The association of angiotensin converting enzyme (ACE) polymorphisms with sleep apnea and hypertension

Sleep. 2007 Apr;30(4):531-3. doi: 10.1093/sleep/30.4.531.

Abstract

Study objectives: To identify the role of polymorphisms in the angiotensin-converting enzyme (ACE) gene in modulating susceptibility to hypertension in sleep apnea.

Design: Observational cross-sectional study.

Participants: Nine hundred seventy-two participants of the Cleveland Family Study who underwent home sleep studies, blood pressure assessments, and genotyping.

Results: After controlling for age, sex, race, and obesity, hypertension risk was reduced in participants who possess the ACE deletion (D) polymorphism with an odds ratio = 0.63 (95% confidence interval: 0.41-0.96) comparing those with 2 versus no D alleles. In analyses stratified by apnea severity, the protective effect of the D allele was most evident in those with severe apnea. Among subjects with severe apnea, the odds ratios for hypertension were 0.47 (0.22-1.00) for 1 D allele and 0.57 (0.26-1.24) for 2 D alleles.

Conclusions: The ACE deletion allele may protect against hypertension in the setting of obstructive sleep apnea. Further research into the potential role of angiotensin in modulating the hypertensive effect of sleep apnea is needed.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Aged
  • Alleles
  • Chromosome Deletion
  • Comorbidity
  • Continuous Positive Airway Pressure
  • Cross-Sectional Studies
  • Female
  • Genetic Predisposition to Disease / genetics
  • Genotype*
  • Humans
  • Hypertension / epidemiology
  • Hypertension / genetics*
  • Hypertension / therapy
  • Longitudinal Studies
  • Male
  • Middle Aged
  • Mutagenesis, Insertional / genetics
  • Peptidyl-Dipeptidase A / genetics*
  • Phenotype
  • Polymorphism, Genetic / genetics*
  • Polysomnography
  • Sleep Apnea, Obstructive / epidemiology
  • Sleep Apnea, Obstructive / genetics*
  • Sleep Apnea, Obstructive / therapy

Substances

  • Peptidyl-Dipeptidase A