Key result
Modulating calcium handling via the ryanodine receptor, sarcoplasmic reticulum Ca ATPase, or Na/Ca exchanger is a potential approach to reduce arrhythmias.
Why the study?
Does modulating calcium handling reduce arrhythmias in patients with genetic diseases or heart failure?
Does modulating calcium handling reduce arrhythmias in patients with genetic diseases or heart failure?
Targeting calcium handling mechanisms represents a potential therapeutic approach for reducing arrhythmias in genetic diseases and heart failure.
Calcium handling modulation may reduce arrhythmias in heart failure; hypothesis-generating review leaves open clinical translation.
Abnormal calcium (Ca) handling can contribute to arrhythmogenesis directly by triggering abnormal depolarizations and indirectly by modulating action potential time course and duration. Recent data have shown the importance of these mechanisms in rare genetic diseases but also in more common conditions such as heart failure. Modulating Ca release from the sarcoplasmic reticulum via the ryanodine receptor, Ca uptake via sarcoplasmic reticulum Ca ATPase or Ca removal from the cell via the Na/Ca exchanger, are potential approaches to reduce arrhythmias. New tools allow exploring these ideas. The principles underlying this approach and the first results are critically reviewed.
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Antoons et al. (2008) conducted a review in Arrhythmias. Targeting calcium handling was evaluated. Modulating calcium handling via the ryanodine receptor, sarcoplasmic reticulum Ca ATPase, or Na/Ca exchanger is a potential approach to reduce arrhythmias.
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