Key result
The presence of the D allele of the ACE gene showed a non-significant trend towards an increased risk of arterial hypertension in patients with COPD (OR 1.26).
Why the study?
Cardiovascular diseases are common in people with COPD and increase hospitalization and mortality, prompting an assessment of the role of the ACE gene polymorphism in the occurrence of arterial hypertension in COPD.
Does the ACE gene I/D polymorphism increase the risk of arterial hypertension in patients with COPD?
Case-Control (n=116)
No
Does the ACE gene I/D polymorphism increase the risk of arterial hypertension in patients with COPD?
Effect estimate: OR 1.26 (95% CI 0.47-2.39)
Absolute Event Rate: 46.4% vs 45%
p-value: p=>0.05
The study found no significant association between ACE gene I/D polymorphism and arterial hypertension in COPD patients, though a non-significant trend suggested the D allele might increase risk.
No significant ACE D allele association with hypertension in COPD; hypothesis-generating and should not change practice pending larger studies.
Background Cardiovascular diseases (CVDs) are common in people with chronic obstructive pulmonary disease (COPD), and their presence is associated with an increased risk for hospitalization, longer length of stay and all-cause and CVD-related mortality. We assessed the role of angiotensin-converting enzyme (ACE) gene polymorphism in the occurrence of arterial hypertension (AH) in patients with COPD. Methods The study group consisted of 96 patients. Group 1 had 25 individuals with COPD, Group 2 had 23 individuals with AH and Group 3 had 28 individuals with COPD and AH. The control group consisted of 20 healthy subjects. I/D genotypes of ACE were determined by polymerase chain reaction amplification. Results The frequency distribution of polymorphic genotypes of the gene encoding ACE and assessment of compliance with the Hardy-Weinberg population equilibrium were carried out in groups of patients with COPD, AH and COPD + AH combination. The frequencies of the genotype responsible for I/D polymorphism of the ACE gene in the control and experimental groups were not found to deviate significantly from the Hardy–Weinberg equilibrium. The results of the study have not demonstrated any significant impact of alleles of ACE genes or ACE genes on occurrence of diseases such as COPD, AH and combinations thereof. However, analysis of odds ratio has demonstrated that the presence of the D allele of the ACE gene may increase the risk for occurrence of the COPD + AH (OR = 1.26). Conclusion The data obtained in the study allow suggesting that the presence of D allele of the ACE gene may increase the risk for AH in patients with COPD.
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Марущак et al. (2019) conducted a case-control in Chronic Obstructive Pulmonary Disease (COPD) and Arterial Hypertension (AH) (n=116). ACE gene D allele vs. Healthy controls was evaluated on Occurrence of combined COPD and arterial hypertension (OR 1.26, 95% CI 0.47-2.39, p=>0.05). The presence of the D allele of the ACE gene showed a non-significant trend towards an increased risk of arterial hypertension in patients with COPD (OR 1.26).
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