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Recent experimental data suggest that current thrombolytic strategies may not yet have achieved their full potential for myocardial salvage. In fact, reperfusion may result in microvascular and myocardial cellular injuries. These may translate into transient loss of contractile function ('myocardial stunning'), and possibly contribute to the ultimate extent of myocardial necrosis. A number of imaging modalities are now available to detect the presence and amount of these dysfunctional but viable myocardial segments. Myocardial reperfusion experiments using animal models have studied possible mechanisms responsible for reperfusion injury. These may help in the search for novel pharmacological and other adjunctive approaches which may overcome potential adverse effects of reperfusion. |
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