Objective: To test the hypothesis that sleep-related breathing disorder (SRBD) is associated with poor blood pressure control in hypertensive patients independent from confounding factors such as age, body mass index, alcohol, smoking and daytime blood gases.
Design and methods: This cross-sectional study of a sleep laboratory cohort was carried out at the University Hospital Sleep Disorders Centre, Marburg. The study comprised 599 patients referred for a sleep study, all of them with a documented history of systemic hypertension and/or previously initiated antihypertensive therapy. Data were obtained from a clinical interview, two unattended sleep studies and assessment of clinic blood pressure, cholesterol level, alcohol and nicotine consumption and daytime blood gases. The main outcome measure was a post hoc analysis of predictors for poor blood pressure control.
Results: Respiratory disturbance index (RDI) was significantly higher in patients with uncontrolled hypertension (blood pressure ≥ 160 and/or 95 mmHg, n = 463) than in those with controlled hypertension (n = 136) (34.0 ± 26.8 versus 27.0 ± 23.5, P <0.01). The relative proportion of patients with uncontrolled hypertension increased significantly as SRBD activity increased (χ2, P <0.05). Body mass index was the only independent predictor (P = 0.006) of uncontrolled hypertension in the whole study sample. However, in the subset of patients aged ≤ 50 years, RDI (P = 0.006) and age (P = 0.016) were the only independent predictors. The probability of uncontrolled hypertension increased by approximately 2% (B = 0.019, P = 0.006) for each RDI unit.
Conclusion: SRBD should be considered, in addition to traditional confounders, as a risk factor for poor blood pressure control in younger hypertensive patients (≤ 50 years of age).
1Department of Clinical Pharmacology and Sleep Laboratory, Pulmonary Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
2Sleep Disorders Centre, University of Marburg, Germany.
3Correspondence and requests for reprints to Ludger Grote, Department of Clinical Pharmacology, Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Tel: +46 31 342 2964; fax: +46 31 826723; e-mail: email@example.com
Sponsorship: This study was supported by research grants from the Deutsche Forschungsgemeinschaft (265/3-2), the Bundesministerium f, r Forschung und Technik (01 KE 8803/8), the Carnegie Foundation and the University of Gothenburg.
Received 23 November 1999 Revised 28 February 2000 Accepted 9 March 2000