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Circ Res. 2015 Jun 5;116(12):1937-55. doi: 10.1161/CIRCRESAHA.116.304691.

Mechanisms of sudden cardiac death: oxidants and metabolism.

Author information

1
From the Department of Pharmacology (K.-C.Y.) and Division of Cardiology, Department of Internal Medicine (K.-C.Y.), National Taiwan University Hospital, Taipei, Taiwan; Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.W.K., J.C.M.); and Lifespan Cardiovascular Institute, the Providence VA Medical Center, and Brown University, RI (S.C.D.).
2
From the Department of Pharmacology (K.-C.Y.) and Division of Cardiology, Department of Internal Medicine (K.-C.Y.), National Taiwan University Hospital, Taipei, Taiwan; Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.W.K., J.C.M.); and Lifespan Cardiovascular Institute, the Providence VA Medical Center, and Brown University, RI (S.C.D.). samuel_dudley@brown.edu jcm@medicine.wisc.edu.

Abstract

Ventricular arrhythmia is the leading cause of sudden cardiac death (SCD). Deranged cardiac metabolism and abnormal redox state during cardiac diseases foment arrhythmogenic substrates through direct or indirect modulation of cardiac ion channel/transporter function. This review presents current evidence on the mechanisms linking metabolic derangement and excessive oxidative stress to ion channel/transporter dysfunction that predisposes to ventricular arrhythmias and SCD. Because conventional antiarrhythmic agents aiming at ion channels have proven challenging to use, targeting arrhythmogenic metabolic changes and redox imbalance may provide novel therapeutics to treat or prevent life-threatening arrhythmias and SCD.

KEYWORDS:

cardiac arrhythmias; death, sudden, cardiac; metabolism; oxidative stress

PMID:
26044249
PMCID:
PMC4458707
DOI:
10.1161/CIRCRESAHA.116.304691
[Indexed for MEDLINE]
Free PMC Article

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