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RIGHT HEART INTERACTION WITH LEFT VENTRICULAR ASSISTANCE

RIGHT HEART INTERACTION WITH LEFT VENTRICULAR ASSISTANCE
右心与左心室辅助的相互作用
批准号:
3343510
负责人:
DAVID J FARRAR
金额:
$13.29万
依托单位国家:
美国
项目类别:
财政年份:
1985
资助国家:
美国
项目状态:
已结题
起止时间:
1985-03-01 至 1988-02-29

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中文摘要
翻译
大约20 - 30%的患者植入了机械左心室 心室辅助装置(LVAD)治疗顽固性心力衰竭 在我们中心和其他中心的心脏直视手术中, 右心衰竭 问题的原因是不知道,但两个 可能性是:1)右室间隔贡献减少 左心室(LV)卸载期间的心室(RV)收缩,和2) 由LVAD引起的静脉回流增加使边缘 RV导致失效。 为了在对照研究中评估这个问题,我们将确定 急性麻醉犬准备中LV辅助的RV功能 使用搏动囊型心室辅助装置 对全球和 使用压力、流量和尺寸测量的区域RV功能, 将测量前负荷、后负荷、收缩性和心率。 数据将 在实验期间,在控制和LV辅助条件下采集 干预措施旨在模拟一系列病理生理和生理 条件 测量心房、心室和动脉压, 肺动脉血流量和心脏尺寸使用超声 将对隔膜以及RV和LV游离壁中的晶体进行取样, 通过计算机分析。 RV功能曲线和RV压力-尺寸 在有和没有LV辅助的情况下, 控制静脉回流和肺动脉束带的变化, 广泛的RV前负荷和后负荷。 在选定的狗群中, 将在间隔和/或RV游离壁缺血期间重复研究, 通过结扎右冠状动脉和/或心脏的隔分支, 左冠状动脉,伴或不伴由 冠脉内利多卡因 使用该IV辅助模型,我们将评估RV功能并测试 主要假设是在间隔缺血的心脏中,右心室游离壁 局部缺血和/或整体心脏抑制,LV辅助导致 RV功能受损,且完全LV卸载进一步 对RV有害。 这些急性动物制剂研究将 补充我们的临床LVAD项目 最终,我们希望利用这个 知识,以改善病人的选择和治疗, 终末期心脏长期植入LVAD的成功应用 失败
英文摘要
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.
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