Otsuji Y, Kisanuki A, Toyonaga K, Hamasaki S, Arima S, Nakao S, Okino H, Toda H, Akiba S, Tanaka H
First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
Am J Cardiol. 1996 Aug 1;78(3):298-303. doi: 10.1016/s0002-9149(96)00281-0.
This study was designed to measure the right ventricular (RV) stiffness (delta P/ delta V) with a new method without estimating the RV volume itself. RV stiffness has rarely been measured due to the difficulty in estimating the RV volume. Without measuring RV volume itself, stiffness can be determined by measuring its volume change (delta V). Tricuspid filling flow volume, which is the diastolic RV delta V, is measurable by using Doppler echocardiography. Thus, RV stiffness may possibly be obtained from Doppler echocardiography combined with high-fidelity RV pressure. Subjects consisted of 8 controls, 8 patients with angina pectoris, 8 with anterior, 8 with posterior, and 8 with inferior prior myocardial infarction. Tricuspid annular dimension was measured by 2-dimensional echocardiography and the tricuspid annular area was calculated. Velocity-time integral of the tricuspid filling flow during the late diastole was measured by pulsed Doppler echocardiography. Then, the late diastolic RV delta V was obtained as the product of the tricuspid annular area and the integral. The late diastolic RV pressure rise (delta P) was also measured with a micromanometer catheter. The RV elastic chamber stiffness constant ([delta P/ delta V]/P) was obtained by dividing simple stiffness by the mean RV pressure during late diastole. The RV elastic chamber stiffness constant did not significantly differ among controls, patients with angina pectoris, and those with anterior and posterior myocardial infarction (0.0054 +/- 0.0009 vs 0.0057 +/- 0.0018 vs 0.0064 +/- 0.002 vs 0.0052 +/- 0.0019 ml-1). However, it was significantly increased in patients with inferior myocardial infarction (0.010 +/- 0.004 ml-1, p < 0.01 or 0.05) compared with those in the other 4 groups. These results suggest (1) that RV stiffness can be measured with a new method without RV volume estimation, and (2) that this new method is useful in evaluating RV diastolic pathophysiology in patients with coronary artery disease.
本研究旨在采用一种无需估计右心室（RV）容积本身的新方法来测量右心室僵硬度（ΔP/ΔV）。由于估计右心室容积存在困难，右心室僵硬度很少被测量。在不测量右心室容积本身的情况下，可通过测量其容积变化（ΔV）来确定僵硬度。三尖瓣充盈血流量，即舒张期右心室ΔV，可通过多普勒超声心动图测量。因此，右心室僵硬度可能通过结合高保真右心室压力的多普勒超声心动图获得。研究对象包括8名对照组、8名心绞痛患者、8名前壁心肌梗死患者、8名后壁心肌梗死患者和8名下壁心肌梗死患者。通过二维超声心动图测量三尖瓣环尺寸并计算三尖瓣环面积。通过脉冲多普勒超声心动图测量舒张晚期三尖瓣充盈血流的速度-时间积分。然后，舒张晚期右心室ΔV作为三尖瓣环面积与积分的乘积获得。舒张晚期右心室压力升高（ΔP）也用微测压导管测量。右心室弹性腔僵硬度常数（[ΔP/ΔV]/P）通过将简单僵硬度除以舒张晚期右心室平均压力获得。对照组、心绞痛患者、前壁和后壁心肌梗死患者的右心室弹性腔僵硬度常数无显著差异（0.0054±0.0009 vs 0.0057±0.0018 vs 0.0064±0.002 vs 0.0052±0.0019 ml-1）。然而，与其他4组相比，下壁心肌梗死患者的该常数显著升高（0.010±0.004 ml-1，p<0.01或0.05）。这些结果表明：（1）无需估计右心室容积即可用新方法测量右心室僵硬度；（2）这种新方法有助于评估冠心病患者的右心室舒张期病理生理学。
