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

Department of Pulmonology (Sleep Unit), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Journal of Sleep Research (Impact Factor: 2.95). 12/2010; 19(4):597-602. DOI: 10.1111/j.1365-2869.2010.00839.x
Source: PubMed

ABSTRACT 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.

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    ABSTRACT: Resistant hypertension in diabetes is associated with poor cardiovascular and renal outcomes. This brief review will examine the definitions and epidemiology of resistant hypertension and consider the differences between apparent resistant hypertension and truly resistant or refractory hypertension. It will review the role of the sympathetic nervous system in resistant hypertension. It will consider the relationship between obesity and leptin resistance and sympathetic signaling; the role of obstructive sleep apnea in resistant hypertension; and the role of aldosterone in resistant hypertension. It will conclude by mentioning briefly renal nerve ablation.
    Current Diabetes Reports 08/2014; 14(8):516. DOI:10.1007/s11892-014-0516-y · 3.38 Impact Factor
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    ABSTRACT: Objective Investigate the clinical features and the blood pressure (BP) pattern of the phenotype of excessive daytime sleepiness (EDS) in OSAHS. Methods A total of 508 Chinese adults with suspected OSAHS were referred to our sleep laboratory from October 2009 to May 2012. On the same night of polysomnography (PSG), the levels of blood pressure were measured before sleeping (bedtime BP) and immediately after waking up in the next morning (morning BP). EDS was recognized as Epworth Sleepiness Scale (ESS)≥9. Subjects were classified into four groups based on the apnea-hypopnea index (AHI) from PSG as follows: control (simple snoring) group (control, n=104) with AHI<5; mild group (mild, n=89) with AHI≥5 and <15; moderate group (moderate, n=70) with AHI≥15 and<30; and severe group (severe, n=245) with AHI ≥30. The differences and correlations between BP and PSG parameters in EDS and non-EDS group of OSAHS patients were analyzed. Results In all subjects, ESS was positively correlated with morning diastolic blood pressure (DBP), Mean arterial pressure (MAP) and bedtime DBP (r=0.144, 0.102 and 0.114, respectively, each P value<0.05). In OSAHS patients, ESS was only positively correlated with morning DBP (r=0.137, P<0.05). OSAHS patients with EDS phenotype were younger and were more likely to have the symptom of waking up feeling tired (36.1% vs. 23.2%, p=0.023), who had lower MSaO2, longer SIT90 (the ratio of time of SpO2 below 90% in total sleep time) and higher DBP (bedtime as well as morning). In patients with AHI≥15, ESS was correlated positively with both bedtime and morning DBP after controlling the confounding effects of age, sex, BMI, AHI and nadir nocturnal oxygen saturation( r=0.126,0.143, respectively, both P values<0.05). And in OSAHS patients of EDS phenotype, the bedtime DBP, bedtime MAP, morning DBP, and morning MAP were 3~5 mm Hg higher than that in patients of non-EDS phenotype(P<0.05). In the moderate and severe OSAHS group, patients with EDS phenotype were younger and had a lower mean blood oxygen saturation (MSaO2), longer time of SpO2 below 90% and higher SIT90 than patients with non-EDS phenotype (P<0.05). In hypertensive OSAHS patients, patients with EDS were also younger and had higher micro-arousal index (MiI), as well as higher morning DBP, morning MAP and bedtime DBP than that in non-EDS group (P<0.05). Conclusions EDS in OSAHS patients is a special phenotype, which was characterized by younger age, higher DBP and more severe hypoxic load. This feature is mainly manifested in moderate and severe OSAHS patients. It is very important to identify the phenotype of EDS in patients with OSAHS, who may meet more benefits from effective treatment of OSAHS by correcting the intermittent nocturnal hypoxia and sleep fragmentation.
    International journal of medical sciences 01/2014; 11(7):713-20. DOI:10.7150/ijms.7487 · 1.55 Impact Factor
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    ABSTRACT: Objective: The high prevalence of obstructive sleep apnea in patients with resistant hypertension could be mediated by an activation of the renin-angiotensin-aldosterone system. This study assessed the impact of continuous positive airway pressure (CPAP) treatment on plasma aldosterone concentration (PAC). Methods: One hundred and twenty-four patients with resistant hypertension were assessed, and those who fulfilled inclusion criteria (n = 116) underwent full night polysomnography, 24-h ambulatory blood pressure monitoring, and PAC measurement. Patients with an apnea-hypopnea index above 15 (n = 102) were randomized to CPAP (n = 50) or to conventional treatment (n = 52) for 3 months. Results: Seventy-eight patients completed the follow-up (36 CPAP, 42 conventional treatment); 58 had true resistant hypertension (74.3%), whereas 20 had white-coat resistant hypertension (25.6%). Most patients were men (70.7%), age 58.3 +/- 9.4 years, and the mean apnea-hypopnea index was 50.1 +/- 21.6. In patients with true resistant hypertension, CPAP achieved a significant decrease in most 24-h BP measurements and a nonsignificant decrease in PAC (25 +/- 8.7 vs. 22.7 +/- 9 ng/dl; P<0.182). In patients with white-coat resistant hypertension, CPAP achieved a significant decrease in PAC (26.1 +/- 11.2 vs. 18.9 +/- 10.1 ng/dl; P<0.041) and in night-time DBP. After adjustment, a weak but significant association was found between cumulative time spent with SaO(2) below 90% (CT90%) and baseline PAC (P<0.047, R-2 0.019), and between changes in PAC and changes in office DBP (P<0.020, R-2 0.083) Conclusions: Night-time hypoxemia and changes in DBP showed an association with baseline and changes in PAC, respectively. CPAP achieved a significant reduction in PAC only in patients with white-coat resistant hypertension, although the CPAP effect on BP was highest in patients with true resistant hypertension.
    Journal of Hypertension 05/2014; 32(8). DOI:10.1097/HJH.0000000000000238 · 4.22 Impact Factor

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