(Circulation. 2001;103:1083.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Cardiology, Baragwanath Hospital, University of the Witwatersrand, Johannesburg, South Africa.
Correspondence to Daniel Skudicky, MD, Department of Cardiology, Baragwanath Hospital, PO Bertsham 2013, Johannesburg, South Africa. E-mail dskudi{at}icon.co.za
BackgroundWe
previously reported beneficial effects of pentoxifylline, a
xanthine-derived agent known to inhibit the production of tumor
necrosis factor-
, in patients with idiopathic dilated cardiomyopathy
treated with diuretics, digoxin, and ACE inhibitors. Since then, 3
large clinical trials showed important clinical benefits of
ß-blockers in this population. Therefore, we designed the present
study to establish whether in patients with heart failure already
receiving treatment with ACE inhibitors and ß-blockers, the addition
of pentoxifylline would have an additive beneficial
effect.
Methods and ResultsIn a single-center, prospective, double-blind, randomized, placebo-controlled study, 39 patients with idiopathic dilated cardiomyopathy were randomized to pentoxifylline 400 mg TID (n=20) or placebo (n=19) if they had a left ventricular ejection fraction <40% after 3 months of therapy with digoxin, ACE inhibitors, and carvedilol. Primary end points were New York Heart Association functional class, exercise tolerance, and left ventricular function. Patients were followed up for 6 months. Five patients died (3 in the placebo group). Patients treated with pentoxifylline had a significant improvement in functional class compared with the placebo group (P=0.01), with an increment in exercise time from 9.5±5 to 12.3±6 minutes (P=0.1). Left ventricular ejection fraction improved from 24±9% to 31±13%, P=0.03, in the treatment group.
ConclusionsIn patients with idiopathic dilated cardiomyopathy, the addition of pentoxifylline to treatment with digoxin, ACE inhibitors, and carvedilol is associated with a significant improvement in symptoms and left ventricular function.
Key Words: cardiomyopathy heart failure apoptosis
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