Tanimoto M, Iwasaki T, Yamamoto T, Makihata S, Konishiike A, Mihata S, Kawakita S, Yamasaki K, Yasutomi N, Kawai Y
J Cardiogr. 1984 Aug;14(2):403-14.
Echocardiographic analysis of right ventricular ejection time (RVET), pre-ejection time (RVPEP), RVPEP/ET and isovolumic relaxation time (RVIRT) was performed in patients with acute or chronic right ventricular pressure overloading. Fifty-five patients undergoing right ventricular cardiac catheterization, were categorized into seven groups; 11 patients with atrial septal defect (ASD) without pulmonary hypertension (PH) (group 1), 12 with ASD with PH (group 2), six with mitral stenosis (MS) without PH (group 3), nine with MS with PH (group 4), seven with primary pulmonary hypertension (PPH) (group 5), seven with acute pulmonary embolism (PE) (group 6), and three patients with convalescence of PE (group 7). Corrected RVIRT (RVIRTc) and RVET (RVETc) were calculated by regression analysis correlating with heart rate in normal subjects. RVIRTc, RVETc, RVPEP and RVPEP/ET in seven groups were significantly correlated with systolic pulmonary artery pressure (SPAP) (r = 0.62, p less than 0.001; r = -0.41, p less than 0.01; r = 0.61, p less than 0.001; r = 0.65, p less than 0.001, respectively), but RVDd did not correlate with SPAP (r = 0.370, p less than 0.05). Comparing acute right ventricular pressure overloading group (group 6) with each of chronic right ventricular pressure overloading groups (groups 2, 4, 5, and 7), RVIRTc and RVDd were significantly increased in the former than the latter, but RVETc, RVPEP and RVPEP/ET were not significantly different in both groups. There was a significant correlation between RVIRTc and RVPEP/ET in chronic pressure overloading, but not in acute pressure overloading. We concluded that early diastolic RV relaxation and systolic performance were both impaired by increased afterload in chronic pressure overloading. In acute pressure overloading, however, early diastolic RV relaxation was more significantly impaired possibly because of acute changes of muscle architectures due to acute right ventricular expansion and anoxia.
对急性或慢性右心室压力负荷过重患者进行了右心室射血时间（RVET）、射血前期（RVPEP）、RVPEP/ET和等容舒张时间（RVIRT）的超声心动图分析。55例行右心室心导管检查的患者被分为七组：11例无肺动脉高压（PH）的房间隔缺损（ASD）患者（第1组），12例有PH的ASD患者（第2组），6例无PH的二尖瓣狭窄（MS）患者（第3组），9例有PH的MS患者（第4组），7例原发性肺动脉高压（PPH）患者（第5组），7例急性肺栓塞（PE）患者（第6组），以及3例PE恢复期患者（第7组）。通过与正常受试者心率相关的回归分析计算校正后的RVIRT（RVIRTc）和RVET（RVETc）。七组中的RVIRTc、RVETc、RVPEP和RVPEP/ET与收缩期肺动脉压（SPAP）显著相关（r分别为0.62，p＜0.001；r为 -0.41，p＜0.01；r为0.61，p＜0.001；r为0.65，p＜0.001），但右心室舒张末期内径（RVDd）与SPAP不相关（r = 0.370，p＜0.05）。将急性右心室压力负荷过重组（第6组）与各慢性右心室压力负荷过重组（第2、4、5和7组）进行比较，前者的RVIRTc和RVDd显著高于后者，但两组的RVETc、RVPEP和RVPEP/ET无显著差异。慢性压力负荷过重时RVIRTc与RVPEP/ET之间存在显著相关性，但急性压力负荷过重时不存在。我们得出结论，在慢性压力负荷过重时，后负荷增加会损害右心室舒张早期的舒张功能和收缩功能。然而，在急性压力负荷过重时，右心室舒张早期的舒张功能可能因急性右心室扩张和缺氧导致的肌肉结构急性改变而受到更显著的损害。
