Exercise-induced ventricular arrhythmias in patients with no structural cardiac disease.
We review the clinical and genetic disorders associated with exercise-induced ventricular arrhythmias in patients with normal hearts. Foremost are those with catecholaminergic polymorphic ventricular tachycardia due to abnormalities in either the ryanodine receptor 2 genes (RyR2) or the calsequestrin genes (CASQ). These patients manifest ventricular premature beats and polymorphic ventricular tachycardia in response to exercise or on exposure to catecholamines. A great deal of basic information has been accumulated suggesting that these arrhythmias are caused by abnormalities in Ca2+ metabolism. The ensuing cytosolic Ca2+ overload results in delayed after-depolarizations and extrasystolic Ca2+ waves, leading to polymorphic ventricular tachycardia. Most of these patients will respond to beta-blocker therapy but a significant minority (30%) will require a defibrillator. Advances in genetic testing allow better understanding of this syndrome.
Scheinman
Melvin M
MM
Department of Medicine, University of California San Francisco, San Francisco, California 94143, USA. scheinman@medicine.ucsf.edu
Lam
Jason
J
D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000502:physiology; D002395:Catecholamines / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology
D015220:Calcium Channels; D002395:Catecholamines; D002118:Calcium