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实验性右心室缺血期间左心室支持对右心室力学的影响。

Effects of left ventricular support on right ventricular mechanics during experimental right ventricular ischemia.

作者信息

Moon M R, Castro L J, DeAnda A, Daughters G T, Ingels N B, Miller D C

机构信息

Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, CA 94305.

出版信息

Circulation. 1994 Nov;90(5 Pt 2):II92-101.

PMID:7955292
Abstract

BACKGROUND

Left ventricular (LV) assist device (LVAD) support has been associated with right ventricular (RV) failure in humans, but the etiology remains unknown. Mechanical LV support apparently does not induce RV pump failure in normal hearts, but controlled studies of LV assistance in hearts with preexistent RV dysfunction have been limited. Therefore, this study was performed to determine if LVAD support impairs RV systolic mechanics during acute RV ischemia.

METHODS AND RESULTS

Five closed-chest, autonomically blocked, sedated dogs were studied after placement of an LVAD (LV-femoral artery bypass), right coronary artery (RCA) occluder, and 27 miniature radiopaque tantalum markers into the LV and RV walls for independent computation of RV and LV volumes. Biplane videofluoroscopic marker images and hemodynamic data were recorded before RCA occlusion with the LVAD off (maximum LV pressure [LVPmax] = 119 +/- 25 mm Hg), after 3 minutes of RCA occlusion with the LVAD off (LVPmax = 84 +/- 18 mm Hg), and then with the LVAD on (LVPmax = 26 +/- 32 mm Hg). Global RV contractility (end-systolic elastance [RV Ees] and preload recruitable stroke work [RV PRSW]), RV power output, and the mechanical (pump) efficiency of converting potential energy to external work (ratio of RV stroke work/total pressure-volume area) were calculated. As expected, with RCA occlusion there were major decreases in RV Ees (from 2.5 +/- 1.2 to 1.4 +/- 0.5 mm Hg/mL, P < .005) and RV PRSW (15 +/- 4 versus 9 +/- 4 mm Hg, P < .001). RV power output (overall pump performance) declined by 39 +/- 20% (P < .025), and mechanical efficiency fell by 38 +/- 13% (P < .001). After initiation of mechanical LV support, however, there was no further impairment of RV contractility or power output (P > .80). Pulmonary artery input impedance (RV afterload) decreased from 848 +/- 628 to 673 +/- 577 dyne.sec-1.cm-5 (P < .01), which led to a 26 +/- 29% improvement in RV pump efficiency (P < .001).

CONCLUSIONS

While right coronary artery occlusion significantly reduced RV systolic performance, LVAD support during acute RV ischemia did not further impair RV contractility or power output. Furthermore, since RV afterload fell with LV unloading, the mechanical pump efficiency of the right ventricle actually improved. These observations demonstrate that LVAD support does not directly induce RV failure in canine hearts with acute isolated RV ischemia.

摘要

背景

左心室(LV)辅助装置(LVAD)支持与人类右心室(RV)衰竭相关,但其病因尚不清楚。机械性左心室支持在正常心脏中显然不会诱发右心室泵衰竭,但对于已有右心室功能障碍的心脏进行左心室辅助的对照研究有限。因此,本研究旨在确定LVAD支持在急性右心室缺血期间是否会损害右心室收缩力学。

方法与结果

对5只开胸、自主神经阻滞、镇静的犬进行研究,在其体内植入LVAD(左心室-股动脉旁路)、右冠状动脉(RCA)闭塞器,并在左心室和右心室壁内植入27个微型不透射线的钽标记物,用于独立计算右心室和左心室容积。在RCA闭塞前(LVAD关闭,最大左心室压力[LVPmax]=119±25mmHg)、RCA闭塞3分钟后(LVAD关闭,LVPmax=84±18mmHg)以及随后LVAD开启(LVPmax=26±32mmHg)时,记录双平面荧光透视标记物图像和血流动力学数据。计算右心室整体收缩性(收缩末期弹性[RV Ees]和可招募前负荷的搏功[RV PRSW])、右心室功率输出以及将势能转化为外部功的机械(泵)效率(右心室搏功/总压力-容积面积之比)。正如预期的那样,RCA闭塞后,RV Ees显著降低(从2.5±1.2降至1.4±0.5mmHg/mL,P<.005),RV PRSW也降低(15±4对9±4mmHg,P<.001)。右心室功率输出(整体泵性能)下降了39±20%(P<.025),机械效率下降了38±13%(P<.001)。然而,在开始机械性左心室支持后,右心室收缩性或功率输出没有进一步受损(P>.80)。肺动脉输入阻抗(右心室后负荷)从848±628降至673±577达因·秒-1·厘米-5(P<.01),这导致右心室泵效率提高了2

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