Ferlinz J, Turbow M E
Am J Cardiol. 1980 Dec 1;46(6):1019-26. doi: 10.1016/0002-9149(80)90361-6.
To determine the metabolic cost of administering an experimental calcium antagonist, verapamil, to patients with coronary artery disease, 12 such patients were studied at rest and during stress with atrial pacing before and after intravenous treatment with verapamil (bolus dose of 0.1 mg/kg body weight, followed by infusion at 0.005 mg/kg per min). The mean (+/- standard deviation) aortic pressure at rest (98 +/- 22 mg Hg), coronary sinus blood flow (88 +/- 17 ml/min) and myocardial oxygen consumption (10.7 +/- 2.4 ml O2/min) decreased to 88 +/- 20 mm Hg (p < 0.0004), 77 +/- 14 ml/min (p < 0.03) and 8.8 +/- 2.5 ml O2/min (p < 0.01), respectively, after administration of verapamil. With atrial pacing, these values were 105 +/- 25 mm Hg, 151 +/- 50 ml/min and 18.5 +/- 6.4 ml O2/min, respectively, before infusion of verapamil, and then decreased to 87 +/- 14 mm Hg (p < 0.006), 107 +/- 31 ml/min (p < 0.0002) and 13.3 +/- 4.4 ml O2/min (p < 0.001) during infusion. Angina occurred in all patients with atrial pacing before verapamil (threshold to pain: 93 +/- 67 seconds). After verapamil, the threshold to pain in six patients increased to 191 +/- 183 seconds; and no pain was experienced by the remaining six (p < 0.0005). Before administration of verapamil lactate extraction decreased from 24 +/- 9 to 10 +/- 11 percent (p < 0.0002) during atrial pacing, and 9 (75 percent) of the 12 patients exhibited electrocardiographic S-T segment depressions. After administration of verapamil lactate extraction normalized to 22 +/- 9 percent during atrial pacing, and the electrocardiogram reverted to baseline in all but one patient. These findings indicate that verapamil decreases left ventricular myocardial metabolic demands, and concomitantly greatly increases the threshold to angina.
为确定给冠心病患者静脉注射实验性钙拮抗剂维拉帕米的代谢成本，对12例此类患者在静息状态下以及在用维拉帕米静脉治疗（静脉推注剂量为0.1mg/kg体重，随后以0.005mg/kg每分钟的速度输注）前后进行心房起搏应激时进行了研究。静息时的平均（±标准差）主动脉压（98±22mmHg）、冠状窦血流量（88±17ml/分钟）和心肌耗氧量（10.7±2.4ml O₂/分钟）在给予维拉帕米后分别降至88±20mmHg（p<0.0004）、77±14ml/分钟（p<0.03）和8.8±2.5ml O₂/分钟（p<0.01）。在心房起搏时，这些值在输注维拉帕米前分别为105±25mmHg、151±50ml/分钟和18.5±6.4ml O₂/分钟，在输注过程中则降至87±14mmHg（p<0.006）、107±31ml/分钟（p<0.0002）和13.3±4.4ml O₂/分钟（p<0.001）。维拉帕米治疗前，所有进行心房起搏的患者均出现心绞痛（疼痛阈值：93±67秒）。维拉帕米治疗后，6例患者的疼痛阈值增至191±183秒；其余6例患者未出现疼痛（p<0.0005）。在给予维拉帕米前，心房起搏期间乳酸摄取率从24±9%降至10±11%（P<0.000）,12例患者中有9例（75%）出现心电图ST段压低。给予维拉帕米后，心房起搏期间乳酸摄取率恢复正常，为22±9%，除1例患者外，所有患者的心电图均恢复至基线水平。这些结果表明，维拉帕米可降低左心室心肌代谢需求，并同时大幅提高心绞痛阈值。
