Farrar D J, Chow E, Compton P G, Foppiano L, Woodard J, Hill J D
Department of Cardiovascular Surgery, Pacific Presbyterian Medical Center, San Francisco, CA 94120.
J Thorac Cardiovasc Surg. 1991 Oct;102(4):588-95.
Systolic ventricular interactions may be partially responsible for right ventricular failure that sometimes occurs during clinical use of prosthetic left ventricular assist devices. In this hypothesis, it is proposed that the left ventricular assist device reduces left ventricular pressure and its contribution to right ventricular performance, thus impairing right ventricular output. On the other hand, these effects may be small compared with other causes of right ventricular failure such as ischemia. To test the systolic interaction hypothesis in the normal and ischemic right ventricle, we used a left ventricular assist device to pressure unload the left ventricle of anesthetized pigs, and we compared its effect on right heart function before and after 2 minutes of acute right coronary artery occlusion as a model of right heart failure. Pigs were instrumented for measurements of septal to left ventricular and right ventricular free wall dimensions with ultrasonic crystals, ventricular chamber pressures, and cardiac output with a pulmonary artery blood flow probe. Without right ventricular ischemia, the left ventricular assist device produced an 80% +/- 6% reduction in left ventricular pressure-time integral while maintaining aortic pressure. This resulted in a leftward septal shift with an 11.6% +/- 1.8% decrease in left ventricular septal-to-free wall dimension and a 12.5% +/- 2.4% increase in right ventricular septal-to-free wall dimension, with no changes in right ventricular cardiac output or stroke work. In contrast, right coronary artery occlusion alone produced right heart failure, with a 50% +/- 6% reduction in right ventricular global stroke work and 26% +/- 6% and 27% +/- 3% reductions in cardiac output and right ventricular peak systolic pressure, respectively. This right heart failure persisted during left ventricular unloading with the left ventricular assist device, which resulted in further leftward septal shifting and unchanged but still depressed stroke work and flow output. These findings support the hypothesis that a preexisting pathologic condition is the dominant factor in determining right ventricular function during prosthetic left ventricular support and that direct anatomic interactions play a minor role.
收缩期心室相互作用可能是临床使用人工左心室辅助装置时有时会发生的右心室衰竭的部分原因。在这一假说中，有人提出左心室辅助装置会降低左心室压力及其对右心室功能的贡献，从而损害右心室输出。另一方面，与右心室衰竭的其他原因（如缺血）相比，这些影响可能较小。为了在正常和缺血的右心室中检验收缩期相互作用假说，我们使用左心室辅助装置对麻醉猪的左心室进行压力卸载，并将急性右冠状动脉闭塞2分钟前后其对右心功能的影响进行比较，急性右冠状动脉闭塞作为右心衰竭的模型。对猪进行仪器植入，以便用超声晶体测量室间隔至左心室和右心室游离壁的尺寸、心室腔压力，并用肺动脉血流探头测量心输出量。在没有右心室缺血的情况下，左心室辅助装置使左心室压力-时间积分降低了80%±6%，同时维持主动脉压力。这导致室间隔向左移位，左心室室间隔与游离壁尺寸减小11.6%±1.8%，右心室室间隔与游离壁尺寸增加12.5%±2.4%，而右心室心输出量或每搏功没有变化。相比之下，单独的右冠状动脉闭塞会导致右心衰竭，右心室整体每搏功降低50%±6%，心输出量和右心室峰值收缩压分别降低26%±6%和27%±3%。在使用左心室辅助装置进行左心室卸载期间，这种右心衰竭持续存在，这导致室间隔进一步向左移位，每搏功和流量输出没有变化但仍处于降低状态。这些发现支持这样一种假说，即在人工左心室支持期间，先前存在的病理状况是决定右心室功能的主要因素，而直接的解剖学相互作用起次要作用。
