This study evaluated the effect of bolus infusion of digoxin (0.014 mg/kg in 10 minutes, intravenously) on large coronary arteries measured by quantitative digital angiography. Twenty-two patients (mean age +/- standard deviation 47 +/- 12 years) divided into 3 groups were studied. The effects of digoxin infusion (after 10 and 20 minutes) and sublingual administration of isosorbide dinitrate were investigated in group I (patients with angiographically normal coronary arteries, n = 9) and in group II (patients with atherosclerotic coronary arteries, n = 8). To determine whether the effects of digoxin were mediated by activation of alpha-adrenergic receptors, coronary angiography was performed in group III after alpha-adrenoceptor blockade (phentolamine 0.11 mg/kg, intravenously) (n = 5). Ten minutes after the end of digoxin infusion, the cross-sectional area decreased from 7.7 +/- 4.1 to 6.0 +/- 2.2 mm2, and after 20 minutes to 5.6 +/- 2.6 mm2 (p < 0.05) in group I. Isosorbide dinitrate reverted digoxin-induced vasoconstriction as cross-sectional area increased to 8.5 +/- 3.4 mm2 (p = not significant versus baseline). Twenty minutes after digoxin infusion, heart rate significantly decreased from 79 +/- 16 to 74 +/- 13 beats/min (p < 0.01). Ten minutes after digoxin infusion, peripheral vascular resistance increased significantly from 1,396 +/- 693 to 1,693 +/- 984 dynes . s . cm-5 (p < 0.05), whereas cardiac output did not change. Twenty minutes after digoxin infusion, minimal stenosis diameter decreased significantly from 1.6 +/- 0.5 to 1.4 +/- 0.5 mm (p < 0.05) in group II. Again, isosorbide dinitrate reverted digoxin-induced vasoconstriction as minimal stenosis diameter increased (p = not significant versus control values). In group III, alpha-adrenoceptor blockade with phentolamine did not prevent the decrease in coroary artery diameter in patients with angiographically normal coronary arteries, from 2.3 +/- 0.7 to 1.9 +/- 0.7 mm (p < 0.001). Thus, bolus infusion of digoxin induced vasoconstriction of normal epicardial coronary arteries and reduced minimal stenosis diameter in patients with coronary artery disease. Digoxin-induced vasoconstriction was not mediated by an alpha-adrenergic mechanism and was revertedby sublingual administration of isosorbide dinitrate.
