Key result
Aberrant intracellular calcium handling, acute myocardial ischemia, neurohumoral changes, and genetic predisposition play key roles in the pathogenesis of sudden cardiac death due to cardiac arrhythmia.
This review highlights the role of aberrant intracellular calcium handling, acute myocardial ischemia, neurohumoral changes, and genetic predisposition in the pathogenesis of sudden cardiac death due to cardiac arrhythmia.
Advances mechanistic insights into sudden cardiac death; leaves open validation of genetic and calcium-handling targets for prevention.
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 Ca 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.
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Michael Rubart (2005) conducted a review in Sudden cardiac death. Aberrant intracellular calcium handling, acute myocardial ischemia, neurohumoral changes, and genetic predisposition play key roles in the pathogenesis of sudden cardiac death due to cardiac arrhythmia.
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