Circulation, Vol 81, 860-864, Copyright © 1990 by American Heart Association
SS Gottlieb, ML Kukin, N Medina, M Yushak and M Packer
Many of the newer antiarrhythmic agents are said to cause minimal
myocardial depression, but their hemodynamic effects have not been
invasively evaluated and compared in patients with severe chronic heart
failure. In a randomized, crossover study, the hemodynamic responses to
single oral doses of procainamide (750 mg), tocainide (600 mg), and
encainide (50 mg) given to 21 patients with severe chronic heart failure
were compared. Cardiac performance decreased with all three drugs, but the
magnitude of deterioration differed among the three agents. Stroke volume
index decreased with procainamide (-5 +/- 1 ml/m2, p less than 0.001),
tocainide (-7 +/- 1 ml/m2, p less than 0.001), and encainide (-8 +/- 1
ml/m2, p less than 0.001), but the decline was significantly greater with
encainide than with procainamide (p less than 0.05). Similarly, left
ventricular filling pressure increased with tocainide and encainide (+4 +/-
1 and +5 +/- 2 mm Hg, respectively; both p less than 0.05), but not with
procainamide; the increase was significantly greater with tocainide and
encainide than with procainamide (p less than 0.001). These deleterious
hemodynamic effects were accompanied by worsening symptoms of heart failure
in six patients with encainide and seven patients with tocainide but in
only two patients with procainamide. Serum levels for all drugs were in the
therapeutic range. In conclusion, although the three type I antiarrhythmic
agents tested may all adversely affect left ventricular function in
patients with heart failure, encainide and tocainide are more likely than
procainamide to cause hemodynamic and clinical deterioration.
ARTICLES
Comparative hemodynamic effects of procainamide, tocainide, and encainide in severe chronic heart failure
Department of Medicine, Mount Sinai School of Medicine, New York, New York.
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