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BMJ 2005;330:1270 (28 May), doi:10.1136/bmj.330.7502.1270-a
| The first 150 words of the full text of this article appear below. |
EditorWe agree with Verma and Strauss that it is naive to consider that angiotensin receptor blockers are like angiotensin converting enzyme (ACE) inhibitors, but without the cough.1 Although the evidence is conflicting, the hypothesis that angiotensin receptor blockers may predispose to myocardial infarction when used in preference to ACE inhibitors warrants further attention.
Long term clinical benefits of treatment with ACE inhibitors, including reduction in fatal and non-fatal myocardial infarction, are well established in chronic heart failure, hypertension, and after myocardial infarction.2 These benefits persist, although serum concentrations of angiotensin II return to pre-treatment values after long term treatment with ACE inhibitors.3
This implies that the mechanism(s) of benefit from ACE inhibitors extend beyond simple antagonism of angiotensin II. The effects of ACE inhibitors are related to the upstream blockade of the renin-angiotensin axis, which not only attenuates the conversion of angiotensin I to angiotensin II but also inhibits the
Zaheer R Yousef, specialist registrar
zypusef@dircon.co.uk
Francisco Leyva, consultant cardiologist, Christopher Gibbs, consultant cardiologist
Department of Cardiology, Good Hope Hospital, Sutton Coldfield, West Midlands B75 7RR