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Calcium Cycling in Heart Failure: The Arrhythmia Connection
Author(s) -
POGWIZD STEVEN M.,
BERS DONALD M.
Publication year - 2002
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2002.00088.x
Subject(s) - medicine , cardiology , heart failure , afterdepolarization , tachycardia , endoplasmic reticulum , ventricular tachycardia , calcium , electrophysiology , repolarization , microbiology and biotechnology , biology
Calcium Cycling in Heart Failure. Ventricular tachycardia in nonischemic heart failure (HF) arises from a nonreentrant mechanism most likely due to delayed afterdepolarizations from activation of a transient inward current (I ti ). We present data and a paradigm in which an up‐regulated Na/Ca exchanger, residual‐adrenergic responsiveness, and decreased inward rectifying K current (I K1 ) in HF all conspire to markedly increase the propensity for triggered arrhythmias. The up‐regulated Na/Ca exchanger plays an additional critical role in unloading the sarcoplasmic reticulum of Ca, thereby causing the mechanical dysfunction. It is imperative that therapeutic approaches for ventricular tachycardia in HF take into consideration cellular Ca handling and excitation‐contractile coupling, and their alteration in the failing heart.