Hess O M, Murakami T, Krayenbühl H P
Medical Polyclinic, University Hospital, Zurich, Switzerland.
Z Kardiol. 1987;76 Suppl 3:82-6.
The effect of 0.1 mg/kg verapamil on left ventricular (LV) diastolic mechanics was evaluated in ten patients with hypertrophic cardiomyopathy and 13 patients with aortic stenosis. LV diastolic function was assessed from simultaneous M-mode echocardiograms and high-fidelity pressure measurements at rest and 10 to 15 min after intravenous administration of verapamil. The time constant of LV pressure decay (T), LV early and mean diastolic filling rate as well as diastolic pressure-diameter relations, were determined before and after verapamil administration. Heart rate, LV peak systolic pressure, maximum and minimum dP/dt remained unchanged in both groups after verapamil administration. LV end-diastolic pressure increased slightly although significantly from 15 to 17 mm Hg (P less than 0.02) in aortic stenosis but remained unchanged in hypertrophic cardiomyopathy. T decreased significantly from 79 to 60 ms (P less than 0.001) in hypertrophic cardiomyopathy but increased from 53 to 68 ms (P less than 0.025) in aortic stenosis. Parallel to the decrease in T, early and mean diastolic lengthening rate increased significantly in hypertrophic cardiomyopathy, but remained unchanged in aortic stenosis before and after verapamil. The diastolic pressure-diameter relation was not affected in both groups by verapamil administration. However, cycle efficiency improved significantly from 71% to 77% (P less than 0.02) in cardiomyopathy but remained unchanged in aortic stenosis (80% versus 80%). Thus, it is concluded that verapamil improves relaxation in hypertrophic cardiomyopathy but delays relaxation in aortic stenosis. The beneficial effect of verapamil in hypertrophic cardiomyopathy is related to improved relaxation and diastolic filling rather than to changes in passive elastic chamber properties.(ABSTRACT TRUNCATED AT 250 WORDS)
在10例肥厚型心肌病患者和13例主动脉瓣狭窄患者中评估了0.1mg/kg维拉帕米对左心室(LV)舒张力学的影响。通过同步M型超声心动图和静息及静脉注射维拉帕米后10至15分钟的高保真压力测量来评估LV舒张功能。在维拉帕米给药前后测定LV压力衰减时间常数(T)、LV早期和平均舒张充盈率以及舒张压-直径关系。维拉帕米给药后两组的心率、LV收缩压峰值、最大和最小dP/dt均保持不变。主动脉瓣狭窄患者的LV舒张末期压力虽有轻微但显著升高,从15mmHg升至17mmHg(P<0.02),而肥厚型心肌病患者的LV舒张末期压力保持不变。肥厚型心肌病患者的T从79ms显著降至60ms(P<0.001),而主动脉瓣狭窄患者的T从53ms升至68ms(P<0.025)。与T的降低平行,肥厚型心肌病患者的早期和平均舒张延长率显著增加,但维拉帕米给药前后主动脉瓣狭窄患者的该指标保持不变。维拉帕米给药对两组的舒张压-直径关系均无影响。然而,心肌病患者的循环效率从71%显著提高至77%(P<0.02),而主动脉瓣狭窄患者的循环效率保持不变(80%对80%)。因此,得出结论,维拉帕米可改善肥厚型心肌病的舒张功能,但会延迟主动脉瓣狭窄的舒张功能。维拉帕米在肥厚型心肌病中的有益作用与舒张功能改善和舒张期充盈有关,而非与被动弹性腔特性的改变有关。(摘要截短至250字)