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Angiotensin II blockers in obstructive pulmonary disease: a randomised controlled trial

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

CORRESPONDENCE: S. Andreas, Lungenfachklinik Immenhausen, Robert-Koch-Str. 3, 34376 Immenhausen, Germany. Fax: 49 5673501101. E-mail: sandreas{at}med.uni-goettingen.de

Keywords: Chronic obstructive pulmonary disease, haematocrit, irbesartan, respiratory muscle

Received: August 22, 2005
Accepted January 11, 2006

In chronic obstructive pulmonary disease (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.

The effects of the angiotensin receptor blocker irbesartan given over 4 months was evaluated in 60 patients with COPD and a forced expiratory volume in one second of <50% of the predicted value and 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 end-point maximum inspiratory pressure. Spirometric results were not affected, but total lung capacity was reduced. Irbesartan led to a significant decrease in haematocrit (46.4±3.6 to 43.9±4.3% versus 47.5±2.4 to 48.7±3.0% with placebo).

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

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