Tomioka Hideyuki, Liakopoulos Oliver J, Buckberg Gerald D, Hristov Nikola, Tan Zhongtuo, Trummer Georg
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:S198-206. doi: 10.1016/j.ejcts.2006.02.051. Epub 2006 Mar 24.
To investigate the effect of biventricular and high septal 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, descending segments, and posterior LV wall within the spatial geometry of the helical heart. Unipolar pacing electrodes stimulated the right atrium (RA) and either the right ventricular apex and left ventricular posterior wall (atrio-biventricular), or the proximal high septum (atrio-high septal). Systemic hemodynamics, QRS-interval, cardiac index (CI), systolic and diastolic LV functions and pressure-dimension loops (P-D) were analyzed and cardiac motion was monitored by video analysis.
Pacing increased normal sinus heart rate (NSR) from 77+/-9 beats/min to 98+/-5 beats/min. Atrial pacing did not change the NSR hemodynamic variables. Conversely, atrio-biventricular pacing prolonged the QRS-interval (91+/-14 ms vs 56+/-11 ms at baseline, p<0.05) and decreased mean arterial pressure (50+/-4 mmHg vs 58+/-12 mmHg), CI (3.4+/-0.3 L/(min m2) vs 4.0+/-0.8 L/(min m2)) and PRSW (71+/-25%) compared to NSR (p<0.05). Furthermore, atrio-biventricular pacing decreased SS% in all segments, especially at the LV posterior wall (71% of baseline, p<0.05), and disrupted the NSR shortening sequence (progression from descending to posterior to ascending regions). Changes were characterized by premature stimulation of the posterior wall 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. In contrast, atrio-high septal pacing restored systemic hemodynamics, LV systolic and diastolic functions to baseline values and preserved the normal sequence of shortening of the ventricular myocardial band.
(1) Biventricular pacing disrupts of the natural sequence of shortening of the myocardial band and results in impaired LV function. (2) High septal pacing preserves the sequential shortening pattern of the myocardial band and LV function.
探讨双心室起搏和高位室间隔起搏对螺旋形心室心肌带正常收缩顺序的影响及其对左心室功能的作用。
10头猪(体重25 - 68千克)通过超声心动图分析节段缩短百分比(SS%),将晶体沿螺旋形心脏空间几何结构内升段、降段及左心室后壁的纤维方向放置。单极起搏电极刺激右心房(RA)以及右心室心尖和左心室后壁(房室双心室起搏)或近端高位室间隔(房室高位室间隔起搏)。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 - 维度环(P - D),并通过视频分析监测心脏运动。
起搏使正常窦性心率(NSR)从77±9次/分钟增加到98±5次/分钟。心房起搏未改变NSR血流动力学变量。相反,房室双心室起搏延长了QRS间期(基线时为56±11毫秒,起搏后为91±14毫秒,p<0.05),并降低了平均动脉压(58±12毫米汞柱对50±4毫米汞柱)、CI(4.0±0.8升/(分钟·平方米)对3.4±0.3升/(分钟·平方米))以及与NSR相比的PRSW(71±25%)(p<0.05)。此外,房室双心室起搏使所有节段的SS%降低,尤其是左心室后壁(降至基线的71%,p<0.05),并打乱了NSR缩短顺序(从降段到后壁再到升段区域的进展)。这些变化的特征是与起搏刺激相邻的后壁节段过早受刺激,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。相比之下,房室高位室间隔起搏使全身血流动力学、左心室收缩和舒张功能恢复到基线值,并保留了心室心肌带缩短的正常顺序。
(1)双心室起搏打乱了心肌带缩短的自然顺序,导致左心室功能受损。(2)高位室间隔起搏保留了心肌带的顺序缩短模式和左心室功能。