Effect of experimentally induced atrial fibrillation on coronary circulation in dogs.

The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2-7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n = 10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78 +/- 6 vs. 75 +/- 5 ml/min X 100 g) while coronary vascular resistance (CVR) (1.16 +/- 0.05 vs. 0.87 +/- 0.07 [m Hg X min X 100 gl/ml [RU], p less than 0.0001) and sinus oxygen saturation (26 +/- 2 vs. 22 +/- 1%, p less than 0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311 +/- 48 vs. 205 +/- 30 ml/min X 100 g, p less than 0.01) and coronary sinus oxygen saturation (65 +/- 6 vs. 42 +/- 6%, p less than 0.01), while CVR (0.27 +/- 0.03 vs. 0.37 +/- 0.04 RU, p less than 0.0001) was 38 +/- 8% (p less than 0.0005) higher during atrial fibrillation than at sinus rhythm. When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n = 11), CBF (92 vs. 125 +/- 14 ml/min X 100 g, p less than 0.001) and sinus oxygen saturation (24 +/- 2 vs. 30 +/- 2%, p less than 0.0025) were higher and CVR (1.16 +/- 0.11 vs. 0.97 +/- 0.10 RU, p less than 0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233 +/- 24 vs. 168 +/- 16 ml/min X 100 g, p less than 0.0005) and sinus oxygen saturation (70 +/- 3 vs. 57 +/- 2%, p less than 0.0005), while CVR (0.25 +/- 0.02 vs. 0.46 +/- 0.02 RU, p less than 0.0005) was lower than during atrial fibrillation. Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.