title: The DD genotype of the angiotensin converting enzyme gene is negatively associated with right ventricular hypertrophy in male patients with chronic obstructive pulmonary disease.
abstract: The renin angiotensin system plays an important role in the development of pulmonary artery remodeling and right ventricular hypertrophy in hypoxia-induced pulmonary hypertension as may occur in patients with COPD. Several polymorphisms of genes encoding for components of the renin angiotensin system such as the M235T polymorphism in the angiotensinogen gene, the 287-base-pair insertion (I)/deletion (D) polymorphism at intron 16 of the ACE gene, and the A1166C polymorphism in the angiotensin II type 1 receptor gene have been associated with an increased risk of cardiovascular diseases. With respect to the pulmonary circulation, only limited data exist on possible associations between polymorphisms of these genes and pulmonary hypertension and/or right ventricular hypertrophy. The objective of the present study was to investigate a possible relationship between polymorphisms of the renin angiotensin system and electrocardiographic evidence of right ventricular hypertrophy in patients with COPD. We therefore determined the angiotensinogen (M235T), angiotensin converting enzyme (I/D), and angiotensin II type 1 receptor (A1166C) genotypes in 87 patients with severe COPD and correlated these data with electrocardiographic parameters of right ventricular hypertrophy. Thirty-one patients (36%) of 87 patients with COPD showed electrocardiographic evidence of right ventricular hypertrophy. In the male, but not in the female, subgroup, the angiotensin-converting enzyme DD genotype was negatively associated with electrocardiographic evidence of right ventricular hypertrophy (male: chi2 = 3.8, p = 0.05; female: chi2 = 0.05, p = 0.82). We found no associations between the investigated polymorphisms in the angiotensinogen and angiotensin II type 1 receptor genes and electrocardiographic evidence of right ventricular hypertrophy.
authors.affiliation: Departments of Pathology, Cardiology, Pulmonology and Asthmacentre, Cardiovascular Research Institute Maastricht, The Netherlands.
authors.forename: R J
authors.initials: RJ
authors.lastname: van Suylen
authors.forename: E F
authors.initials: EF
authors.lastname: Wouters
authors.forename: H J
authors.initials: HJ
authors.lastname: Pennings
authors.forename: E C
authors.initials: EC
authors.lastname: Cheriex
authors.forename: P E
authors.initials: PE
authors.lastname: van Pol
authors.forename: A W
authors.initials: AW
authors.lastname: Ambergen
authors.forename: A M
authors.initials: AM
authors.lastname: Vermelis
authors.forename: M J
authors.initials: MJ
authors.lastname: Daemen
mesh_terms: D000368:Aged; D000808:Angiotensinogen / Q000235:genetics; D004251:DNA Transposable Elements; D004562:Electrocardiography; D005260:Female; D017353:Gene Deletion; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D017380:Hypertrophy, Right Ventricular / Q000150:complications* / Q000175:diagnosis / Q000235:genetics*; D008173:Lung Diseases, Obstructive / Q000150:complications*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000235:genetics; D012727:Sex Characteristics
chemical_list: D004251:DNA Transposable Elements; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A