RIGHT HEART INTERACTION WITH LEFT VENTRICULAR ASSISTANCE

约20%至30%的患者植入了机械左 心脏辅助装置(LVAD)治疗顽固性心力衰竭 在我们中心和其他中心的心内直视手术有并发症 右心衰竭。这个问题的原因尚不清楚，但有两个 可能的情况是：1)右间隔贡献减少 左心室(LV)卸载时的右室收缩，以及2) 左前降支引起的静脉回流增加使边缘不堪重负 房车造成故障。 为了在对照研究中评估这个问题，我们将确定 急性麻醉犬在左心室辅助下的右室功能 使用脉动囊型VAD。详细评估全球和 使用压力、流量和尺寸测量的区域RV函数 将测量前负荷、后负荷、收缩能力和心率。数据将 在实验期间，在控制和LV辅助条件下收集 旨在模拟一系列病理生理学和生理学的干预措施 条件。测量房室和动脉的压力， 应用超声测量肺动脉血流量和心脏内径 间隔和RV和LV游离壁中的晶体将被取样并 用计算机进行分析。RV函数曲线和RV压力-尺寸 有无LV援助的关系将在#年确定 静脉回流和肺动脉环扎的可控性变化 广泛的房车预载和后载。在选定的几组狗中， 在间隔和/或右室游离壁缺血期间将重复研究，产生 结扎右冠状动脉和/或右冠状动脉隔支 左冠状动脉，伴或不伴全球心脏压低 冠状动脉内注射利多卡因。 使用该模型的LV辅助，我们将评估RV功能和测试 主要假说在间隔缺血的心脏中，右室游离壁 缺血和/或全身性心脏抑制，LV辅助会导致 RV功能受损，完全LV卸载进一步 对房车不利。这些在急性动物制剂中的研究将 补充我们的临床LVAD计划。最终我们希望使用这一点 改善患者选择和治疗的知识，并促进 慢性植入LVAD在终末期心脏中的成功应用 失败了。

Approximately 20 to 30% of patients implanted with mechanical left ventricular assist devices (LVADs) for refractory cardiac failure after open heart surgery at our center and at others have had complications of right heart failure. The cause of the problem is not known but two possibilities are: 1) there is reduced septal contribution to right ventricular (RV) contraction during left ventricular (LV) unloading, and 2) the increased venous return resulting from the LVAD overloads the marginal RV resulting in failure. In order to evaluate this problem in a controlled study, we will determine RV function with LV assistance in an acute anesthetized dog preparation using a pulsatile sac-type VAD. Detailed evaluations of global and regional RV function using pressure, flow, and dimensional measurements of preload, afterload, contractility, and heart rate will be made. Data will be collected under control and LV assist conditions during experimental interventions designed to model a range of pathophysiologic and physiologic conditions. Measurements of atrial, ventricular, and arterial pressure, pulmonary artery blood flow, and cardiac dimensions using ultrasonic crystals in the septum and RV and LV free walls, will be sampled and analyzed by computer. RV function curves and RV pressure-dimension relations with and without LV assistance will be determined during controlled changes in venous return and pulmonary artery banding to provide a wide range of RV preload and afterload. In selected groups of dogs the study will be repeated during septal and/or RV free wall ischemia, produced by ligation of the right coronary artery and/or the septal branch of the left coronary artery, with or without global cardiac depression produced by intracoronary lidocaine. Using this model of lV assistance we will evaluate RV function and test the major hypothesis that in hearts with septal ischemia, RV free wall ischemia, and/or global cardiac depression, LV assist results in an impairment of RV function, and that complete LV unloading is further detrimental to the RV. These studies in an acute animal preparation will complement our clinical LVAD program. Ultimately we wish to use this knowledge to improve patient selection and treatment and to promote successful utilization of chronically implanted LVADs for end stage heart failure.