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Published online before print January 30, 2006
Eur Respir J 2006, doi:10.1183/09031936.06.00098105
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ORIGINAL ARTICLE

Angiotensin II blockers in obstructive pulmonary disease. A randomized, controlled trial

S. Andreas 1*, C. Herrmann-Lingen 2, T. Raupach 3, L. Lüthje 3, J.A. Fabricius 3, N. Hruska 3, W. Körber 4, B. Büchner 2, C-P. Criée 4, G. Hasenfuß 3, P. Calverley 5

1 Lungenfachklinik Immenhausen; and Dept of Cardiology and Pneumology, Georg-August-Universitat Göttingen, Germany
2 Dept of Psychosomatics and Psychotherapy, section of Psychocardiology; Georg-August-Universitat Göttingen, Germany
3 Dept of Cardiology and Pneumology, Georg-August-Universitat Göttingen, Germany
4 Bereich Pneumologie Evangelisches Krankenhaus Göttingen Weende e.v., Germany
5 Dept of Medicine, University Hospital Aintree, Liverpool, UK

* To whom correspondence should be addressed. E-mail: sandreas{at}med.uni-goettingen.de.


   Abstract

In COPD, the sympathetic nervous system as well as the renin-angiotensin system is activated with possible negative systemic effects on skeletal muscles. Angiotensin II type 1 receptor blockers inhibit the sympathetic and renin-angiotensin systems and might improve skeletal and respiratory muscle strength in patients in whom these systems are activated.

We evaluated the effects of the angiotensin receptor blocker irbesartan given over 4 months to 60 patients with COPD and an FEV1<50% predicted without obvious cardiovascular disease that would necessitate the administration of an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.

Irbesartan was well tolerated, but did not exert a significant effect on the primary endpoint maximum inspiratory pressure. Spirometry was not affected but total lung capacity was reduced. Irbesartan led to a significant decrease in hematocrit (46.4±3.6 to 43.9±4.3% vs. 47.5±2.4 to 48.7±3.0 with placebo; p ANOVA<0.0005).

In conclusion respiratory muscle strength in COPD patients was not influenced by angiotensin II receptor blockade. However, the changes in hematocrit and total lung capacity following irbesartan raise the possibility that well known cardiovascular drugs can produce unanticipated beneficial effects in COPD patients.

Keywords:  Chronic obstructive lung disease, hematocrit, irbesartan, respiratory muscle




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