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Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated
Christophe Meune1, Isabelle Mahé, Jean-Jacques Mourad
1Internal Medicine, Hospital Lariboisière, Paris, France. christophe.meune@cch.ap-hop-paris.fr
Insights
Aspirin negatively impacts arterial function in chronic heart failure (CHF) patients on ACE inhibitors, with higher doses causing more significant adverse effects on arterial properties.
Area of Science:
- Cardiovascular Pharmacology
- Vascular Physiology
Background:
- Aspirin's inhibition of prostaglandin synthesis may adversely affect arterial function and ACE inhibitor efficacy in chronic heart failure (CHF).
- Understanding aspirin's impact on arterial properties in CHF patients receiving ACE inhibitors is crucial.
Purpose of the Study:
- To prospectively assess the effects of aspirin on arterial functional properties in CHF patients treated with ACE inhibitors.
Main Methods:
- Prospective, single-blind study involving 18 CHF patients over three 7-day periods: placebo, aspirin 100 mg/day, and aspirin 325 mg/day.
- Evaluated reflected wave analysis, pulse wave velocity, blood pressure, thromboxane B2 (TxB2), and prostaglandins.
- Radial applanation tonometry was used for arterial assessment.
Main Results:
- Aspirin 325 mg/day significantly increased augmentation index and decreased reflected wave traveling times.
- Aspirin 100 mg/day showed a similar, non-significant trend.
- Both aspirin doses significantly reduced serum TxB2, but did not affect prostaglandin I2 metabolites.
Conclusions:
- Aspirin exerts a dose-dependent, detrimental effect on arterial functional properties in CHF patients treated with ACE inhibitors.
- This highlights potential risks associated with aspirin use in this patient population.
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.
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