Bussmann W D, Seher W, Grüngras M
Dtsch Med Wochenschr. 1983 Jul 8;108(27):1047-53. doi: 10.1055/s-2008-1069690.
In a prospective, randomized and controlled study, 29 patients received i.v. verapamil, 5-10 mg/h for two days, at a mean of eight hours after onset of myocardial infarction. In a control group, 25 patients received no specific treatment. In all patients, left ventricular end-diastolic pressure was initially less than 15 mm Hg. The two groups were comparable as to age, infarct site and haemodynamics (measured via Swan-Ganz catheter). CK and CKMB peaks were significantly lower in the verapamil than the control group (CK 547 vs 703 U/1, P less than 0.05; CKMB 51 vs 68 U/1, P less than 0.025), as well as infarct weight (CK = 48 vs 65 g-equivalent; P less than 0.03; CKMB = 31 vs 49 g-equivalent; P less than 0.005). Arterial blood pressure was lower by 10 mm Hg than in the control group. Peripheral resistance and filling pressure remained unchanged. In patients without left ventricular failure verapamil reduces the infarct size by about 30%. The most prominent haemodynamic change is a reduction in blood pressure.
在一项前瞻性、随机对照研究中,29例患者在心肌梗死发作平均8小时后静脉注射维拉帕米,剂量为5 - 10毫克/小时,持续两天。在对照组中,25例患者未接受特殊治疗。所有患者的左心室舒张末期压力最初均低于15毫米汞柱。两组在年龄、梗死部位和血流动力学(通过Swan - Ganz导管测量)方面具有可比性。维拉帕米组的肌酸激酶(CK)和肌酸激酶同工酶(CKMB)峰值显著低于对照组(CK:547 vs 703 U/L,P < 0.05;CKMB:51 vs 68 U/L,P < 0.025),梗死重量也较低(CK = 48 vs 65克当量;P < 0.03;CKMB = 31 vs 49克当量;P < 0.005)。动脉血压比对照组低10毫米汞柱。外周阻力和充盈压保持不变。在无左心室衰竭的患者中,维拉帕米可使梗死面积缩小约30%。最显著的血流动力学变化是血压降低。