Nocturnal blood pressure and nocturnal blood pressure fluctuations: the effect of short-term CPAP therapy and their association with the severity of obstructive sleep apnea

Objective. To evaluate the effect of antihypertensive therapy (AHT) and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea (OSA) syndrome in association with arterial hypertension (AH). Materials and methods. The study included 43 male patients with severe OSA syndrome (Apnea-Hypopnea Index 52.4 [46.1; 58.6]) and AH (systolic blood pressure 144.0 [142.0; 156.0] mm Hg, diastolic blood pressure 90.9 [88.3; 93.5] mm Hg). Treatment with angiotensin-converting enzyme inhibitors, calcium antagonists, and thiazide-like diuretics was performed till target BP level measured with Korotkoff method was achieved. The patients who had reached target BP level (BP≤140/90 mm Hg) were randomized into two groups: group 1 included 23 patients who continued taking the AHT, group 2 included 22 patients who continued taking the AHT to which CPAP therapy was added. Peripheral blood lymphocyte immunophenotyping, cytokine panel test (IL-1β, IL-6, tumor necrosis factor a, IL-2Ra, sCD40L), adhesion molecule analysis (ICAM-1, VCAM-1), thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1a), and endothelin-1 levels in blood serum were evaluated at admission, after target BP level achievement (2nd visit) and after 3 months of AHT or AHT+CPAP therapy (3rd visit). Flow-mediated dilation of brachial artery was assessed using reactive hyperemia test by D.Celermajer. Results. Against the background of combined AHT the target BP level was achieved by 95% of patients. After target BP level achievement a significant decrease of IL-1β -0.16 [-0.5; 0], p=0.000 level and number of CD50+ cells (lymphocytes with inter-cellular adhesion molecule ICAM-3) from 2158.5 [1884.7; 2432.3] to 1949.6 [1740.9; 2158.3], p=0.050 were observed in patients with severe OSA associated with AH. There were no significant changes in vascular endothelial function observed in patients taking only AHT. Significant decrease of fibrinogen (-0.3 [-0.4; -0.1], p=0.002) and homocystein (-2.03 [-3.8; -0.2], p=0.03) levels was observed in patients taking both AHT and CPAP therapy. Conclusion. The combination of AHT and CPAP therapy in patients with severe OSA and AH not only allows reaching the target BP level but also leads to inflammatory and endothelial dysfunction markers levels decrease.

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Effect of Maternal Obstructive Sleep Apnea-Hypopnea on 24-Hour Blood Pressure, Nocturnal Blood Pressure Dipping and Arterial Stiffness in Hypertensive Disorders of Pregnancy

Frontiers in Physiology ◽

10.3389/fphys.2021.747106 ◽

2021 ◽

Vol 12 ◽

Author(s):

Pattaraporn Panyarath ◽

Noa Goldscher ◽

Sushmita Pamidi ◽

Stella S. Daskalopoulou ◽

Robert Gagnon ◽

...

Keyword(s):

Blood Pressure ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Arterial Stiffness ◽

Hypertensive Disorders Of Pregnancy ◽

Adjusted Analysis ◽

Nocturnal Blood Pressure ◽

Hypertensive Disorders ◽

Obstructive Sleep ◽

The Impact

Rationale: Maternal obstructive sleep apnea-hypopnea (OSAH) is associated with hypertensive disorders of pregnancy (HDP). Attenuation of the normal nocturnal blood pressure (BP) decline (non-dipping) is associated with adverse pregnancy outcomes. OSAH is associated with nocturnal non-dipping in the general population, but this has not been studied in pregnancy. We therefore analyzed baseline data from an ongoing RCT (NCT03309826) assessing the impact of OSAH treatment on HDP outcomes, to evaluate the relationship of OSAH to 24-h BP profile, in particular nocturnal BP dipping, and measures of arterial stiffness.Methods: Women with a singleton pregnancy and HDP underwent level II polysomnography. Patients with OSAH (apnea-hypopnea index (AHI) ≥ 5 events/h) then underwent 24-h ambulatory BP monitoring and arterial stiffness measurements (applanation tonometry, SphygmoCor). Positive dipping was defined as nocturnal systolic blood pressure (SBP) dip ≥ 10%. The relationships between measures of OSAH severity, measures of BP and arterial stiffness were evaluated using linear regression analyses.Results: We studied 51 HDP participants (36.5 ± 4.9 years, BMI 36.9 ± 8.6 kg/m2) with OSAH with mean AHI 27.7 ± 26.4 events/h at 25.0 ± 4.9 weeks’ gestation. We found no significant relationships between AHI or other OSA severity measures and mean 24-h BP values, although BP was generally well-controlled. Most women were SBP non-dippers (78.4%). AHI showed a significant inverse correlation with % SBP dipping following adjustment for age, BMI, parity, gestational age, and BP medications (β = −0.11, p = 0.02). Significant inverse correlations were also observed between AHI and DBP (β = −0.16, p = 0.01) and MAP (β = −0.13, p = 0.02) % dipping. Oxygen desaturation index and sleep time below SaO2 90% were also inversely correlated with % dipping. Moreover, a significant positive correlation was observed between carotid-femoral pulse wave velocity (cfPWV) and REM AHI (β = 0.02, p = 0.04) in unadjusted but not adjusted analysis.Conclusion: Blood pressure non-dipping was observed in a majority of women with HDP and OSAH. There were significant inverse relationships between OSAH severity measures and nocturnal % dipping. Increased arterial stiffness was associated with increasing severity of OSAH during REM sleep in unadjusted although not adjusted analysis. These findings suggest that OSAH may represent a therapeutic target to improve BP profile and vascular risk in HDP.

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