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Chronic hibernation and chronic stunning: a continuum
1Department of Veterans Affairs Western New York Health Care System and the Department of Medicine, University at Buffalo, School of Medicine and Biomedical Sciences, NY 14214, USA. canty@buffalo.edu
Insights
Identifying myocardial viability is crucial for patients with coronary artery disease. Chronic stunning and hibernating myocardium are distinct but related mechanisms of viable, dysfunctional heart muscle.
Area of Science:
- Cardiology
- Physiology
- Pathophysiology
Background:
- Myocardial viability assessment is vital for managing coronary artery disease and left ventricular dysfunction.
- Contractile dysfunction in viable myocardium results from reversible ischemia via multiple mechanisms.
- Distinguishing between chronic stunning and hibernating myocardium is key for treatment decisions.
Purpose of the Study:
- To review pathophysiologic studies on chronic stunning and hibernating myocardium.
- To support the distinct nature of these entities in viable, dysfunctional myocardium.
- To position them as ends of a continuum.
Main Methods:
- Review of basic and clinical pathophysiologic studies.
- Analysis of mechanisms underlying contractile dysfunction in ischemic heart disease.
- Synthesis of evidence on the progression from chronic stunning to hibernation.
Main Results:
- Chronic stunning involves contractile dysfunction with normal resting perfusion.
- Hibernating myocardium exhibits reduced resting flow secondary to contractile dysfunction.
- Repetitive ischemia drives progression from stunning to hibernation.
Conclusions:
- Chronic stunning and hibernating myocardium are distinct pathophysiologic entities.
- These conditions represent different points on a continuum of viable, dysfunctional myocardium.
- Understanding these mechanisms aids in predicting functional recovery after revascularization.
Abstract:
Identification of myocardial viability is of increasing clinical importance in managing patients with coronary artery disease and advanced left ventricular dysfunction. Although viable chronically dysfunctional myocardium is always the result of repetitive episodes of reversible ischemia, there may be multiple mechanisms responsible for the contractile dysfunction. Many patients have contractile dysfunction with normal resting perfusion, as determined by imaging, that is related to chronic myocardial stunning. Viability studies are generally unnecessary because normal resting perfusion would preclude significant fibrosis. The clinical problem arises in evaluating patients with depressed resting flow that can be due to hibernating myocardium or nontransmural infarction. In this circumstance viability studies are required to assess the likelihood of functional recovery after revascularization. Although hibernating myocardium was originally posited to develop in response to prolonged episodes of myocardial ischemia (experimentally termed "short-term hibernation"), subsequent studies have shown that this tenuous balance can only be maintained for a period of several hours before resulting in some degree of subendocardial infarction. More recent experimental studies have demonstrated that there is a progression from chronic stunning with normal flow to hibernating myocardium with reduced resting flow. This presumably arises from repetitive episodes of spontaneous ischemia that increase in frequency as the physiologic significance of a coronary stenosis progresses. Thus in this new paradigm reduced flow is a result, rather than the cause, of the contractile dysfunction. This review summarizes basic and clinical pathophysiologic studies supporting the claim that chronic stunning and hibernation are distinct entities that may represent opposite ends of a continuum of mechanisms in viable chronically dysfunctional myocardium.
