Hirose K, Shimada T, Matsumura T, Iwata M, Yasunaga K, Hori K, Matsusaka J
J Cardiogr. 1981 Dec;11(4):1223-32.
In order to determine the effect of verapamil, a calcium-channel blocking agent, on systolic performance and relaxation in hypertrophic cardiomyopathy (HCM), 12 patients with HCM and 10 normal subjects were studied. Echocardiograms, phonocardiograms, carotid pulses, and apex cardiograms were recorded simultaneously at the control state and 5, 10, and 15 min after intravenous injection of 10 mg of verapamil. After verapamil administration, heart rate was unchanged, while systolic blood pressure was slightly reduced in both groups. In normal subjects no significant changes were observed in systolic time intervals, such as ET, delta ET, PEP, delta PEP and PEP/ET, and mean VCF, except slightly prolonged delta ET after 5 min of the injection. The duration of isovolumic relaxation, (IIa-D) interval, taken as the period from the aortic valve closure (IIa) to the onset of mitral valve cusp separation and the time from IIa to the O point of the apex cardiogram, (IIa-O) interval, were 58 +/- 5 and 123 +/- 16 msec, respectively. The maximum velocity of the left ventricular posterior wall in early diastole (PWDV) was 128 +/- 10 mm/sec. These intervals and the velocity were not significantly changed after verapamil administration. In patients with HCM, ET and delta ET were unchanged, but PEP and delta PEP prolonged at 10 and 15 min after verapamil administration. PEP/ET was increased and mean VCF was reduced at 15 min after injection. In comparison with normal subjects, IIa-D interval and Ha-O interval were prolonged definitely at control, 92 +/- 21 and 190 +/- 28 msec, respectively. PWDV was slower than normal, 86 +/- 18 mm/sec at control. After verapamil, these intervals were shortened and PWDV fastened significantly. These results indicated that verapamil is regarded to have slight intrinsic negative inotropic action, suggesting the beneficial effect to reduce intraventricular pressure gradient, and also improve impaired myocardial relaxation in HCM.
为了确定钙通道阻滞剂维拉帕米对肥厚型心肌病（HCM）患者心脏收缩功能及舒张功能的影响，我们对12例HCM患者和10名正常受试者进行了研究。在对照状态以及静脉注射10mg维拉帕米后5分钟、10分钟和15分钟时，同步记录超声心动图、心音图、颈动脉搏动图和心尖搏动图。注射维拉帕米后，两组患者的心率均未改变，而收缩压均略有下降。在正常受试者中，收缩期时间间期，如射血时间（ET）、射血时间变化率（delta ET）、射血前期（PEP）、射血前期变化率（delta PEP）和PEP/ET，以及平均圆周纤维缩短速度（mean VCF）均未发生显著变化，仅在注射后5分钟时delta ET略有延长。等容舒张期时长，即从主动脉瓣关闭（IIa）至二尖瓣瓣叶分离开始的时间段（IIa-D间期），以及从IIa至心尖搏动图O点的时间（IIa-O间期），分别为58±5毫秒和123±16毫秒。左心室后壁舒张早期最大速度（PWDV）为128±10毫米/秒。注射维拉帕米后，这些间期和速度均未发生显著变化。在HCM患者中，ET和delta ET未改变，但在注射维拉帕米后10分钟和15分钟时，PEP和delta PEP延长。注射后15分钟时，PEP/ET升高，mean VCF降低。与正常受试者相比，HCM患者在对照时IIa-D间期和IIa-O间期明显延长，分别为92±21毫秒和190±28毫秒。对照时PWDV比正常受试者慢，为86±18毫米/秒。注射维拉帕米后，这些间期缩短，PWDV显著加快。这些结果表明，维拉帕米被认为具有轻微的内在负性肌力作用，提示其对降低心室内压力梯度有益，并且还可改善HCM患者受损的心肌舒张功能。
