Effect of digoxin on coronary blood flow and myocardial oxygen consumption in patients with chronic coronary artery disease

In 10 patients with chronic coronary artery disease and without clinical evidence of congestive heart failure, the effects of 1.0 mg of digoxin intravenously on systemic hemodynamics, coronary blood flow, myocardial oxygen consumption and myocardial lactate extraction were studied both at rest and during atrial pacing. Atrial stimulation at a rate just below the threshold for angina led to a significant decrease in left ventricular enddiastolic pressure, from 10.6 ± 1.6 to 7.1 ± 0.8 mm Hg, associated with a significant decrease in left ventricular stroke work index per beat, from 76.7 ± 5.11 to 40.3 ± 4.01 g-m/m². After digoxin, nearly identical results in stroke work index could be observed at rest and during stimulation (75.2 ± 6.74 and 44.1 ± 5.92, respectively). However, left ventricular enddiastolic pressure decreased significantly before and during atrial stimulation (8.1 ± 1.29 and 4.7 ± 1.09 mm Hg, respectively). Cardiac index decreased from 3.08 ± 0.20 to 2.73 ±0.17 liters/min per m² at rest but during pacing it no longer differed before and after digoxin (3.17 ± 0.22 and 3.10 ± 0.20 liters/min per m², respectively). Myocardial oxygen consumption and lactate extraction remained unchanged after digoxin both at rest and during atrial pacing.It is concluded that some deficiency in left ventricular function is present in patients with chronic coronary artery disease even without clinical evidence of congestive heart failure. Digoxin improves left ventricular performance at rest and during stress conditions. An expected increase in myocardial oxygen consumption due to enhanced contractility is completely counterbalanced, probably by a decrease in left ventricular volume after digoxin.