This study was supported in part by the Herman C. Krannert Fund, Indianapolis, Indiana; and Grant HL-52323-01 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
Unequal Atrial Stretch in dogs Increases Dispersion of Refractoriness Conducive to developing Atrial Fibrillation
Article first published online: 29 APR 2007
Journal of Cardiovascular Electrophysiology
Volume 7, Issue 9, pages 833–842, September 1996
How to Cite
SATOH, T. and ZIPES, D. P. (1996), Unequal Atrial Stretch in dogs Increases Dispersion of Refractoriness Conducive to developing Atrial Fibrillation. Journal of Cardiovascular Electrophysiology, 7: 833–842. doi: 10.1111/j.1540-8167.1996.tb00596.x
- Issue published online: 29 APR 2007
- Article first published online: 29 APR 2007
- Manuscript received 15 February 1996; Accepted for publication 15 April 1996
- atrial refractoriness;
- thick region;
- thin region;
- regional atrial stretch;
Atrial Stretch Precipitates Atrial Fibrillation. Introduction: We have shown previously that acute atrial dilation prolonged atrial refractoriness. We hypothesized that this increase in refractoriness might be heterogeneous and could create an electrophysiologic substrate leading to atrial fibrillation. The purpose of the present study was to test that hypothesis.
Methods and Results: We studied 23 anesthetized open chest dogs. Bipolar plunge electrodes were placed in the medial free wall of the right atrium (thin region) and in the lower crista terminalis of the right atrium (thick region). Two bipolar plunge electrodes were also placed in the left ventricular apex to stimulate and record. Atrial effective refractory period (ERP) was measured in a group of nine dogs using the atrial extrastimulus method (A1A2) in two ways: during atrial pacing (AP) and during simultaneous atrioventricular (AV) pacing that achieved an AV interval of 0 msec (AV = 0). One liter/hour of normal saline was infused intravenously to elevate right atrial pressure and produce right atrial stretch. Atrial ERPs were measured before and after the normal saline infusion. To compare the extent of atrial stretch produced by volume overload, two pairs of sonomicrometer transducers were implanted in the thick and thin regions in a separate group of six dogs. The area encompassed by sonomicrometers was measured before and after saline infusion. The inducibility of atrial fibrillation was compared before and after saline infusion using rapid AP in another group of five dogs. Atrial pressure during sinus rhythm increased from 5.1 ± 0.96 mmHg to 6.3 ± 0.93 mmHg after normal saline infusion (P < 0.01). ERP increased in the thin free wall from 151 ± 14.3 to 172 ± 14.7 msec (AV = 0), and from 149 ± 12.0 to 170 ± 14.3 msec (AP). ERP increased in the thick crista terminalis from 134 ± 9.9 to 147 ± 10.2 msec (AV = 0), and from 133 ± 7.9 to 146 ± 9.8 msec (AP) (P < 0.01). The increase in ERP in the thin free wall exceeded that in the thick crista terminalis (P < 0.01), increasing the dispersion of atrial ERP. After 500-mL saline infusion for 30 minutes, the increase of area in the thin region was 12.8%± 3.7%, and that in the thick was 3.5%± 3.2%. The increase of the area in the thin region after 1000 mL for 1 hour was 18.8%± 6.2%. and that in the thick region was 6.3%± 5.1% (P < 0.01). Atrial fibrillation was not induced in any dog before saline infusion, hut induced in all five dogs after saline infusion.
Conclusions: Atrial ERP in the thin right atrial free wall exceeds the ERP of the thick cristaterminalis, and an increase in atrial pressure produced by saline infusion exaggerates this ditterence by stretching thin segments of the atrial myocardium more than it stretches thick regions. Thus, atrial stretch, by increasing the dispersion of atrial ERP, may be conducive to the development of atrial fibrillation.