Reversible congestive heart failure caused by myocardial hibernation.

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RESUMO

Myocardial hibernation is reversible contractile dysfunction of cardiac myocytes caused by chronic ischemia. Animal studies and observations in human beings suggest that the term hibernation is a misnomer. Repetitive ischemic insult that does not produce necrosis results in functional and histologic tissue deterioration, which culminates in myocyte apoptosis. Revascularization of "hibernating" myocardium results in partial or complete recovery of function, depending upon the duration of ischemia and the severity of cellular degeneration. Improvement in global left ventricular function is proportional to the quantity of hibernating tissue that is revascularized, but this threshold quantity has not been determined with certainty. Diagnostic methods used to detect viable tissue within akinetic left ventricular segments depend upon the recognition of recruitable contractile function or the active concentration of a radioactive tracer. No diagnostic method has shown clear superiority. The most sensitive methods appear to be single-photon emission computed tomographic imaging after reinjection of thallium-201 at 24 hours and positron-emission tomographic imaging with 18F-fluorodeoxyglucose. The most specific diagnostic method appears to be measurement of dobutamine-stimulated contractile function, using either echocardiography or gated magnetic resonance imaging. We present a review of the pathophysiology, diagnosis, and treatment of myocardial hibernation, and include an illustrative case report involving a 57-year-old man with myocardial hibernation.

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