Septal function during left ventricular unloading.
Septal function during left ventricular unloading.
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DOI：
10.1161/01.cir.95.5.1320
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发表时间：
1997-03
期刊：
影响因子：
37.8
通讯作者：
M. Moon;A. Bolger;Abelardo DeAnda;M. Komeda;G. Daughters;S. Nikolic;D. C. Miller;N. Ingels
中科院分区：
文献类型：
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作者：
M. Moon;A. Bolger;Abelardo DeAnda;M. Komeda;G. Daughters;S. Nikolic;D. C. Miller;N. Ingels
背景：机械支持装置的左心室(LV)卸载可改变双室几何结构并损害右室(RV)收缩功能，但其对室间隔收缩功能的影响尚不清楚。方法与结果7只开胸麻醉犬，采用压力控制伺服机构从左房抽血，通过夹闭左房压力在0~-2 mm Hg范围内，突然降低左心房前负荷，以评价左心室容量和压力卸载对室间隔形态和功能的影响。阻断左房压力后，LV最大压力下降30+/-12%(平均+/-SD)(P<；0.0001)，LV舒张末横截面积(二维超声心动图测定)下降53+/-16%(P<；0.0001)。这导致室间隔左移(右室间隔游离壁内径增大；P<；.004)和变平(曲率半径增大；P<；.0002)，而左室间隔游离壁内径减小(P<；.0001)。室间隔舒张末厚度增加23+/-15%(P<；.0005)，反映室间隔前负荷下降。收缩期室间隔增厚减少(P<；0.002)，而收缩期室间隔输出量(间隔输出量=室间隔增厚×心率)从30+/-17降至15+/-22 cm/min(P<；.002)。这与沿间隔Frank-Starling等值(间隔输出量与舒张期末期间隔厚度[前负荷]的关系)向曲线中较少的部分移动有关。结论LV减负不仅改变了室间隔的几何形态，而且降低了室间隔的收缩厚度和心输出量，这可能是机械LV支持过程中右室收缩功能受损的原因之一。
BACKGROUND Left ventricular (LV) unloading with mechanical support devices alters biventricular geometry and impairs right ventricular (RV) contractility, but its effect on septal systolic function remains unknown. METHODS AND RESULTS To evaluate the effects of LV volume and pressure unloading on septal geometry and function, LV preload was abruptly reduced by clamping left atrial pressure between 0 and -2 mm Hg in seven open-chest, anesthetized dogs by use of a pressure-control servomechanism to withdraw blood from the left atrium. With left atrial pressure clamping, maximal LV pressure decreased 30 +/- 12% (mean +/- SD) (P < .0001) and LV end-diastolic cross-sectional area (determined by two-dimensional echocardiography) decreased by 53 +/- 16% (P < .0001). This caused the septum to shift toward the left (RV septal free-wall dimension increased; P < .004) and flatten (radius of curvature increased; P < .0002), while LV septal free-wall dimension fell (P < .0001). Septal end-diastolic thickness increased 23 +/- 15% (P < .0005), reflecting a decline in septal preload. Systolic septal thickening decreased (P < .002), while systolic septal output (Septal Output = Septal Thickening x Heart Rate) fell from 30 +/- 17 to 15 +/- 22 cm/min (P < .002). This was associated with movement along the septal Frank-Starling equivalent (septal output versus end-diastolic septal thickness [preload] relation) to a less productive portion of the curve. CONCLUSIONS LV unloading not only altered interventricular septal geometry but also reduced septal systolic thickening and output, all of which may contribute to impaired RV contractility during mechanical LV support.