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Targeted SERCA2a Gene Expression Identifies Molecular Mechanism and Therapeutic Target for Arrhythmogenic Cardiac Alternans
Circulation: Arrhythmia and Electrophysiology, 10/08/09

Cutler MJ et al. – The data provide new evidence that SR Ca2+ reuptake directly modulates susceptibility to cellular alternans. Moreover, SERCA2a overexpression suppresses cellular alternans, interrupting an important pathway to cardiac fibrillation in the intact heart.

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David S. Rosenbaum, 10/08/09

T-wave alternans arises from beat to beat alternans of cellular repolarization is a recognized marker of risk for sudden cardiac death (SCD). Previously, we reported an association between deficient expression of SERCA2a, the protein responsible for calcium re-uptake into sarcoplasmic reticulum, and resistance to alternation of calcium transients. In the present study, we demonstrated that targeted in vivo gene transfer of SERCA2a significantly suppresses cellular alternans in the intact heart and voltage-clamped myocytes isolated from these hearts. These findings provided definitive evidence for a primary role of intra-cellular calcium cycling in the mechanism of cardiac alternans. Moreover, SERCA2a gene transfer reduced susceptibility to inducible ventricular arrhythmias in the intact beating heart. Taken together, these data point to a novel molecular target for ameliorating cardiac electrical instability, and suggest possible approaches for genetically engineering hearts that are resistant to ventricular arrhythmias. .

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