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Volume 10, Issue 10, Pages 1107-1111 (December 2009)


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Reciprocal interactions of obstructive sleep apnea and hypertension associated with ACE I/D polymorphism in males

Renata G. Koyamaab, Luciano F. Dragercd, Geraldo Lorenzi-Filhod, Fátima D. Cintraa, Alexandre C. Pereirac, Dalva Poyaresa, José Eduardo Kriegerc, Rosa M.R.P.S. Castroa, Sérgio Tufika, Marco Túlio de Melloab, Mario PedrazzoliaCorresponding Author Informationemail address

Received 17 October 2008; received in revised form 17 December 2008; accepted 17 December 2008.

Abstract 

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±13y, body mass index=29±5kg/m2, AHI=34±25events/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.

a Department of Psychobiology, Universidade Federal de São Paulo, Brazil

b Psychobiology and Exercise Research Center, Universidade Federal de São Paulo/UNIFESP, Rua Napoleão de Barros, 925, Vila Clementino, 04024-002 São Paulo, Brazil

c Hypertension Unit, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil

d Sleep Laboratory, Pulmonary Division, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil

Corresponding Author InformationCorresponding author. Tel.: +55 11 21490155/251; fax: +55 11 21490155.

PII: S1389-9457(09)00136-1

doi:10.1016/j.sleep.2008.12.012


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