Key result
Apoptosis primarily occurs after reperfusion following ischemia, and its attenuation represents a potentially beneficial strategy for salvaging jeopardized myocardium.
Attenuating apoptosis after ischemia-reperfusion may salvage jeopardized myocardium, but better markers are needed to quantify its extent.
Apoptosis attenuation after reperfusion may salvage myocardium; leaves open optimal agents and markers for trials.
OBJECTIVES: We consider the conundrum suggested by myocardial hibernation and late restoration of function despite the absence of a substantial lateral peri-infarction border zone with respect to oxygenation, and suggest a pivotal role for apoptosis and its attenuation in salvaging jeopardized myocardium. METHODS: Selective pertinent literature is reviewed, and some recent observations indicating difficulties in identifying and quantifying apoptosis microscopically are summarized. RESULTS: Apoptosis seems to occur primarily after reperfusion following ischemia rather than persistent ischemia leading to necrosis. Refinements of markers of its presence are needed in vitro for use ultimately in vivo and should be pivotal in defining the extent to which tissue-protective interventions can salvage myocardium in the context of a fixed magnitude and duration of ischemia. CONCLUSION: Apoptosis is strongly implicated in the overall demise of jeopardized myocardium. Its attenuation seems likely to be potentially beneficial. Validation of this hypothesis will require progress in identification, delineation, and assessment of the extent of apoptosis in the threatened heart.
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Sobel et al. (2008) conducted a review in Myocardial hibernation and ischemia/reperfusion injury. Attenuation of apoptosis was evaluated. Apoptosis primarily occurs after reperfusion following ischemia, and its attenuation represents a potentially beneficial strategy for salvaging jeopardized myocardium.
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