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[The viable myocardium: metabolic, diagnostic and therapeutic aspects]
Insights
Stunned myocardium involves reversible post-ischemic dysfunction, while hibernating myocardium shows depressed contractility due to chronic hypoperfusion. Both conditions may improve with revascularization.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Context:
- Post-ischemic myocardial dysfunction, termed stunned myocardium, persists after restored coronary flow.
- Hibernating myocardium describes contractile depression from chronic hypoperfusion, reversible with revascularization.
- Understanding these conditions is crucial for managing ischemic heart disease.
Purpose:
- To review the underlying biochemical and physiopathological mechanisms of stunned and hibernating myocardium.
- To explore hypotheses explaining myocardial stunning, including free radicals, energy deficit, and calcium overload.
- To differentiate the mechanisms of dysfunction in stunned versus hibernating myocardium.
Summary:
- Stunned myocardium results from reversible post-ischemic dysfunction, potentially caused by free radicals, energy deficit, or calcium overload.
- Calcium ion transport and accumulation alterations, linked to Na+/Ca++ pump deficits, are implicated in contractile dysfunction.
- Hibernating myocardium involves metabolic down-regulation and reduced energy consumption for survival in hypoperfused areas.
Impact:
- Clarifies the distinct pathophysiological pathways of myocardial stunning and hibernation.
- Provides insights into potential therapeutic targets for improving cardiac function after ischemia.
- Enhances understanding of myocardial adaptation to chronic hypoperfusion and acute ischemic events.
Abstract:
The term stunned myocardium is used to indicate a reversible post-ischemic dysfunction of the ventricular mechanism which may persist for hours, days or weeks after the restoration of coronary flow following spontaneous or pharmacological thrombolysis, transluminal coronary angioplasty, aorto-coronary bypass and ischemic attacks. Hibernating myocardium is used to describe a depression of ventricular contractility in the presence of chronic hypoperfusion which may be reversed following revascularization as a result of aorto-coronary by-pass surgery. Three biochemical and physiopathological hypotheses are currently acknowledged to explain the phenomenon of stunning: the hypothesis of free oxygen radicals, the hypothesis related to an energy deficit and that involving a calcium overload. It is possible that oxydizing stress induced by free radicals may modify the activity of one or more sarcolemmic proteins which regulate the flow of calcium or other ions. Alterations in the transport and accumulation of calcium ions due to a Na+/Ca++ pump deficit and calcium-ATPase of the sarcoplasmatic reticle appear to be responsible for contractile dysfunction. The hypothesis concerning an energy deficit appears to be least probable since even if ATP levels are low the intracellular energy status does not appear to be a factor which limits mechanical function which may be stimulated in the absence of further variations in the content of highly energetic phosphates. There is also reduced myofibrillar creatinkinase activity. In hibernating myocardium the mechanical dysfunction is due to a metabolic and therefore contractile "down-regulation' with low myocardial energy and oxygen consumption to ensure the survival of chronically hypoperfused areas.(ABSTRACT TRUNCATED AT 250 WORDS)