Botti G, Bonatti V, Taccardi B, Rolli A, Favaro L, Musso E
G Ital Cardiol. 1981;11(9):1242-51.
The effects of Verapamil on main haemodinamic parameters and on Max sigma pos., sigma Q15, Max sigma pos./Max sigma neg. and sigma ST, studied by automatic recording of thoracic maps, were evaluated in 11 patients with acute myocardial infarction within 6 hours from pain onset. Verapamil was given at the dose of 0.1 mg/Kg followed by infusion of 0.035 mg/min. Hemodynamic measurements were made before and 15 minutes after Verapamil; the maps were recorded before and 5, 15 and 30 minutes after Verapamil. Heart rate and sistolic arterial pressure were reduced, though not significantly: right atrial pressure, pulmonary pressures and capillary pulmonary pressure remained unchanged. On the contrary, the reduction of diastolic arterial pressure (from 94 +/- 4.2 to 88 +/- 4.5 mmHg; P less than 0.05) and of cardiac index (from 3.1 +/- 0.11 to 3 +/- 0.11; P less than 0.05) was important. Max sigma pos. increased after 15 minutes from 11619 +/- 1970 to 12349 +/- 2151 microV (P less than 0.01), but il decreased after 30 minutes to 11037 +/- 2042 microV (P less than 0.05). Max sigma pos./Max sigma neg. ratio increased significantly after 5 and 15 minutes. Sigma Q15 increased significantly only after 30 minutes (from 7198 +/- 1643 to 8688 +/- 1541 microV; P less than 0.05). Sigma ST showed a transient, non significant increase after 5 minutes, but decreased significantly after 30 minutes (from 76664 +/- 19505 to 67157 +/- 18581 microV; P less than 0.05). The results show that Verapamil does not cause worsening of main haemodinamic parameters during acute, non complicated myocardial infarction and reduces significantly ST segment elevation. The Authors discuss also a possible electrophysiological effect of Verapamil on action potential of ischemic cells, responsible for early increase of sigma ST observed in some patients.
通过自动记录胸电图,研究了维拉帕米对11例疼痛发作后6小时内的急性心肌梗死患者主要血液动力学参数以及最大正向σ波、Q15时段σ波、最大正向σ波/最大负向σ波和ST段σ波的影响。维拉帕米的给药剂量为0.1mg/kg,随后以0.035mg/min的速度输注。在维拉帕米给药前及给药后15分钟进行血液动力学测量;在维拉帕米给药前及给药后5、15和30分钟记录胸电图。心率和收缩压有所降低,但不显著:右心房压力、肺血管压力和肺毛细血管压力保持不变。相反,舒张压(从94±4.2降至88±4.5mmHg;P<0.05)和心脏指数(从3.1±0.11降至3±0.11;P<0.05)的降低较为显著。最大正向σ波在15分钟后从11619±1970微伏增加到12349±2151微伏(P<0.01),但在30分钟后降至11037±2042微伏(P<0.05)。最大正向σ波/最大负向σ波比值在5分钟和15分钟后显著增加。Q15时段σ波仅在30分钟后显著增加(从7198±1643微伏增加到8688±1541微伏;P<0.05)。ST段σ波在5分钟后出现短暂的、不显著的增加,但在30分钟后显著降低(从76664±19505微伏降至67157±18581微伏;P<0.05)。结果表明,在急性非复杂性心肌梗死期间,维拉帕米不会导致主要血液动力学参数恶化,且能显著降低ST段抬高。作者还讨论了维拉帕米对缺血细胞动作电位可能的电生理作用,这可能是部分患者早期观察到的ST段σ波增加的原因。