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Eur Respir J 2006; 28:670
Copyright ©ERS Journals Ltd 2006

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

M. Meysman

Respiratory Division, University Hospital AZ VUB, Brussels, Belgium.

To the Editors:

In a recent issue of the European Respiratory Journal, Andreas et al. 1 explored the effect of the angiotensin II type-1 receptor blocker irbesartan on skeletal and respiratory muscle strength in Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage III and IV chronic obstructive pulmonary disease (COPD) patients.

Although I agree that there is only sparse evidence of any systemic or pulmonary effect of angiotensin-converting enzyme (ACE) inhibitors in COPD, there are some indications that increased rennin–angiotensin system activity may contribute to the pathogenesis and progression of COPD. Captopril, at a dose of 25 mg, is associated with lower exertional pulmonary artery pressure, lower pulmonary vascular resistance, higher mixed venous oxygen saturation, and lower lactate levels in selected COPD patients 2. In several studies, Kanazawa and co-workers 3–5 demonstrated that these effects might be ACE genotype dependent. Based on the presence (insertion) or absence (deletion) of some alleles, they demonstrated that increased pulmonary arterial pressure is associated with the angiotensin deletion allele, which was confirmed by an independent Slovakian group 6. The deletion allele is also associated with greater quadriceps strength in COPD patients 7.

So if we want to study the effects of angiotensin-converting enzyme blockers on the exercise capacity in chronic obstructive pulmonary disease patients, we should not only power the study to detect modest changes in maximal oxygen uptake, but also stratify for angiotensin-converting enzyme gene polymorphism as this could potentially effect the oxygen delivery to the working muscle.

REFERENCES

  1. 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]
  2. 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]
  3. 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]
  4. Kanazawa H, Otsuka T, Hirata K, Yoshikawa J. Association between the angiotensin-converting enzyme gene polymorphisms and tissue oxygenation during exercise in patients with COPD. Chest 2002;121:697–701.[Abstract/Free Full Text]
  5. Kanazawa H, Hirata K, Yoshikawa J. Influence of oxygen administration on pulmonary haemodynamics and tissue oxygenation during exercise in COPD patients with different ACE genotypes. Clin Physiol Funct Imaging 2003;23:332–336.[CrossRef][ISI][Medline] [Order article via Infotrieve]
  6. Tkacova R, Joppa P, Stancak B, Salagovic J, Misikova S, Kalina I. The link between angiotensin-converting enzyme genotype and pulmonary artery pressure in patients with COPD. Wien Klin Wochenschr 2005;117:210–214.[ISI][Medline] [Order article via Infotrieve]
  7. 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]



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R. Tkacova and P. Joppa
Angiotensin-converting enzyme genotype and C-reactive protein in patients with COPD
Eur. Respir. J., April 1, 2007; 29(4): 816 - 817.
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