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Interaction between cyclooxygenase and the renin-angiotensin-aldosterone system: rationale and clinical relevance
Christophe Meune
Department of Cardiology, Cochin Hospital, Rene Descartes University, Paris, France
Jean-Jacques Mourad
Department of Internal Medicine, Georges Pompidou European Hospital, Paris, France
Jean-François Bergmann
Department of Internal Medicine, Lariboisière Hospital, Paris, France
Christian Spaulding
Department of Cardiology, Cochin Hospital, Rene Descartes University, Paris, France, christian.spaulding{at}cch.ap-hop-paris.fr
Increased understanding of pathophysiological mechanisms of cardiovascular diseases has shown that the renin-angiotensin-aldosterone system (RAAS) is activated in this setting and suggests a central role for the angiotensin-converting enzyme (ACE). ACE transforms angiotensin I (Ang I) to angiotensin II (Ang II), and also promotes the degradation of bradykinin into inactive metabolites. These bradykinins stimulate nitric oxide synthesis and vasodilatator prostaglandin synthesis via a cyclooxygenase (COX) pathway.
COX inhibitors may therefore be deleterious in cardiovascular disease and/or counteract part of ACE inhibitor (ACE-I) efficacy. This has been clearly demonstrated with non-steroidal anti-inflammatory drugs (NSAIDs), including high-dose aspirin, in avoiding their use in such patients. hypertension, coronary artery disease and chronic heart failure (CHF); most guidelines recommend avoiding their use in such patients.
Theoretically, this effect is dose-mediated and the existence of an identical deleterious effect with low-dose aspirin has been an area of intense debate. In this article, we review studies, most of them conducted in CHF, that pointed out such a possible deleterious effect and a counteraction of ACE-Is with low-dose aspirin , using various criteria of assessment.
However, there are no prospective long-term studies that have validated such an effect, and the role of other anti-aggregating agents has not been evaluated. Until such studies are published, the use of low-dose aspirin (100 mg/day) in such patients can be recommended.
Key Words: angiotensin II • angiotensin-converting enzyme • aspirin • heart failure
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Journal of Renin-Angiotensin-Aldosterone System, Vol. 4, No. 3,
149-154 (2003)
DOI: 10.3317/jraas.2003.023
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