OBJECTIVE:To determine the effects of ventricular pacing on the normal contraction sequence of the helical ventricular myocardial band, and its' impact on left ventricular function. METHODS:Ten pigs (25-68 kg) underwent analysis of percent segmental shortening (%SS) by sonomicrometry, with crystals placed along the fiber orientation of the ascending and descending segments, and posterior LV wall of the geometry of the helical heart. Unipolar pacing electrodes stimulated either the right atrium (RA), right ventricular apex (RVA) and outflow tract (RVOT), or posterior LV wall. Systemic hemodynamics, QRS-interval, cardiac index (CI), systolic and diastolic LV function and pressure-dimension (P-D) loops were analyzed and cardiac motion was monitored by video analysis. RESULTS:Normal sinus heart rate (NSR) was elevated from 84+/-15 beats/min to 113+/-22 beats/min by pacing (p<0.05). The variables of NSR were not changed by atrial pacing. Conversely, compared with NSR, ventricular pacing (RVA, RVOT, LV) significantly (p<0.05) prolonged the QRS-interval (94-111 ms vs 52+/-7 ms, p<0.05) decreased mean arterial pressure (46-47 mmHg vs 62+/-11 mmHg), CI (2.7-3.4 L/(min m2) vs 4.9+/-0.9L/(min m2)) and systolic LV pressure (56-61 mmHg vs 92+/-10 mmHg). Furthermore, ventricular pacing decreased peak +dP/dt and -dP/dt (p<0.05) and lowered PRSW to 59-77%, with most profound change after RVA pacing (p<0.05). Each ventricular pacing intervention decreased SS% significantly in the descending, ascending, and posterior LV segments compared with NSR. Disruption of the normal NSR sequence of shortening (progression from descending to posterior to ascending regions) followed each pacing intervention. Changes were characterized by premature stimulation of the segment adjacent to the pacer stimulus, with associated (1) decrease of pressure-dimension loop area, (2) desynchronization of P-D loops and (3) consistent loss of the twisting pattern of visible cardiac motion. CONCLUSIONS:Ventricular pacing disrupts the natural sequence of shortening along the myocardial band, and the resultant dyssynchrony impairs LV function.

译文

目的:确定心室起搏对正常人螺旋形心肌心肌收缩序列的影响及其对左心室功能的影响。
方法:十只猪(25-68公斤)通过体测法进行节段缩短百分比(%SS)的分析,晶体沿上升节段和下降节段的纤维方向放置,并且螺旋心的几何形状位于左后壁。单极起搏电极刺激右心房(RA),右心室尖(RVA)和流出道(RVOT)或左后壁。分析系统的血液动力学,QRS间隔,心脏指数(CI),收缩压和舒张压LV功能以及压力尺寸(P-D)回路,并通过视频分析监测心脏运动。
结果:正常窦性心率(NSR)通过起搏从84 / -15拍/分钟提高到113 / -22拍/分钟(p <0.05)。 NSR的变量不会因心房起搏而改变。相反,与NSR相比,心室起搏(RVA,RVOT,LV)显着(p <0.05)延长了QRS间隔(94-111 ms vs 52 / -7 ms,p <0.05)降低了平均动脉压(46-47) mmHg vs 62 / -11 mmHg),CI(2.7-3.4 L /(min m2)vs 4.9 /-0.9L/(min m2))和收缩压LV压力(56-61 mmHg vs 92 / -10 mmHg)。此外,心室起搏可降低峰值dP / dt和-dP / dt(p <0.05),PRSW降低至59-77%,RVA起搏后变化最大(p <0.05)。与NSR相比,每次心室起搏干预在LV下降段,上升段和后段均显着降低SS%。每次起搏干预后,正常NSR缩短序列(从下降区域到后区域再到上升区域的进展)的破坏。变化的特征是过早刺激了与起搏器刺激相邻的节段,并伴有(1)压力环面积的减小,(2)P-D环的失步和(3)可见心脏运动扭曲模式的持续丧失。
结论:心室起搏破坏了沿心肌带缩短的自然顺序,并且由此引起的不同步性损害了左室功能。

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