Abstract
In two groups, each comprising 10 patients with advanced coronary artery disease, disopyramide, 2 mg/kg over a period of 5 minutes, or lidocaine, 100 mg as a bolus dose, was injected intravenously. Disopyramide increased diastolic and mean arterial pressures significantly because of its vasoconstrictive properties. Cardiac index decreased from 3.7 ± 0.3 to 3.2 ±0.1 liters/min per m 2 at 10 minutes and to 3.1 ± 0.2 30 minutes after the injection was begun. After lidocaine no changes in hemodynamic variables were observed. Disopyramide revealed potent coronary constrictive activity, whereas lidocaine was a mild coronary vasodilator. Coronary blood flow increased significantly from 68.2 ± 4.3 ml/ min × 100 g to 74.8 ± 4.1 directly after injection of 100 mg lidocaine and to 75.5 ± 5.0 25 to 30 minutes later. Disopyramide decreased coronary blood flow significantly from 73.8 ± 3.8 to 67.8 ± 2.7 ml/ min × 100 mg during the 5 minute period after drug infusion. Coronary vascular resistance increased very significantly from 0.94 ± 0.1 to 1.14 ± 0.1 units. Because of an extreme increase in the arterial-coronary sinus oxygen difference, myocardial oxygen consumption (MVO 2) increased at the same time from 9.9 ± 0.6 to 10.6 ± 0.5 ml/ min × 100 g. At 25 to 30 minutes after the start of the dlsopyramide infusion MVO 2 increased significantly to 11.9 ± 0.6 because the coronary blood flow increased to 79.1 ± 2.8. However, the arterial-coronary sinus oxygen difference remained significantly elevated and coronary vascular resistance declined only moderately. Myocardial lactate extraction did not change. Apparently a metabolism-induced dilatation in coronary vasculature actually overcomes the vasoconstriction by disopyramide and prevents serious myocardial ischemia, but a vasoconstrictive effect of disopyramide is still present. The potent coronary constrictive activity of intravenous disopyramide in the presence of increased myocardial oxygen need may be hazardous in specific clinical situations.
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