Effects of verapamil on coronary hemodynamic function and vasomobility relative to its mechanism of antianginal action*

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The effect of intravenous verapamil on systemic and coronary hemodynamic function was studied at cardiac catheterization in 12 patients with coronary artery disease. Verapamil was administered as a 2-minute bolus (0.145 mg/kg) followed by an infusion (0.005 mg/kg/min). Cardiac output and coronary sinus blood flow were measured by thermodilution techniques. Caliber of the large coronary arteries and of diseased segments was determined from the coronary angiogram using a computer-assisted method. Verapamil reduced mean arterial pressure 14% (p <0.001), systemic vascular resistance 21% (p <0.01), and stroke work index 16% (p <0.001). Coronary vascular resistance decreased 24% (p <0.01) with a small increase in coronary sinus blood flow (+13%, difference not significant [NS]). Myocardial oxygen consumption determined in 5 patients showed no significant change with verapamil. Luminal area in 39 coronary lesions was measured in the “normal” portion of the diseased segment and at its maximal constriction, and an estimate of flow resistance in the stenosis was computed. Overall, 50% of “normal” and of diseased coronary segments dilated significantly with verapamil. Stenosis dilation resulted in an average 14% reduction (p <0.01) in estimated flow resistance. In 8 patients, the luminal changes (n = 27) induced by sublingual nitroglycerin were compared with those induced by verapamil. Nitroglycerin induced a significantly greater increase in coronary caliber in both normal and diseased segments; estimated stenosis flow resistance decreased 28% with nitroglycerin compared with 14% with verapamil (p <0.01).

Thus, verapamil moderately dilates the systemic and coronary small vessel resistance bed without apparently increasing myocardial metabolic demand. Furthermore, verapamil mildly dilates large coronary conductance vessels in both “normal” and diseased segments, although significantly less than does nitroglycerin.

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    *

    This study was supported in part by the Medical Research Service of Veterans Administration (1102-01), Washington, D.C.; Grants HL 13517, HL 19451, and HL 18805 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; and Grant-In-Aid 592-01 from the American Heart Association-Greater Los Angeles.

    1

    Dr. Brown is an Established Investigator of the American Heart Association.

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