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  • Journal
    Digital Access
    Provider
    Version
    Sage
    v. 3-, 2014-
    PubMed Central
    v. 4-, 2015-
  • Book
    François Ellenberger.
    Print c1988-
  • Article
    Singh BN, Roche AH.
    Am Heart J. 1977 Nov;94(5):593-9.
    The hemodynamic effects of intravenous verapamil (10 mg.) were evaluated in 13 patients with coronary artery disease and in seven patients with rheumatic valvular disease during cardiac catheterization. The peak effects were apparent at 3 to 5 minutes after injection and lasted about 10 minutes. The mean arterial pressure fell from 97.8 +/- 3.4 to 85.9 +/- 2.7 mm. Hg (-12%; p less than 0.01) accompanied by a significant decrease (-21%, p less than 0.001) in systemic vascular resistance (from 1435 +/- 80 to 1131 +/- 82 dynes-sex.-cm.-5) with an increase in left ventricular end-diastolic pressure (from 11.0 +/- 0.9 to 15.0 +/- 1.0 mm. Hg; +36%, p less than 0.01) and a reduction in LV dp/dt max (from 1343 +/- 152 to 1007 +/- 102 mm. Hg/sex.; -25%, p less than 0.05). The changes in heart rate (from 75.7 +/- 3.0 to 80.2 +/- 2.8 beats/min.), cardiac index (from 3.17 +/- 0.15 to 3.61 +/- 0.17 L./min./M.2), left ventricular minute work (from 3.63 +/- 0.28 to 3.31 +/- 0.23 Kg.-m./min./M.2) and mean pulmonary artery pressures (from 15.7 +/- 1.0 to 18.1 +/- 0.8 mm. Hg) were not statistically significant. The intrinsic negative inotropic action of verapamil is, therefore, minimized by its effect on afterload so that cardiac index is not reduced by the drug in patients with cardiac disease.
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