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European Heart Journal 1994 15(Supplement D):145-154; doi:10.1093/eurheartj/15.suppl_D.145
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Biochemical and Electrophysiological Alterations Underlying Ventricular Arrhythmias in the Failing Heart

S. M. Pogwizd and P. B. Corr

Department of Internal Medicine, Cardiovascular Division and Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis Missouri, U.S.A.

Correspondance: Dr Steven M Pogwizd. Washington University School of Medicine. Cardiovawular Division. Box 8086.660 South Eudid Avenue. St. Louis, MO 63110, U.S.A.

Our understanding of the electrophysiological and biochemical mechanism underlying malignant ventricular arrhythmias in the setting of heart failure has been limited, in large part because of the lack of experimental preparations of heart failure that demonstrate spontaneously occurring ventricular arrhythmias Recent 3-dimensional cardiac mapping studies in experimental preparations of heart failure, as well as the failing human heart, have demonstrated that focal non-reentrant mechanisms may underlie ventricular tachycardia occurring spontaneously or induced by programmed electrical stimulation This non-reentrant activation may be due to triggered activity arising from delayed after depolarization. Alterations of calcium homeostasis in the failing heart involving a number of ionic channels and membrane transporters may contribute to increased levels of intracellular calcium and the activation of a transient inward current. Modulation of calcium flux by and padrenergic stimulation may impact significantly on development of arrhythmias in the failing heart. Activation of the renin-angiotensin system and the generation of free radicals may also contribute. A thorough understanding of the underlying electrophysiological and biochemical alterations responsible for arrhythmogenesis in the failing heart will be critical for the development of therapeutic agents to prevent suddent death in patients with congestive heart failure.

Key Words: Ventricular tachycardia • cardiomyopathy • calcium • sympathetic nervous system


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