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European Journal of Heart Failure 2003 5(3):271-279; doi:10.1016/S1388-9842(03)00006-0
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© 2003 European Society of Cardiology

Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated deleterious effect

Christophe Meunea,*, Isabelle Mahéa, Jean-Jacques Mouradb, Alain Cohen-Solalc, Bernard Levyd, Jean-Philippe Kevorkiana, Guillaume Jondeaue, Aïda Habibf, Marilyne Lebretf, Anne-Laure Knellwolfa, Guy Simoneaua, Charles Caulina and Jean-François Bergmanna

a Internal Medicine, Hospital Lariboisière Paris, France
b Internal Medicine, Hospital Saint-Michel Paris, France
c Department of Cardiology, Hospital Beaujon Clichy, France
d Functional Explorations, Hospital Lariboisière Paris, France
e Department of Cardiology, Hospital Ambroise Paré Boulogne, France
f Inserm 348, Hospital Lariboisière Paris, France

* Corresponding author. Department of Cardiology, Hospital Cochin, 27 rue du Faubourg Saint-Jacques, 75014 Paris Cedex, France. Tel.: +33-1-58-41-16-21; fax: +33-1-58-41-16-05. E-mail address: christophe.meune{at}cch.ap-hop-paris.fr


   Abstract

Background: By inhibiting prostaglandin synthesis, aspirin can interfere with both arterial functional and angiotensin-converting enzyme inhibitor (ACEI) properties and be deleterious in chronic heart failure (CHF).

Aim: Our aim was to prospectively evaluate the effect of aspirin on arterial functional properties in CHF patients treated with ACEIs.

Methods and results: Over three consecutive treatment periods of 7 days, 18 patients received placebo, followed by aspirin 100 mg/day, and then aspirin 325 mg/day. Single blind prospective assessment of reflected wave and time reflection by radial applanation tonometry; pulse wave velocity; blood pressure; thromboxane B2 (TxB2) and prostaglandins in plasma and urine was performed. Aspirin 325 mg/day induced a significant increase in augmentation index of reflected wave (P<0.0001 and P=0.0013 vs. placebo and aspirin 100 mg, respectively) and a significant decrease in reflected wave traveling times (P=0.0007 vs. placebo). Aspirin 100 mg/day produced a similar, though non-significant, trend in these parameters compared with placebo. Both aspirin treatments produced a statistically significant decrease in serum TxB2 (P<0.0001) but did not have an effect on the metabolite of prostaglandin I2 (P=0.136).

Conclusion: This study demonstrates the existence of a dose-mediated deleterious effect of aspirin upon arterial functional properties in CHF patients treated with ACEI.

Key Words: Angiotensin-converting enzyme inhibitors • Aspirin • Heart failure • Bradykinin

Received June 26, 2001; Revised October 17, 2002; Accepted December 18, 2002


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