, LV functional recovery may occur in partially infarcted segments where there has been an antecedent ischemic insult of sufficient duration to result in some degree of myocardial necrosis. Certain acute coronary syndromes characterized by nonsustained coronary occlusion followed by spontaneous reperfusion (e.g., non-Q-wave AMI) or drug-induced reperfusion induced by the exogenous administration of thrombolytic therapy are associated with incomplete, delayed recovery of LV function as detected clinically by partial improvement in serial radionuclide-ejection measurement, enhanced metabolic integrity of cardiac tissue by F-18 deoxyglucose myocardial imaging, and scintigraphic findings of reverse thallium redistribution--findings that support the presence of partially viable myocardium that has been incompletely salvaged during reperfusion late after AMI. Experimentally, delayed LV functional recovery has been reported in animal models in which prolonged coronary occlusion (hours to days) followed by reperfusion is associated with late recovery of regional LV function in myocardial segments subtending border (stunned) zones and central infarct (maimed) zones. In studies in animals and human beings, postextrasystolic potentiation and pharmacologic inotropic interventions may augment maimed and stunned segments, although the magnitude of regional contractile reserve that can be unmasked with these interventions is quantitatively less in the maimed than in stunned segments. In summary, the propensity of intensely injured or partially infarcted LV segments to display intermediate functional recovery followed by reperfusion late after coronary occlusion suggests that even severely depressed but residually viable cardiac muscle can be salvaged incompletely over time.(ABSTRACT TRUNCATED AT 400 WORDS)