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