• John N Catanzaro, John Makaryus, Jonathan Vafai, Amgad N Makaryus, Ram Jadonath, and Stuart Beldner.
• Department of Cardiology, Division of Electrophysiology, North Shore University Hospital, Manhasset, New York 11030, USA.
• Tex Heart Inst J. 2009 Jan 1;36(4):352-4.

AbstractAtrioventricular nodal re-entry tachycardia is the most common form of regular paroxysmal tachycardia in the adult population. This tachycardia is a re-entrant rhythm that uses the anatomic location of the atrioventricular node and its surrounding perinodal atrial tissue. The simplest concept regarding the atrioventricular nodal physiology that allows re-entry is founded upon the postulated existence of 2 atrioventricular nodal pathways with different conduction velocities and refractory periods. Herein, we present the case of a 64-year-old man who had a history of paroxysmal atrial fibrillation; he had a permanent pacemaker for sick-sinus syndrome. He developed a tachycardia-induced cardiomyopathy with a perpetual dual response to the pacemaker stimulus. The tachycardia displayed characteristic dual atrioventricular-nodal physiology that was suppressed by amiodarone therapy, leading to a reversal of the cardiomyopathy. We discuss the mechanisms that surround such phenomena.

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