Hibernating myocardium in patients with coronary artery disease: Identification and clinical importance

Abstract

The term hibernating myocardium describes a particular outcome of myocardial ischemia in which myocytes show a chronically depressed contractile ability but remain viable. Revascularization of hibernating tissue causes a recovery of mechanical function that correlates with long-term survival. Therefore it is important clinically to distinguish hibernating from infarcted myocardium, since asynergies due to hibernation will improve on reperfusion, whilst those due to infarct will not. One suggested technique to identify hibernating myocardium is to stimulate the myocytes acutely, but briefly, by administration of inotropic agents while monitoring contractile function by echocardiography. We report our experience on the use of low dosages of dobutamine. Myocardial viability was validated by measuring the recovery in contraction of the akinetic areas after coronary artery bypass surgery by means of intraoperative epicardial echocardiography. The test has a sensitivity of 93% and a specificity of 78%. It is useful for identification of viable myocardium and also for quantification of intraoperative risk in individual patients. Limitations of this test are related to the presence of downregulation of beta receptors and to the impossibility of differentiating hibernating from stunned myocardium. Another useful technique of identifying hibernating myocardium is the use of radionuclear markers for viability. In our experience the two most important tests are (1) rest-redistribution imaging of thallium 201 (which has a high sensitivity of 93% but a low specificity of 44%) and (2) 99mTc-Sestamibi imaging, which provides information on both perfusion and function with a single injection. This latter technique allows differentiation between stunning and hibernating on the basis of coronary flow which is preserved in stunning and reduced in hibernation.

Myocardial perfusion and function in dogs with moderate coronary stenosis

“…This may possibly have led to a higher interanimal variation that, when coupled with our small sample size, may have prevented us from achieving statistically significant measurements that might be obtainable with a larger sample size or less interanimal variation. At the dosage level of dobutamine used (10 pg/kg/min), echocardiographic studies have shown that areas with diminished blood supply due to moderate stenoses will be dyskinetic or hypokinetic; whereas at lower dobutamine levels ( e g , 2.5 pglkglmin), contraction is maintained in these areas (42)(43)(44). Our findings in the ANT region at the StD state are consistent with these echocardiographic studies.…”

Predicting the outcome of revascularization in ischaemic left ventricular dysfunction

“…The most useful investigations are echocardiography at rest and with dobutamine stress, and nuclear cardiology using either single photon (SPET) or positron emitting (PET) tracers of myocardial viability and perfusion. Contrast echocardiography, ultrasonic tissue characterization, gated SPET and PET and magnetic resonance imaging and spectroscopy have also shown their potential but they are less widely used [13,14] In general terms, the functional techniques (stress echocardiography and magnetic resonance imaging) are specific but insensitive for the prediction of segmental functional recovery, and the radionuclide tracer techniques are sensitive but non-specific [15,16] . It is possible that the lower specificity of the tracer techniques is not a drawback since they have been shown to predict improvement in symptoms and outcome and, as explained above, recovery of segmental function may not be the only important factor.…”

On some pathogenetic and adaptation mechanisms of acute coronary disease

“…Acute coronary failure with foci of degeneration is a focal ischemic myocardial injury without necrosis; it can be reversible ("hibernated myocardium") [2,8,9]. Coronary bloodflow deficit in hibernated myocardium is insufficient for necrosis development, but it can cause pH changes, which, in turn, impairs contractile function of cardiomyocytes [7]. Clinically this form of coronary disease differs little from small focal myocardial infarction.…”