Common intronic D variant of ACE gene is associated with endothelial dysfunction in COPD

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Pathogenesis of chronic obstructive lung disease (COPD) includes primary inflammatory events, multiple vascular reactions, remodeling of bronchial and vascular walls. The aim of present single-center study was to assess relations between angiotensin-converting enzyme (ACE) gene and prevalence of clinical symptoms characteristic to COPD. The study involved sixty-three male patients with COPD (44-86 years old, a mean of 60.4 years). COPD diagnostics was performed according to common criteria, including evaluation of systolic pressure in pulmonary artery (SPPA) and endothelial disfunction (ED). Genotyping of ACE I/D was performed by means of gene-specific PCR. 1. Allele distribution of studied gene alleles among COPD patients did not differ from control age-matched group. 2. Detectable endothelial dysfunction in COPD patients was shown to correlate with high-producer D allele of ACE gene, at an odds ratio of 6.632 (CI=1.67-26.31; chi2=8.39, p=0.004). Moreover, detectable ED correlated with numbers of COPD exacerbations per year. These findings suggest possible association of the functional ACE D allele with altered vascular responses that may modulate development of distinct COPD symptoms. The results are obtained in a limited clinical cohort, and deserve repeated trials in other groups of COPD patients.