Hemodynamic effects of disopyramide at rest and during exercise in normal subjects

Abstract

The hemodynamic effects of disopyramide phosphate, 2.0 mg/kg body weight, given intravenously over a period of five minutes were studied at rest and during exercise in ten patients without clinical or angiographic evidence of heart disease. Following disopyramide, the resting cardiac index was lower (4.0 +/- 0.6 vs 4.3 +/- 0.6 liters/min/m2, mean +/- 1 SD,P less than 0.05), while left ventricular end-diastolic pressure (16 +/- 4 vs 11 +/- 4 mm Hg, P less than 0.001), pulmonary arterial (PA) mean pressure (20 +/- 5 vs 17 +/- 5 mm Hg, P less than 0.05), and brachial arterial (BA) mean pressure (105 +/- 8 vs 96 +/- 7 mm Hg, P less than 0.05), were higher than the pre-infusion resting values. During exercise, there was no change in left ventricular end-diastolic pressure while cardiac index rose from 4.0 +/- 0.6 to 6.5 +/- 0.6 liters/min/m2 (P less than 0.001) and left ventricular stroke work index increased from 62 +/- 19 to 84 +/- 22 gm/beat/m2 (P less than 0.001). The normal hemodynamic response during exercise after disopyramide despite the apparent depression of left ventricular function at rest probably reflects the positive inotropic effect of enhanced sympathoadrenergic activity.

Hemodynamics Changes after Tilting and the Efficacy of Preventive Drugs

“…The dis‐res group was the only group in our study to show a significant increase of DBP and TPR from pre‐ to post‐disopyramide administration. It was reported that intravenous disopyramide increased DBP in normal patients 33 …”

Negative inotropic effects of disopyramide on guinea‐pig papillary muscles

“…Disopyramide decreases the rate of diastolic depolarization during phase 4 of the action potential decreases the upstroke velocity of phase 0 of the action potential and prolongs the duration of the action potential and the refractory period (phases 2 and 3). In addition, a negative inotropic effect of disopyramide has been identified in animal experiments (Nayler, 1979;Walsh & Horwitz, 1979;Abdollah et al, 1984;Beltrame et al, 1984) and has been detected by echocardiography (Martin et al, 1980;Pollick et al, 1982;Holt et al, 1983), radionuclide angiography (Wisenberg et al, 1984) and during cardiac catheterisation (Thadani et al, 1981) in normal volunteers. In some haemodynamic studies on patient groups, the effects of disopyramide on myocardial performance have been minimal (Marrott et al, 1976;Sutton, 1976), but in patients with preexisting left ventricular function abnormalities, negative inotropic effects are more marked (Hills et al, 1976;Jensen et al, 1976;Sutton, 1976;Davies et al, 1979;Hulting & Rosenhamer, 1979;Naqui et al, 1979;Scheinman et al, 1980;Gottdiener et al, 1983;Greene et al, 1983;Marrott et al, 1983;Cameron et al, 1984).…”