Abernathy W S, Ferrier G R, Moe G K
Am Heart J. 1978 Apr;95(4):489-96. doi: 10.1016/0002-8703(78)90241-7.
The mechanism by which atrial systeole influences the efficacy of ventricular capture by a failing pacemaker was investigated in 12 dogs with atrioventricular heart block. Atrial systole caused facilitation of ventricular capture in eight dogs, and inhibition of capture in 10 dogs. Interpolating atrial extrasystoles caused an enhancement or depression of the hemodynamic performance of the atrial systole that affected the efficacy of the pacemaker stimulus. These interpolation experiments showed that atrial systole influenced the efficacy of capture by a mechanical mechanism and not by an electrotonic mechanism. Atrial systole probably caused motion of the endocardial pacing catheter and/or ventricular myocardium. This motion increased or decreased the contact between the pacing electrode and the endocardium with subsequent changes in the efficacy of capture. In three dogs with pacing through epicardial electrodes, atrial systole had no effect on the efficacy of capture.
在12只患有房室传导阻滞的犬中，研究了心房收缩影响功能衰竭起搏器心室夺获效能的机制。心房收缩在8只犬中促进了心室夺获，而在10只犬中抑制了夺获。插入房性期前收缩导致影响起搏器刺激效能的心房收缩血流动力学表现增强或减弱。这些插入实验表明，心房收缩通过机械机制而非电紧张机制影响夺获效能。心房收缩可能导致心内膜起搏导管和/或心室心肌运动。这种运动增加或减少了起搏电极与心内膜之间的接触，进而使夺获效能发生改变。在3只通过心外膜电极起搏的犬中，心房收缩对夺获效能没有影响。
