Effect of verapamil on regional coronary and myocardial perfusion during acute coronary occlusion

To elucidate the mechanism of action of the calcium antagonist verapamil, S-T segment mapping, retrograde coronary flow and regional coronary resistance were studied in 28 dogs subjected to acute coronary occlusion. Retrograde coronary flow was measured directly through catheterization of the distal...

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Veröffentlicht in:The American journal of cardiology 1980-02, Vol.45 (2), p.269-275
Hauptverfasser: da Luz, Protásio L., de Barros, L.F.Monteiro, Leite, João Jorge, Pileggi, Fúlvio, Décourt, Luiz V.
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Sprache:eng
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Zusammenfassung:To elucidate the mechanism of action of the calcium antagonist verapamil, S-T segment mapping, retrograde coronary flow and regional coronary resistance were studied in 28 dogs subjected to acute coronary occlusion. Retrograde coronary flow was measured directly through catheterization of the distal occluded coronary artery. Regional coronary resistance was calculated by dividing mean distal coronary pressure by coronary flow. Verapamil (0.8 mg/kg) administered intravenously to eight dogs 30 minutes before coronary occlusion significantly reduced S-T segment elevation as compared with occlusion alone (p < 0.025); heart rate and diastolic pressure were also reduced (p < 0.05) but systolic pressure remained essentially unchanged. When verapamil was given to seven dogs within 30 minutes after coronary occlusion, there was a significant increase in retrograde coronary flow (p < 0.05) and a decrease in regional coronary resistance (p < 0.05). Simultaneously, heart rate and heart rate-blood pressure product declined significantly (p < 0.05), suggesting a reduction in myocardial oxygen consumption. Systolic blood pressure was unaltered, and diastolic pressure decreased only transiently. In 13 control dogs there was no significant change in any of these variables during the observation period. Thus, verapamil during acute coronary occlusion protects the ischemic myocardium by both increasing perfusion and reducing myocardial oxygen consumption.
ISSN:0002-9149
1879-1913
DOI:10.1016/0002-9149(80)90645-1