(Circulation. 2006;113:2566-2568.)
© 2006 American Heart Association, Inc.
Editorial |
From the Department of Cardiology, Western Infirmary, Scotland, UK.
Correspondence to Dr J.J.V. McMurray, Department of Cardiology, Western Infirmary, Scotland G11 6NT, UK. E-mail j.mcmurray@bio.gla.ac.uk
Key Words: Editorials angiotensin-converting enzyme inhibitors aspirin heart failure pharmacology
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Fourteen years ago, Hall and colleagues1 reported observations that initiated a vigorous debate about a possible interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors that continues to this day. That debate centers on whether the apparent pharmacological interaction between aspirin and ACE inhibitors might influence clinical outcomes and has been heightened greatly by the provocative suggestion that long-term aspirin use might not be beneficial in patients with chronic coronary heart disease, including those with heart failure.2 The arguments used in the debate and the studies on which they are based highlight the strengths and weaknesses of many of the main strands of modern cardiovascular therapeutic research and illustrate many useful lessons about the interpretation of these different types of study.
Article p 2572
Hall et al1 carried out what might be called a "mechanistic" study, demonstrating that the short-term hemodynamic effects of an ACE inhibitor in patients with severe heart failure were attenuated by aspirin. Many but not all subsequent studies have supported this finding.36 Although interesting, the clinical importance of this observation is uncertain. First, whether the effect of aspirin persists in the longer term is unknown. Second, we do not know how an ACE inhibitor exerts its beneficial effect and therefore how important its hemodynamic or other actions are. Third, experience has taught us that however plausible a pharmacological mechanism may seem, it may not lead to the expected effect on clinical outcome. Consequently, studies on the actions of drugs on potentially important biological mechanisms can only be
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