© 2004 European Society of Cardiology
Letter to the Editor
Department of Cardiology and Intensive Care General Hospital Wels, Grieskirchnerstraße 42, Wels 4600, Austria
* Corresponding author. Tel.: +43-7242-415-2215; fax: +43-7242-415-3992
Increased aortic stiffness measured by pulse-wave velocity is an independent predictor of peak exercise oxygen consumption and could partially explain exercise intolerance in patients with heart failure [1]. The article by Meune and colleagues in a recent issue of the European Journal of Heart Failure described the existence of a dose-mediated deleterious effect of aspirin upon arterial function properties in patients with chronic heart failure treated with ACE inhibitors [2]. The authors assessed the reflected pulse wave and time to aortic arrival of the reflected wave by radial applanation tonometry following treatment with aspirin 100 mg/die, and then 325 mg/die. While low-dose aspirin produced an effect on arterial function that was not significantly different compared to placebo, higher-dose aspirin induced a significant increase in augmentation index and a significant decrease in reflected wave travelling times [2].
We investigated the effect of aspirin on arterial function in a larger unselected population (n=84; 74% male; 80% ischemic heart disease; all patients on ACE-inhibitors) of heart failure patients undergoing cardiac catheterisation for evaluation of underlying coronary artery disease. Patients were in New York Heart Association (NYHA) functional class I, II, III, and IV in 42%, 31%, 25%, and 2%, respectively. Arterial function was assessed by applanation tonometry of the radial artery and calculated from the derived central aortic pressure pulse curve [3–6]. Study patients were divided into two groups according to treatment or no treatment with aspirin. All aspirin treated patients had a daily dose of 100 mg orally. Baseline characteristics and applanation tonometry measurements of both patient groups are shown in Table 1. We found no significant difference in timing and magnitude of pulse wave reflections, expressed as augmentation index, augmented pressure and time to return of the reflected wave. Thus, the present data, although obtained in an observational study, support the findings by Christophe Meune and colleagues [2] that in contrast to higher doses (325 mg/die or more), low-dose aspirin (up to a daily dose of 100 mg) had no significant effect on arterial function as expressed by augmentation index (AIx) and reflected wave travelling time.
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Facing the large proportion of heart failure patients with underlying ischemic heart disease (who are usually treated with the combination of ACE inhibitors [7] and aspirin [8]) the clinical relevance of this finding is of vital importance. Our data are in agreement with a recently published meta-analysis [9] and therefore support the statement of Christophe Meune and coworkers [2] that low-dose aspirin can be recommended in heart failure patients who concomitantly need therapy with acetylsalicylic acid.
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[Abstract/Free Full Text] - Meune C., Mahe I., Mourad J.J., et al. Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated deleterious effect. Eur J Heart Fail (2003) 5:271–279.
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- Garg R., Yusuf S. Overview of randomised trials of angiotensin converting enzyme inhibitors on mortality and morbidity in patients with heart failure. J Am Med Assoc (1995) 273:1450–1456. The Collaborative Group on ACE Inhibitor Trials.
[Abstract/Free Full Text] - Antiplatelet trialist collaboration. Collaborative overview of randomised trials of antiplatelet therapy. Part I. Prevention of death, myocardial infarction and strole by prolonged antiplatelet therapy in various categories of patients. Br Med J (1994) 308:81–106.
[Abstract/Free Full Text] - Teo K.K., Yusuf S., Pfeffer M., Torp-Pedersen C., Kober L., Hall A., et al. ACE Inhibitors Collaborative Group. Effects of long-term treatment with angiotensin-converting-enzyme inhibitors in the presence or absence of aspirin: a systematic review. Lancet (2002) 360:1037–1043.[CrossRef][Web of Science][Medline]
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