BACKGROUND: The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism gene contributes to the genesis of hypertension (HTN) and may help explain the relationship between obstructive sleep apnea (OSA) and HTN. However, ACE is a pleiotropic gene that has several influences, including skeletal muscle and control of ventilation. We therefore tested the hypothesis that ACE polymorphism influences OSA severity. METHODS: Male OSA patients (apnea-hypopnea index [AHI]>5 events/h) from 2 university sleep centers were evaluated by polysomnography and ACE I/D polymorphism genotyping. RESULTS: We studied 266 males with OSA (age=48+/-13 y, body mass index=29+/-5 kg/m(2), AHI=34+/-25 events/h). HTN was present in 114 patients (43%) who were older (p<0.01), heavier (p<0.05) and had more severe OSA (p<0.01). The I allele was associated with HTN in patients with mild to moderate OSA (p<0.01), but not in those with severe OSA. ACE I/D polymorphism was not associated with apnea severity among normotensive patients. In contrast, the only variables independently associated with OSA severity among patients with hypertension in multivariate analysis were BMI (OR=1.12) and II genotype (OR=0.27). CONCLUSIONS: Our results indicate reciprocal interactions between OSA and HTN with ACE I/D polymorphism, suggesting that among hypertensive OSA males, the homozygous ACE I allele protects from severe OSA.
BACKGROUND: The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism gene contributes to the genesis of hypertension (HTN) and may help explain the relationship between obstructive sleep apnea (OSA) and HTN. However, ACE is a pleiotropic gene that has several influences, including skeletal muscle and control of ventilation. We therefore tested the hypothesis that ACE polymorphism influences OSA severity. METHODS: Male OSA patients (apnea-hypopnea index [AHI]>5 events/h) from 2 university sleep centers were evaluated by polysomnography and ACE I/D polymorphism genotyping. RESULTS: We studied 266 males with OSA (age=48+/-13 y, body mass index=29+/-5 kg/m(2), AHI=34+/-25 events/h). HTN was present in 114 patients (43%) who were older (p<0.01), heavier (p<0.05) and had more severe OSA (p<0.01). The I allele was associated with HTN in patients with mild to moderate OSA (p<0.01), but not in those with severe OSA. ACE I/D polymorphism was not associated with apnea severity among normotensive patients. In contrast, the only variables independently associated with OSA severity among patients with hypertension in multivariate analysis were BMI (OR=1.12) and II genotype (OR=0.27). CONCLUSIONS: Our results indicate reciprocal interactions between OSA and HTN with ACE I/D polymorphism, suggesting that among hypertensive OSA males, the homozygous ACE I allele protects from severe OSA.
Authors: Fábio S Lira; Gustavo D Pimentel; Ronaldo Vt Santos; Lila M Oyama; Ana R Damaso; Cláudia M Oller do Nascimento; Valter Ar Viana; Rita A Boscolo; Viviane Grassmann; Marcos G Santana; Andrea M Esteves; Sergio Tufik; Marco T de Mello Journal: Lipids Health Dis Date: 2011-07-06 Impact factor: 3.876
Authors: Alberto R Ramos; Pedro Figueredo; Shirin Shafazand; Alejandro D Chediak; Alexandre R Abreu; Salim I Dib; Carlos Torre; Douglas M Wallace Journal: Front Neurol Date: 2017-12-05 Impact factor: 4.003