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Cardiac alternans, in the form of microvolt T-wave alternans, is an important clinical sign of heart disease that frequently emerges as a diagnostic manifestation of disease severity in cardiomyopathies such as heart failure, coronary artery disease, genetic and acquired channelopathies, and even in electrolyte disturbances of the body.1 During cardiac alternans, there is a beat-to-beat oscillation between strong and weak contractions, and although the heart keeps a regular pace, cardiac alternans ultimately spawns lethal arrhythmias, serving as a valuable risk stratification factor for sudden cardiac death and helping guide arrhythmia treatment.2Article, see p 846At the cellular level, cardiac alternans manifests as a cyclic, simultaneous alternation of 3 of the fundamental events of cardiomyocyte physiology: action potential duration (APD), intracellular Ca2+ transient (CaT) amplitude, and contraction amplitude. Because action potentials trigger cytosolic CaTs, and CaTs in turn influence the amplitude and duration of the action potentials through various Ca2+-dependent ionic currents, in this inescapable bidirectional coupling there is barely an instance in which APD alternans becomes dissociated from CaT alternans and in reality, one faithfully follows the other. But which one has the primary role? The question seems of fundamental importance if one is to understand the hierarchical role of distinct cellular processes and target the roots of this arrhythmogenic event through rationalized therapy.The prominence of membrane currents in the genesis of cardiac alternans was demonstrated as early as 1968 by Nolasco and Dahlen3 in their classical experiments of APD restitution. They observed that in electrically paced frog ventricular muscle strips, APD shortened as they accelerated the pacing rate. This phenomenon appeals to logic because the cardiac cycle length decreases considerably during increased metabolic demand, and it must do so by means of shortening both, APD and diastolic interval (DI). Typically, DI …

Mechanisms of Cardiac Alternans in Atrial Cells