Leeuwenburgh Boudewijn P J, Helbing Willem A, Steendijk Paul, Schoof Paul H, Baan Jan
Departments of Pediatric Cardiology, Cardiology, CardioThoracic Surgery, Leiden University Medical Center, The Netherlands.
J Thorac Cardiovasc Surg. 2003 Mar;125(3):481-90. doi: 10.1067/mtc.2003.28.
Right ventricular pressure overload occurs in several types of (congenital) heart disease, as well as in pulmonary disease. Clinical outcome in some of these patient groups might in part be related to left ventricular loading conditions. The effects of left ventricular unloading on the function of the hypertrophic right ventricle have not been studied. We aimed to study the effects of left ventricular unloading on right ventricular hemodynamics and contractility in an animal model of chronic right ventricular pressure overload.
In lambs the pulmonary artery was chronically banded to increase right ventricular pressure to systemic levels. After 8 weeks, right ventricular contractility and hemodynamic function were assessed in these lambs, as well as in age-matched control animals, by using a combined pressure-conductance catheter in the right ventricle during baseline conditions and during complete bypass of the left ventricle.
In both groups acute left ventricular unloading significantly decreased left ventricular pressure to low levels while aortic pressure was maintained. In the right ventricle of the control group, both end-systolic and end-diastolic volumes increased with left ventricular unloading (P <.01) while end-systolic pressure was maintained. Cardiac output was unchanged despite decreased right ventricular contractility. In the banding group acute left ventricular unloading also decreased right ventricular contractility but increased cardiac output. During acute left ventricular unloading, diastolic stiffness was unchanged in the control group, whereas it was significantly decreased in the banding group.
Both in normal hearts and in hearts subject to chronic right ventricular pressure overload, acute left ventricular unloading decreases right ventricular contractility. Although no effects on cardiac output are encountered in normal hearts during left ventricular bypass, cardiac output is improved in right ventricular pressure-overloaded hearts, most likely related to improved right ventricular diastolic compliance.
右心室压力超负荷发生于多种类型的(先天性)心脏病以及肺部疾病中。在其中一些患者群体中,临床结局可能部分与左心室负荷情况有关。左心室卸载对肥厚性右心室功能的影响尚未得到研究。我们旨在研究在慢性右心室压力超负荷动物模型中左心室卸载对右心室血流动力学和收缩性的影响。
对羔羊进行肺动脉长期束带术,以使右心室压力升高至体循环水平。8周后,在这些羔羊以及年龄匹配的对照动物中,通过在右心室使用压力 - 电导联合导管,在基线状态和左心室完全旁路期间评估右心室收缩性和血流动力学功能。
在两组中,急性左心室卸载均显著降低左心室压力至较低水平,同时维持主动脉压力。在对照组的右心室中,随着左心室卸载,收缩末期和舒张末期容积均增加(P <.01),而收缩末期压力保持不变。尽管右心室收缩性降低,但心输出量未改变。在束带组中,急性左心室卸载也降低了右心室收缩性,但增加了心输出量。在急性左心室卸载期间,对照组的舒张硬度未改变,而束带组的舒张硬度显著降低。
在正常心脏和慢性右心室压力超负荷的心脏中,急性左心室卸载均会降低右心室收缩性。尽管在左心室旁路期间正常心脏的心输出量未受影响,但右心室压力超负荷的心脏的心输出量会增加,这很可能与右心室舒张顺应性改善有关。