Effect of the atrioventricular relationship on atrial refractoriness in humans.
Atrial arrhythmias occur frequently in the setting of increased atrial size and pressure. This may result from contraction-excitation feedback. The objective of this study was to investigate the effect of alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness, and on the frequency of induction of atrial fibrillation. Twenty-seven patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory period (ARP) were measured during AV pacing at a cycle length of 400 msec and AV intervals of 0, 120, and 160 msec. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined during continuous pacing using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval was increased from 0 to 160 msec, the peak right atrial pressure decreased from 16 +/- 4 mmHg to 7 +/- 3 mmHg and the mean right atrial pressure decreased from 7 +/- 3 mmHg to 3 +/- 22 mmHg (P less than 0.001). The atrial ERP and ARP did not change with alterations in the AV interval. There was no difference in the frequency of induction of atrial fibrillation. Similar results were obtained during autonomic blockade. These findings suggests that the phenomenon of contraction-excitation feedback may not be of importance in the development of atrial arrhythmias in patients without structural heart disease.
Calkins
H
H
University of Michigan Medical Center, Division of Cardiology, Ann Arbor 48109-0022.
el-Atassi
R
R
Leon
A
A
Kalbfleisch
S
S
Borganelli
M
M
Langberg
J
J
Morady
F
F
D000328:Adult; D001281:Atrial Fibrillation / Q000503:physiopathology*; D016275:Atrial Function / Q000502:physiology*; D001283:Atrioventricular Node / Q000502:physiology*; D001285:Atropine; D001341:Autonomic Nervous System / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D004594:Electrophysiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D011433:Propranolol
D001285:Atropine; D011433:Propranolol