Key result
T-wave alternans arises from multiple cellular mechanisms including electrical restitution, transient outward current, early afterdepolarizations, and intracellular calcium cycling alternans.
This review outlines the cellular mechanisms underlying T-wave alternans and their contribution to lethal cardiac arrhythmias and sudden cardiac death.
May inform TWA-based arrhythmia risk assessment; leaves open mechanism-specific interventions pending trials.
T-wave alternans, a manifestation of repolarization alternans at the cellular level, is associated with lethal cardiac arrhythmias and sudden cardiac death. At the cellular level, several mechanisms can produce repolarization alternans, including: 1) electrical restitution resulting from collective ion channel recovery, which usually occurs at fast heart rates but can also occur at normal heart rates when action potential is prolonged resulting in a short diastolic interval; 2) the transient outward current, which tends to occur at normal or slow heart rates; 3) the dynamics of early afterdepolarizations, which tends to occur during bradycardia; and 4) intracellular calcium cycling alternans through its interaction with membrane voltage. In this review, we summarize the cellular mechanisms of alternans arising from these different mechanisms, and discuss their roles in arrhythmogenesis in the setting of cardiac disease.
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Zhilin Qu (2010) conducted a review in Cardiac arrhythmias. T-wave alternans was evaluated. T-wave alternans arises from multiple cellular mechanisms including electrical restitution, transient outward current, early afterdepolarizations, and intracellular calcium cycling alternans.
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