Treatment of acute myocardial infarction with verapamil. Hemodynamic effects and electrical changes studied by body surface maps
Botti, G.; Bonatti, V.; Taccardi, B.; Rolli, A.; Favaro, L.; Musso, E.
Giornale Italiano di Cardiologia 11(9): 1242-1251
1981
ISSN/ISBN: 0046-5968 PMID: 7327333 Document Number: 180551
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.