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Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose‐mediated deleterious effect
Author(s) -
Meune Christophe,
Mahé Isabelle,
Mourad JeanJacques,
CohenSolal Alain,
Levy Bernard,
Kevorkian JeanPhilippe,
Jondeau Guillaume,
Habib Aïda,
Lebret Marilyne,
Knellwolf AnneLaure,
Simoneau Guy,
Caulin Charles,
Bergmann JeanFrançois
Publication year - 2003
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/s1388-9842(03)00006-0
Subject(s) - aspirin , medicine , placebo , thromboxane b2 , blood pressure , thromboxane , prostaglandin , cardiology , thromboxane a2 , metabolite , anesthesia , platelet , alternative medicine , pathology
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.