Abstract
Possible mechanisms of myocardial stunning at the cellular level include oxygen free radical production, neutrophil-induced damage, accelerated degradation of adenosine triphosphate (ATP), ischemia-induced myofibrillar damage, and calcium overload due to abnormal sodium/calcium exchange. Although the role of free radicals is generally accepted, their source(s) and clinical importance remain controversial. Similarly, an association of a declining ATP pool with myocardial stunning is well established but may not have clinical relevance as treatments that result in functional recovery do not always increase ATP levels. Little evidence exists for a strong link between myofibril damage and myocardial stunning. In contrast to these mechanisms, altered calcium homeostasis is an attractive hypothesis because: normal hearts perfused with high levels of calcium develop contractile dysfunctions similar to stunning; stunned hearts perfused with low calcium have increased function; calcium overload inhibition attenuates stunning; and reduced calcium ATPase activities have been found in sarcoplasmic reticulum from stunned hearts. Future research efforts should strive to simultaneously evaluate flow, function, and metabolic changes that occur in the stunned heart. Changes in the latter may eventually be studied using the techniques of molecular biology, integrating knowledge at the molecular level with clinical needs.
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