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Radiofrequency catheter ablation for incessant atrioventricular nodal reentrant tachycardia normalized H-V block associated with tachycardia-induced cardiomyopathy

https://doi.org/10.1016/j.jelectrocard.2004.07.009Get rights and content

Abstract

A 30-year-old man was admitted for treatment of tachycardia-induced cardiomyopathy caused by incessant atrioventricular nodal reentrant tachycardia (AVNRT). An echocardiogram revealed dilatation of all cardiac chambers with severe globally depressed biventricular systolic function. During an electrophysiologic study, HV interval was prolonged to 118 ms by atrial extrastimulus and 2:1 HV block was documented during AVNRT. Four weeks after catheter ablation for AVNRT, an echocardiogram demonstrated regression of the wall motion abnormality of both ventricles and of their dimensions. In the electrophysiologic study, the HV conduction disturbance disappeared. So far, this is the first case in which tachycardia-induced cardiomyopathy was accompanied by transient His-Purkinje conduction abnormality.

Section snippets

Case

A 30-year-old man had a history of palpitation attacks which occurred several times per year and terminated within a few minutes. No cardiac abnormality had ever been identified during annual physical examinations. Three weeks before admission to our hospital, the frequency of his palpitation attack increased and he complained of coincident dyspnea and fainting, upon admission to another hospital. An electrocardiogram displayed supraventricular tachycardia at a rate of 200 beats/min. He was

Discussion

A state resembling dilated cardiomyopathy can be induced by atrial fibrillation with rapid ventricular responses 3, 5, 7, atrial tachycardia 8, 9, accessory pathway reciprocating tachycardias (6), and AVNRT3, 10. Termination of the tachycardia leads to a regression of myocardial dysfunction. The precise mechanisms responsible for the so-called tachycardia-induced cardiomyopathy have not been elucidated. Hypotheses include depletion of myocardial high-energy phosphate stores 1, 11, altered

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    2016, HeartRhythm Case Reports
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    To our knowledge, this is the first report of typical AVNRT provoking tachycardia-induced cardiomyopathy in an otherwise healthy individual and the first description of AVNRT associated with intracardiac thrombosis and pulmonary emboli. Although supraventricular tachycardia typically presents with palpitations and shortness of breath, heart rates ≥170 beats/min are more likely to be associated with disabling symptoms such as syncope and dizziness.3–6 Since AVNRT is almost always associated with palpitations, is often self-remitting, and rarely goes unrecognized for weeks on end, tachycardia-induced ventricular dilation and dysfunction appear to be exceedingly rare.

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