Mechanisms of sudden cardiac death
Michael Rubart, Douglas P. Zipes
Michael Rubart, Douglas P. Zipes
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Science in Medicine

Mechanisms of sudden cardiac death

Abstract

Despite recent advances in preventing sudden cardiac death (SCD) due to cardiac arrhythmia, its incidence in the population at large has remained unacceptably high. Better understanding of the interaction among various functional, structural, and genetic factors underlying the susceptibility to, and initiation of, fatal arrhythmias is a major goal and will provide new tools for the prediction, prevention, and therapy of SCD. Here, we review the role of aberrant intracellular Ca2+ handling, ionic imbalances associated with acute myocardial ischemia, neurohumoral changes, and genetic predisposition in the pathogenesis of SCD due to cardiac arrhythmia. Therapeutic measures to prevent SCD are also discussed.

Authors

Michael Rubart, Douglas P. Zipes

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Schematic illustration of intracellular Ca2+ cycling and associated seco...
Schematic illustration of intracellular Ca2+ cycling and associated second messenger pathways in cardiomyocytes (figure modified from ref. 84). AC, adenylyl cyclase; α, G protein subunit α; α-receptor, α-adrenergic receptor; β, G protein subunit β; β-receptor, β-adrenergic receptor; γ, G protein subunit γ; LTCC, L-type Ca2+ channel; CAMKII, Ca2+-calmodulin kinase II; I-1, inhibitor 1; NCX, Na+/Ca2+ exchanger; P, phosphate group; PLC, phospholipase C; PLN, phospholamban; PP1, protein phosphatase 1; PP2A, protein phosphatase 2A; SERCA2a, SR Ca2+-ATPase isoform 2a; T-tubule, transverse tubule.