Ravelli F, Allessie M
Medical Biophysics, Centro Materiali e Biofisica Medica, Trento, Italy.
Circulation. 1997 Sep 2;96(5):1686-95. doi: 10.1161/01.cir.96.5.1686.
Atrial fibrillation (AF) is frequently observed under conditions that are associated with atrial dilatation. The aim of this study was to investigate the effects of atrial dilatation on the substrate of AF.
In 15 Langendorff-perfused rabbit hearts, the interatrial septum was perforated, and after occlusion of the caval and pulmonary veins, biatrial pressure was increased by raising the level of an outflow cannula in the pulmonary artery. Right and left atrial effective refractory periods (AERPs), monophasic action potentials (MAPs), and inducibility of AF by single premature stimuli were measured as a function of atrial pressure. Increasing the atrial pressure from 0.5+/-0.7 to 16.2+/-2.2 cm H2O resulted in a progressive shortening of the right AERP from 82.2+/-9.8 to 48.0+/-5.1 ms. In the left atrium, an increase in pressure up to 7.4+/-0.3 cm H2O had no effect on the AERP. At higher pressures, however, the left AERP also shortened, from 67.5+/-7.5 to 49.3+/-2.0 ms. The duration of MAPs also decreased by an increase in atrial pressure, showing a high correlation with the shortening in AERP (r=.94, P<.01). All these changes were completely reversible within 3 minutes after release of the atrial stretch. Dilatation of the atria was a major determinant for the vulnerability to AF. The inducibility of AF increased from 0% at low pressures to 100% when the atrial pressure was >10 cm H2O. Release of the atrial wall stress resulted in prompt cardioversion of AF. The increased vulnerability for AF was highly correlated with the shortening in AERP (logistic regression r=.97). No correlation was found with the spatial dispersion between right and left AERPs.
Increased atrial pressure in the isolated rabbit heart resulted in a significant increase in vulnerability to AF that was closely correlated to shortening of the AERP. These changes were completely reversible within 3 minutes after release of the atrial stretch, resulting in prompt termination of AF.
心房颤动（AF）常在与心房扩张相关的情况下出现。本研究旨在探讨心房扩张对房颤基质的影响。
在15个经Langendorff灌注的兔心脏中，穿破房间隔，在腔静脉和肺静脉闭塞后，通过提高肺动脉流出插管的水平来增加双房压力。测量右心房和左心房有效不应期（AERPs）、单相动作电位（MAPs）以及单个早搏刺激诱发房颤的易感性，并将其作为心房压力的函数。将心房压力从0.5±0.7 cm H₂O升高至16.2±2.2 cm H₂O，导致右心房AERP从82.2±9.8毫秒逐渐缩短至48.0±5.1毫秒。在左心房，压力升高至7.4±0.3 cm H₂O时对AERP无影响。然而，在更高压力下，左心房AERP也缩短，从67.5±7.5毫秒缩短至49.3±2.0毫秒。MAPs的持续时间也因心房压力升高而缩短，与AERP缩短高度相关（r = 0.94，P < 0.01）。所有这些变化在解除心房牵张后3分钟内完全可逆。心房扩张是房颤易感性的主要决定因素。房颤的诱发率从低压时的0%增加到心房压力>10 cm H₂O时的100%。解除心房壁应力可使房颤迅速转复。房颤易感性增加与AERP缩短高度相关（逻辑回归r = 0.97）。未发现与左右心房AERP之间的空间离散度相关。
离体兔心脏中，心房压力升高导致房颤易感性显著增加，且与AERP缩短密切相关。这些变化在解除心房牵张后3分钟内完全可逆，从而使房颤迅速终止。
