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No immediate change to SCD prevention; leaves open integration of genetic and calcium-handling insights into risk models.
Despite recent findings on the functional, structural and genetic background of sudden cardiac death, the incidence is still relatively high in the entire population. A thorough knowledge on susceptibility, as well as pathophysiology behind the development of malignant arrhythmias will help us to identify individuals at risk and prevent sudden cardiac death. This article presents a review of the current literature on the role of altered intracellular Ca2+ handling, acute myocardial ischaemia, cardiac autonomic innervation, renin-angiotensin-aldosterone system, monogenic and complex heritability in the pathogenesis of sudden cardiac death.
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Simkó et al. (2012) studied this question.
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