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From the authors

Lungenfachklinik Immenhausen, Immenhausen, Germany.

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.

REFERENCES

1. Andreas S, Anker SD, Scanlon PD, Somers VK. Neurohumoral activation as a link to systemic manifestation of chronic lung disease. Chest 2005;128:3618–3624.[Abstract/Free Full Text]
2. Kanazawa H, Okamoto T, Hirata K, Yoshikawa J. Deletion polymorphisms in the angiotensin converting enzyme gene are associated with pulmonary hypertension evoked by exercise challenge in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000;162:1235–1238.[Abstract/Free Full Text]
3. Kanazawa H, Hirata K, Yoshikawa J. Effects of captopril administration on pulmonary haemodynamics and tissue oxygenation during exercise in ACE gene subtypes in patients with COPD: a preliminary study. Thorax 2003;58:629–631.[Abstract/Free Full Text]
4. Hopkinson NS, Nickol AH, Payne J, et al. Angiotensin converting enzyme genotype and strength in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2004;170:395–399.[Abstract/Free Full Text]
5. Andreas S, Herrmann-Lingen C, Raupach T, et al. Angiotensin II blockers in obstructive pulmonary disease: a randomised controlled trial. Eur Respir J 2006;27:972–979.[Abstract/Free Full Text]
6. Farber HW, Loscalzo J. Pulmonary arterial hypertension. N Engl J Med 2004;351:1655–1665.[Free Full Text]

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