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Stunned myocardium and the attenuation of stunning by calcium antagonists
Abstract:
Myocardial "stunning" is characterized by a reversible postischemic contractile dysfunction despite full restoration of blood flow. The underlying mechanisms are not clearly understood. Inadequate energy supply and impaired sympathetic neurotransmission may have been excluded. Potential mechanisms, which are not mutually exclusive, may include damage to membranes and enzymes by free radicals, an increase in free cytosolic calcium during ischemia and reperfusion, and a lower calcium sensitivity of myofibrils. The equally pronounced increases in regional contractility in normal and stunned myocardium during postextrasystolic potentiation and the infusion of calcium or the calcium-sensitizing agent AR-L-57, however, suggest an unchanged calcium sensitivity in reperfused myocardium. Pretreatment with calcium antagonists before ischemia attenuates myocardial stunning. This effect is probably related to a lessened myocardial calcium overload during early ischemia. The potential benefit of treatment with calcium antagonists after reperfusion is established remains controversial.
Insights
Myocardial stunning, a reversible heart dysfunction after ischemia, may involve free radicals and calcium overload. Calcium antagonists before ischemia show benefit, but their use after reperfusion is debated.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Ischemic Heart Disease
Background:
- Myocardial stunning is reversible contractile dysfunction post-ischemia despite restored blood flow.
- Underlying mechanisms remain unclear, with potential roles for free radicals and calcium dysregulation.
- Impaired energy supply and sympathetic neurotransmission are less likely causes.
Purpose of the Study:
- To elucidate the mechanisms of myocardial stunning.
- To investigate the role of calcium sensitivity and overload in stunning.
- To evaluate the efficacy of calcium antagonists in preventing and treating myocardial stunning.
Main Methods:
- Assessed myocardial stunning characterized by reversible postischemic contractile dysfunction.
- Investigated potential mechanisms including free radical damage, cytosolic calcium increase, and myofibril calcium sensitivity.
- Evaluated effects of postextrasystolic potentiation, calcium infusion, and AR-L-57 on contractility.
- Examined the impact of calcium antagonist pretreatment before ischemia and post-reperfusion.
Main Results:
- Myocardial calcium sensitivity appears unchanged in reperfused myocardium.
- Pretreatment with calcium antagonists before ischemia significantly attenuates myocardial stunning.
- This protective effect is likely due to reduced calcium overload during early ischemia.
Conclusions:
- Myocardial stunning mechanisms may involve calcium overload rather than altered calcium sensitivity.
- Calcium antagonists are effective in preventing myocardial stunning when administered before ischemia.
- The therapeutic benefit of calcium antagonists after reperfusion for established stunning remains uncertain.