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European Journal of Heart Failure 2000 2(3):237-240; doi:10.1016/S1388-9842(00)00084-2
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© 2000 European Society of Cardiology

‘ACE inhibitors are better than AT1 receptor blockers (ARBs)’ — controversies in heart failure

Hazel L. White* and Alistair S. Hall

Institute for Cardiovascular Research, Universtity of Leeds Leeds LS2 9JT, UK

* Corresponding author. Tel.: +44-113-233-4820; fax: +44-113-233-4803.

Received April 17, 2000; Accepted April 20, 2000

The first 150 words of the full text of this article appear below.


   1. Overview
 
Angiotensin-converting enzyme (kininase II) governs the equilibrium between the renin–angiotensin system and the kallakrein–kinin system. This in turn influences a wide variety of pathophysiological mechanisms including water and salt homeostasis, vascular tone, fibrinolysis, cell growth and inflammation, all of which are implicated in cardiac failure and two of the main underlying pathologies: coronary artery disease and systemic hypertension. ACE inhibitors, by adjusting this balance, play a pivotal role in the natural history of cardiac failure, a phenomenon reflected by the survival benefit observed in the numerous large-scale clinical trials of ACE inhibitors. In contrast, similar trials performed with the AT1, angiotensin II receptor blockers (ARBs) have yielded very disappointing results with a statistically non-significant excess of deaths.


   2. Angiotensin II concentrations
 
The deleterious effects of angiotensin II are well described. Systemically, it is a potent pressor agent also promoting salt and water retention. At a cellular level angiotensin II has been shown to . . . [Full Text of this Article]


   3. AT2 receptor-mediated effects
 

   4. Bradykinin potentiation
 

   5. Anti-thrombotic and anti-inflammatory effect
 

   6. ACE: survival studies
 

   7. ACE vs. ARB: survival studies
 

   8. Conclusion
 

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