Obstructive sleep apnoea and 24‐h blood pressure in patients with resistant hypertension

• Published in: Journal of sleep research Vol. 19; no. 4; pp. 597 - 602
• Main Authors: LLOBERES, PATRICIA, LOZANO, LOURDES, SAMPOL, GABRIEL, ROMERO, ODILE, JURADO, MARÍA J., RÍOS, JOSÉ, UNTORIA, MARÍA D., TOVAR, JOSÉ L.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.12.2010
• Subjects: Age Factors; ambulatory blood pressure monitoring; Blood Pressure - physiology; blood pressure predictors; Body Mass Index; excessive daytime sleepiness; Female; Humans; Hypertension - complications; Hypertension - physiopathology; Linear Models; Male; Middle Aged; obstructive sleep apnoea; Polysomnography; resistant hypertension; Sex Factors; Sleep Apnea, Obstructive - complications; Sleep Apnea, Obstructive - physiopathology; Statistics, Nonparametric
• ISSN: 0962-1105; 1365-2869
• DOI: 10.1111/j.1365-2869.2010.00839.x

Summary Obstructive sleep apnoea (OSA) is common in patients with resistant hypertension, but understanding of the pathogenic mechanisms linking both conditions is limited. This study assessed the prevalence of OSA and the relationships between OSA and 24‐h blood pressure (BP) in 62 consecutive patients with resistant hypertension, defined as clinic BP values ≥ 140/90 despite the prescription of at least three drugs at adequate doses, including a diuretic. In order to exclude a ‘white coat effect’, only patients with ambulatory 24‐h BP values ≥ 125/80 were recruited. Patients underwent polysomnography, 24‐h ambulatory BP monitoring and completed the Epworth sleepiness scale (ESS). OSA was defined as an apnoea–hypopnoea index (AHI) ≥ 5 and excessive daytime sleepiness (EDS) by an ESS ≥ 10. A multiple linear regression analysis was used to assess the association of anthropometric data, OSA severity measures and ESS with 24‐h systolic and diastolic BP. Mean 24‐h BP values were 139.14/80.98 mmHg. Ninety per cent of patients had an AHI ≥ 5 and 70% had an AHI ≥ 30. Only the ESS was associated with 24‐h diastolic BP [slope 0.775, 95% confidence interval (CI) 0.120–1.390, P < 0.02); age was associated negatively with 24‐h diastolic BP (slope −0.64, 95% CI −0.874 to −0.411, P < 0.001). Compared with those without EDS, patients with EDS showed a significantly higher frequency of diastolic non‐dipping pattern (69.2% versus 34.7%, P < 0.032). Our results demonstrate a high prevalence of severe OSA in patients with resistant hypertension and suggest that EDS could be a marker of a pathogenetic mechanism linking OSA and hypertension.