What is the clinical evidence from this study?

Study design: Observational. Population: Catecholaminergic polymorphic ventricular tachycardia (CPVT) (n=8). Intervention: Catecholaminergic polymorphic ventricular tachycardia (CPVT). Primary outcome: Frequency of sinus node dysfunction and inducible atrial tachyarrhythmias.

January 1, 2007Circulation Journal132 citationsOpen Access

Association of Atrial Arrhythmia and Sinus Node Dysfunction in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia

NSNaokata Sumitomo HSHarumizu Sakurada KTKazuo Taniguchi

Key Result

Patients with CPVT frequently exhibit sinus node dysfunction and inducible atrial tachyarrhythmias, indicating that the disease's arrhythmogenic substrate involves supraventricular tissues.

Study Design

Type

Observational (n=8)

Structured PICO

Population

8 patients (mean age 16.8 years, 87.5% female) with catecholaminergic polymorphic ventricular tachycardia referred for arrhythmia evaluation who underwent electrophysiological study.

Exposure

Electrophysiological study including low-rate atrial pacing and isoproterenol infusion

Outcome

Frequency of supraventricular arrhythmia and sinus node (SN) dysfunctionsurrogate

Patients with CPVT frequently exhibit sinus node dysfunction and inducible atrial tachyarrhythmias, suggesting the disease pathogenesis involves broader regions of the heart beyond the ventricular myocardium.

Limitations

Extremely small number of patients limits the electrophysiologic findings
Sinus node recovery time and sino-atrial conduction time could change with age and maturation of autonomic tone
The entire RyR2 gene was not analyzed (only 33 of the 105 exons)

Abstract

BACKGROUND: This study was performed to investigate the frequency and importance of supraventricular arrhythmia and sinus node (SN) dysfunction in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT). METHODS AND RESULTS: Eight patients with CPVT (mean age: 16.8+/-8.1 years) underwent an electrophysiological study. SN recovery time (1,389+/-394 ms) was slightly prolonged, and 4 of 8 patients had abnormal values. Atrial flutter (AF) was induced by low-rate atrial pacing in 2 patients and by isoproterenol infusion in 1 patient. Atrial fibrillation (Af) was induced by isoproterenol infusion in 2 patients. One patient presented with Af during the follow-up period, and 2 of 4 patients with AF/Af presented with increased SN recovery time. CONCLUSIONS: Patients with CPVT frequently have associated with SN dysfunction, and inducible atrial tachyarrhythmias, which indicate that the pathogenesis of CPVT is limited not only to the ventricular myocardium, but also to broad regions of the heart, including the SN and atrial muscle.

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