Abstract
An arrhythmic mechanism seen only in heart failure (HF) that involves increased mitochondrial Ca2+ handling, selective transfer of Ca2+ to the sarcoplasmic reticulum (SR), and SR Ca2+ leak. Modeling suggests mitochondrial Ca2+ transfer to the SR via sarco/endoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) is crucial to this arrhythmic mechanism. Here, we tested the role of SERCA2a in arrhythmias during ischemic HF. Myocardial infarction (MI) was induced in wild type (Wt) and SERCA2a heterozygous knockdown (SERCA+/-) mice.
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