Furuta T, Kondo T, Watanabe Y, Okamura M, Shimokata T, Hishida H, Mizuno Y, Anno H, Takeuchi A, Koga S
Department of Internal Medicine, Fujita-Gakuen Health University School of Medicine, Toyoake.
J Cardiol. 1988 Jun;18(2):477-91.
To assess the interaction and interdependence of left and right ventricular function, ECG-gated radionuclide angiocardiography was performed immediately after cardiac catheterization during right atrial pacing for 11 patients with old myocardial infarction (MI), two with non-obstructive hypertrophic cardiomyopathy, one with aortic stenosis (AS), two with pulmonary infarction (PI), and one with neurocirculatory asthenia (NCA). Absolute left ventricular (LV) volume curves were obtained by the count-based method with attenuation factor corrections. Biventricular pressure and volume curves were digitized and synchronized to end-diastole, and pressure-volume (P-V) loops were constructed throughout a cardiac cycle. The stroke work index (SWI), the work index per min (WI/M) and the contractility index (CNTI) were calculated from the P-V loops. In a patient with NCA, LV end-diastolic volume decreased during rapid pacing, but no significant change in the LV end-systolic P-V relation was recognized. However, the entire right ventricular (RV) P-V loop was shifted toward the left during rapid pacing. In a patient with AS, the LV P-V loop was markedly enlarged and every parameter of LV function was much greater than that of the right ventricle due to increased LV afterload. The areas of RV P-V loops in two patients with PI were larger than those of other patients, because RV pressure was relatively high, and RV volume was increased. It is suggested that RV pressure and volume overloads prevail in patients with PI. In four MI patients with three vessel disease and having collateral circulation, the LV end-systolic P-V relationship was shifted toward the lower right, and every parameter (SWI, WI/M, CNTI) of LV function decreased by rapid pacing. Myocardial ischemia may be induced by rapid pacing stress, causing decreased LV contractility. It was concluded that the P-V loops obtained by RNA and catheterization are clinically useful for estimating the interaction and interdependence between right and left ventricular hemodynamics.
为评估左、右心室功能的相互作用和相互依存关系,对11例陈旧性心肌梗死(MI)患者、2例非梗阻性肥厚型心肌病患者、1例主动脉瓣狭窄(AS)患者、2例肺梗死(PI)患者和1例神经循环衰弱(NCA)患者,在心脏导管插入术后立即进行右心房起搏时行心电图门控放射性核素心血管造影。采用基于计数法并进行衰减因子校正获取绝对左心室(LV)容积曲线。将双心室压力和容积曲线数字化并同步至舒张末期,在整个心动周期构建压力-容积(P-V)环。根据P-V环计算每搏功指数(SWI)、每分钟功指数(WI/M)和收缩性指数(CNTI)。在1例NCA患者中,快速起搏时左心室舒张末期容积减小,但左心室收缩末期P-V关系未见明显变化。然而,快速起搏时整个右心室(RV)P-V环向左移位。在1例AS患者中,由于左心室后负荷增加,左心室P-V环明显增大且左心室功能的各项参数均远高于右心室。两名PI患者的右心室P-V环面积大于其他患者,因为右心室压力相对较高且右心室容积增加。提示PI患者以右心室压力和容积超负荷为主。在4例三支血管病变且有侧支循环的MI患者中,快速起搏时左心室收缩末期P-V关系向右下移位,左心室功能的各项参数(SWI、WI/M、CNTI)均降低。快速起搏应激可能诱发心肌缺血,导致左心室收缩力下降。结论是,通过放射性核素心血管造影和导管插入术获得的P-V环在临床上有助于评估左右心室血流动力学之间的相互作用和相互依存关系。