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Shortened Ca2+ Signaling Refractoriness Underlies Cellular Arrhythmogenesis in a Postinfarction Model of Sudden Cardiac Death
AE Belevych, D Terentyev, R Terentyeva... - Circulation ..., 2012 - Am Heart Assoc Abstract Rationale: Diastolic spontaneous Ca 2+ waves (DCWs) are recognized as important contributors to triggered arrhythmias. DCWs are thought to arise when [Ca 2+] in sarcoplasmic reticulum ([Ca 2+] SR) reaches a certain threshold level, which might be ...
Methods and Results: The frequency of DC Ws, recorded during periodic pacing in the presence of a β-adrenergic receptor agonist isoproterenol, was significantly higher in VF myocytes than in normal controls. Rather than occurring immediately on reaching a final [Ca2+]SR, DC Ws arose with a distinct time delay after attaining steady [Ca2+]SR in both experimental groups. Although the rate of [Ca2+]SR recovery after the SR Ca2+ release was similar between the groups, in VF myocytes the latency to DC Ws was shorter, and the [Ca2+]SR at DCW initiation was lower. The restitution of depolarization-induced Ca2+ transients, assessed by a 2-pulse protocol, was significantly shorter in VF myocytes than in control. The VF-related alterations in myocyte Ca2+ cycling were mimicked by the Ry R2 agonist, caffeine. The reducing agent, mercaptopropionylglycine, or the Ca MKII inhibitor, KN93, decreased DCW frequency and normalized restitution of Ca2+ release in VF myocytes.
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Shortened Ca2+ Signaling Refractoriness Underlies Cellular Arrhythmogenesis in a Postinfarction Model of Sudden Cardiac Death |
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