Kussmaul W G, Wieland J M, Laskey W K
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia.
Cardiovasc Res. 1988 Sep;22(9):627-38. doi: 10.1093/cvr/22.9.627.
Because exercise induced pulmonary hypertension may disturb optimal coupling between the right ventricle and pulmonary artery in coronary artery disease, high fidelity pulmonary artery and right ventricular pressure and electromagnetic pulmonary artery flow velocity data were recorded at rest and during supine exercise in 10 control subjects free of detectable cardiovascular disease and in 11 patients with coronary artery disease. The pulmonary artery impedance and power spectra were calculated from Fourier analysis of pressure and flow waveforms. Total hydraulic power expended per unit of forward flow was computed as an index of right ventricular-pulmonary artery coupling. In coronary artery disease exercise produced substantial increases in pulmonary artery pressure, pulmonary artery characteristic impedance, and total power per unit flow. These changes did not occur in control subjects. Despite a significant exercise increase in right ventricular end diastolic pressure and peak right ventricular dP/dt, and independent of the presence of right coronary artery involvement, the right ventricular stroke output response during exercise was significantly blunted in the coronary artery disease patients. Pulmonary vascular resistance was unchanged by exercise in either group. Exercise induced ischaemia presents an increased pulsatile hydraulic load to the right ventricle. Increased pulmonary artery input impedance impairs the hydraulic efficiency of right ventricular-pulmonary artery coupling and may contribute to the limitation of right ventricular ejection performance in coronary artery disease.
由于运动诱发的肺动脉高压可能会扰乱冠状动脉疾病患者右心室与肺动脉之间的最佳耦合，因此对10名无明显心血管疾病的对照受试者和11名冠状动脉疾病患者在静息状态和仰卧运动期间记录了高保真肺动脉和右心室压力以及电磁肺动脉流速数据。通过对压力和流量波形进行傅里叶分析来计算肺动脉阻抗和功率谱。计算每单位前向血流所消耗的总水力功率，作为右心室-肺动脉耦合的指标。在冠状动脉疾病中，运动导致肺动脉压力、肺动脉特征阻抗和每单位流量的总功率大幅增加。这些变化在对照受试者中未出现。尽管运动使右心室舒张末期压力和右心室峰值dP/dt显著增加，且与右冠状动脉受累情况无关，但冠状动脉疾病患者运动期间的右心室搏出量反应明显减弱。两组运动后肺血管阻力均未改变。运动诱发的缺血会给右心室带来增加的搏动性水力负荷。肺动脉输入阻抗增加会损害右心室-肺动脉耦合的水力效率，并可能导致冠状动脉疾病患者右心室射血功能受限。
