Liakopoulos Oliver J, Tomioka Hideyuki, Buckberg Gerald D, Tan Zhongtuo, Hristov Nikola, Trummer George
Department of Surgery, Division of Cardiothoracic Surgery, David Geffen School of Medicine at University of California Los Angeles, 10833 Le Conte Avenue, 62-258 CHS, Los Angeles, CA 90095-1741, USA.
Eur J Cardiothorac Surg. 2006 Apr;29 Suppl 1:S188-97. doi: 10.1016/j.ejcts.2006.02.053. Epub 2006 Mar 24.
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.
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.
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.
Ventricular pacing disrupts the natural sequence of shortening along the myocardial band, and the resultant dyssynchrony impairs LV function.
确定心室起搏对螺旋状心室心肌带正常收缩序列的影响及其对左心室功能的影响。
十只猪(体重25 - 68千克)通过超声心动图分析法进行节段缩短百分比(%SS)分析,晶体沿螺旋状心脏几何结构的升段、降段及左心室后壁的纤维方向放置。单极起搏电极分别刺激右心房(RA)、右心室心尖部(RVA)、流出道(RVOT)或左心室后壁。分析全身血流动力学、QRS间期、心脏指数(CI)、左心室收缩和舒张功能以及压力 - 维度(P - D)环,并通过视频分析监测心脏运动。
起搏使正常窦性心率(NSR)从84±15次/分钟升高至113±22次/分钟(p<0.05)。心房起搏未改变NSR的各项变量。相反,与NSR相比,心室起搏(RVA、RVOT、LV)显著(p<0.05)延长QRS间期(94 - 111毫秒对52±7毫秒,p<0.05),降低平均动脉压(46 - 47毫米汞柱对62±11毫米汞柱)、CI(2.7 - 3.4升/(分钟·平方米)对4.9±0.9升/(分钟·平方米))以及左心室收缩压(56 - 61毫米汞柱对92±10毫米汞柱)。此外,心室起搏降低了峰值 +dP/dt和 -dP/dt(p<0.05),并使PRSW降至59 - 77%,RVA起搏后变化最为显著(p<0.05)。与NSR相比,每次心室起搏干预均显著降低了降段、升段及左心室后壁的SS%。每次起搏干预后均破坏了正常的NSR缩短序列(从降段到后壁再到升段区域的进展)。变化特征为紧邻起搏刺激部位的节段过早激动,并伴有(1)压力 - 维度环面积减小,(2)P - D环不同步,以及(3)可见心脏运动扭转模式持续丧失。
心室起搏破坏了沿心肌带的自然缩短序列,由此产生的不同步损害了左心室功能。