13th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 1998

January 24-31, 1998
Marilleva, Trento, Italy

RT-246

Changes in atrial effective refractory period in patients with induced atrial fibrillation

Andrzej Lubinski, Ewa Lewicka-Nowak, Maciej Kempa, Grzegorz Raczak, Grazyna Swiatecka.
II Department of Cardiology, Medical University of Gdansk, Poland

Abstract

There is evidence from recent experimental studies that pacing-induced atrial fibrillation modifies electrophysiological properties of atria by shortening of atrial refractory period. The present study was performed to assess the influence of induced atrial fibrillation (AF) on atrial effective refractory period (ERP) in patients with structural heart disease.
Method. The study was performed in 7 pts with coronary artery disease or dilated cardiomyopathy without spontaneous AF episodes in their history. AF was induced by fast atrial stimulation (300-1500/min). If sinus rhythm restored within 10 min AF was reinduced. Atrial ERP was measured during atrial pacing at basic cycle length of 550 msec, before AF induction and after its conversion to the sinus rhythm. After restoration of sinus rhythm a time course of atrial ERP recovery was assessed.
results. Atrial ERP before AF was 236 ± 22 msec. ERP shortening following AF was observed after 2 min of AF. After 9 min 30 sec (8 min 40 sec-10 min 50 sec) of AF ERP achieved minimal value of 145 ± 29 msec. ERP returned to the initial value during 9 min (6-10 min) after conversion of AF. A tendency to prolongation in duration of consecutive AF episodes and facilitation of their induction was observed.
Conclusion. The present study confirms that in humans short episodes of atrial fibrillation may markedly decrease duration of atrial refractoriness. In patients with structural heart disease atrial ERP shortening after AF was found to be reversible during approximately 10 min after arrhythmia termination.

Key Words

Atrial fibrillation - electrophisiology
pacing-induced AF, atrial effective refractory period, coronary artery disease, dilated cardiomyopathy, mechanisms of AF perpetuation, OA

 

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