Chew C Y, Brown B G, Singh B N, Wong M M, Pierce C, Petersen R
Am J Cardiol. 1983 Mar 1;51(5):699-705. doi: 10.1016/s0002-9149(83)80118-0.
The effect of intravenous verapamil on systemic and coronary hemodynamic function was studied at cardiac catheterization in 12 patients with coronary artery disease. Verapamil was administered as a 2-minute bolus (0.145 mg/kg) followed by an infusion (0.005 mg/kg/min). Cardiac output and coronary sinus blood flow were measured by thermodilution techniques. Caliber of the large coronary arteries and of diseased segments was determined from the coronary angiogram using a computer-assisted method. Verapamil reduced mean arterial pressure 14% (p less than 0.001), systemic vascular resistance 21% (p less than 0.01), and stroke work index 16% (p less than 0.001). Coronary vascular resistance decreased 24% (p less than 0.01) with a small increase in coronary sinus blood flow (+13%, difference not significant [NS]). Myocardial oxygen consumption determined in 5 patients showed no significant change with verapamil. Luminal area in 39 coronary lesions was measured in the "normal" portion of the diseased segment and at its maximal constriction, and an estimate of flow resistance in the stenosis was computed. Overall, 50% of "normal" and of diseased coronary segments dilated significantly with verapamil. Stenosis dilation resulted in an average 14% reduction (p less than 0.01) in estimated flow resistance. In 8 patients, the luminal changes (n = 27) induced by sublingual nitroglycerin were compared with those induced by verapamil. Nitroglycerin induced a significantly greater increase in coronary caliber in both normal and diseased segments; estimated stenosis flow resistance decreased 28% with nitroglycerin compared with 14% with verapamil (p less than 0.01). Thus, verapamil moderately dilates the systemic and coronary small vessel resistance bed without apparently increasing myocardial metabolic demand. Furthermore, verapamil mildly dilates large coronary conductance vessels in both "normal" and diseased segments, although significantly less than does nitroglycerin.
在12例冠心病患者进行心导管检查时，研究了静脉注射维拉帕米对全身和冠状动脉血流动力学功能的影响。维拉帕米以2分钟推注（0.145mg/kg）给药，随后进行输注（0.005mg/kg/min）。心输出量和冠状窦血流量通过热稀释技术测量。使用计算机辅助方法从冠状动脉造影确定大冠状动脉和病变节段的管径。维拉帕米使平均动脉压降低14%（p<0.001），全身血管阻力降低21%（p<0.01），每搏功指数降低16%（p<0.001）。冠状动脉血管阻力降低24%（p<0.01），冠状窦血流量略有增加（+13%，差异无统计学意义[NS]）。在5例患者中测定的心肌耗氧量，维拉帕米治疗后无显著变化。在病变节段的“正常”部分及其最大狭窄处测量了39个冠状动脉病变的管腔面积，并计算了狭窄处血流阻力的估计值。总体而言，50%的“正常”和病变冠状动脉节段在维拉帕米作用下显著扩张。狭窄扩张导致估计的血流阻力平均降低14%（p<0.01）。在8例患者中，比较了舌下含服硝酸甘油和维拉帕米引起的管腔变化（n=27）。硝酸甘油在正常和病变节段均引起冠状动脉管径显著更大的增加；与维拉帕米相比，硝酸甘油使估计的狭窄血流阻力降低28%，而维拉帕米为14%（p<0.01）。因此，维拉帕米适度扩张全身和冠状动脉小血管阻力床，而不会明显增加心肌代谢需求。此外，维拉帕米在“正常”和病变节段均轻度扩张大冠状动脉传导血管，尽管明显小于硝酸甘油。
