From the authors
I would like to thank M. Meysman for raising the interesting aspect of the angiotensin-converting enzyme (ACE) genotype in chronic obstructive pulmonary disease (COPD) patients. I fully agree that the activation of the rennin–angiotensin system is likely to contribute to inflammation, cachexia, pulmonary hypertension and skeletal muscle dysfunction in COPD 1. M. Meysman cited interesting studies by Kanazawa and co-workers 2, 3 and Hopkins et al. 4 pointing to an effect of the ACE genotype on pulmonary hypertension and muscle strength in COPD patients.
My study group evaluated the effects of an angiotensin-receptor blocker in patients with COPD and found no significant effect on the primary end-point, maximum inspiratory pressure. However, total lung capacity and haematocrit were affected 5. It was reasoned that well-known cardiovascular drugs can produce unanticipated effects in COPD patients. Pulmonary haemodynamics were not evaluated because this was a noninvasive study. However, echocardiography was used without noticing a significant effect of angiotensin I inhibition on right ventricular dimension. Furthermore, the rennin–angiotensin system is unlikely to be a major determinant of pulmonary vascular pathology in therapeutic trials 6.
Albeit it must be acknowledged that there is a clear benefit of angiotensin-converting enzyme and angiotensin I inhibition in large randomised cardiovascular trials, pharmacogenomics probably help to improve individual tailored therapy. Thus, I value the suggestion to assess the effect of angiotensin-converting enzyme genotype in further therapeutic studies on chronic obstructive pulmonary disease patients.
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