Abstract
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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