Satoh T, Zipes D P
Krannert Institute of Cardiology, Indiana University, School of Medicine, Indianapolis 46202-4800, USA.
J Cardiovasc Electrophysiol. 1996 Sep;7(9):833-42. doi: 10.1111/j.1540-8167.1996.tb00596.x.
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.
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 and 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 169 +/- 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 (AV) (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 infusion, but induced in all five dogs after saline infusion.
Atrial ERP in the thin right atrial free wall exceeds the ERP of the thick crista terminalis, and an increase in atrial pressure produced by saline infusion exaggerates this difference 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.
我们之前已经表明，急性心房扩张会延长心房不应期。我们推测这种不应期的增加可能是不均匀的，并且可能会产生导致心房颤动的电生理基质。本研究的目的是验证这一假设。
我们研究了23只麻醉开胸犬。将双极插入电极置于右心房内侧游离壁（薄区域）和右心房下部界嵴（厚区域）。还在左心室心尖放置了两个双极插入电极用于刺激和记录。使用心房期外刺激法（A1A2）以两种方式在一组9只犬中测量心房有效不应期（ERP）：在心房起搏（AP）期间以及在实现房室（AV）间期为0毫秒（AV = 0）的同时房室起搏期间。以1升/小时的速度静脉输注生理盐水以升高右心房压力并使右心房伸展。在输注生理盐水前后测量心房ERP。为了比较容量超负荷引起的心房伸展程度，在另一组6只犬的厚区域和薄区域植入了两对超声心动图换能器。在输注生理盐水前后测量超声心动图换能器所包围的面积。在另一组5只犬中，使用快速AP比较输注生理盐水前后心房颤动的诱发性。窦性心律时的心房压力在输注生理盐水后从5.1±0.96 mmHg增加到6.3±0.93 mmHg（P <0.01）。薄游离壁的ERP在（AV = 0时）从151±14.3毫秒增加到172±14.7毫秒，在（AP时）从169±12.0毫秒增加到170±14.3毫秒。厚界嵴的ERP在（AV = 0时）从134±9.9毫秒增加到147±10.2毫秒，在（AV时）从133±7.9毫秒增加到146±9.8毫秒（P <0.01）。薄游离壁中ERP的增加超过厚界嵴中的增加（P <0.01），增加了心房ERP的离散度。在输注500 mL生理盐水30分钟后，薄区域的面积增加为12.8％±3.7％，厚区域为3.5％±3.2％。在输注1000 mL生理盐水1小时后，薄区域的面积增加为18.8％±6.2％，厚区域为6.3±5.1％（P <0.01）。输注前没有任何犬诱发心房颤动，但输注生理盐水后所有5只犬均诱发心房颤动。
右心房薄游离壁的心房ERP超过厚界嵴的ERP，并且输注生理盐水引起的心房压力增加通过比厚区域更显著地拉伸心房心肌的薄段而夸大了这种差异。因此，心房伸展通过增加心房ERP的离散度，可能有助于心房颤动的发生发展。
