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Arrhythmia substrate and management in hypertrophic cardiomyopathy: from molecules to implantable card ioverter-defibrillators

M.J. Janse*,1 and J.M.T. De Bakker2

a Cardiovascular Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
b The Heart Lung Institute, University of Utrecht, Utrecht, The Netherlands

* Correspondence: Michiel J. Janse, Cardiovascular Research, Academic Medical Center J1–27, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.

Abstract

Ventricular arrhythmias and sudden death are among the characteristics of hypertrophic cardiomyopathy. Experience with the implantable cardioverter-defibrillator has shown that sudden death is caused by ventricular tachycardia or fibrillation. Several triggers for sudden death have been proposed: arrhythmias; ischaemia; and abnormal response to exercise. The substrates for arrhythmias includes hypertrophy itself, predisposing to triggered activity based on delayed afterdepolarizations; fibrosis, leading to abnormal, zig-zag conduction and fractionated extracellular electrograms; and abnormal distribution of gap junctions, especially in areas of myofibrillar disarray, which also may lead to conduction abnormalities. The latter two factors predispose to re-entry.

Key Words: Triggered activity • delayed afterdepolarizations • fibrosis • abnormal gap junction distribution • re-entry


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