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J Am Coll Cardiol, 1999; 34:363-373 © 1999 by the American College of Cardiology Foundation |
a Department of Cardiology, University of Bonn, Bonn, Germany
Manuscript received September 21, 1998; revised manuscript received March 6, 1999, accepted April 15, 1999.
Reprint requests and correspondence: Dr. Burghard Schumacher, University Hospital Mannheim, University of Heidelberg, Theodor-Kutzer-Uber 1-3, 68167 Mannheim, Germany.
burghard.schumacher{at}med2.ma.uni-heidelberg.de
OBJECTIVES
In this study, the transverse conduction capabilities of the crista terminalis (CT) were determined during pacing in sinus rhythm in patients with atrial flutter and atrial fibrillation.
BACKGROUND
It has been demonstrated that the CT is a barrier to transverse conduction during typical atrial flutter. Mapping studies in animal models provide evidence that this is functional. The influence of transverse conduction capabilities of the CT on the development of atrial flutter remains unclear.
METHODS
The CT was identified by intracardiac echocardiography. The atrial activation at the CT was determined during programmed stimulation with one extrastimulus at five pacing sites anteriorly to the CT in 10 patients with atrial flutter and 10 patients with atrial fibrillation before and after intravenous administration of 2 mg/kg disopyramide. Subsequently, atrial arrhythmias were reinduced.
RESULTS
At baseline, pacing with longer coupling intervals resulted in a transverse pulse propagation across the CT. During shorter coupling intervals, split electrograms and a marked alteration of the activation sequence of its second component were found, indicating a functional conduction block. In patients with atrial flutter, the longest coupling interval that resulted in a complete transverse conduction block at the CT was significantly longer than that in patients with atrial fibrillation (285 ± 49 ms vs. 221 ± 28 ms; p < 0.05). After disopyramide administration, a transverse conduction block occurred at longer coupling intervals as compared with baseline (287 ± 68 ms vs. 250 ± 52 ms; p < 0.05). Subsequently, a sustained atrial arrhythmia was inducible in 15 of 20 patients. This was atrial flutter in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients.
CONCLUSIONS
It was found that the CT provides transverse conduction capabilities and that the conduction block during atrial flutter is functional. Limited transverse conduction capabilities of the CT seem to contribute to the development of atrial flutter.
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