Effects of CPAP Therapy on Systemic Blood Pressure, Cardiac Rhythm and Catecholamines Concentration in Patients with Obstructive Sleep Apnea

One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles of normoxia-hypoxia, when administered to rats for 35 days, allows examination of the chronic cardiovascular response to intermittent hypoxia patterned after the episodic desaturation seen in humans with sleep apnea. The result of this type of intermittent hypoxia in rats is a 10- to 14-mmHg increase in resting (unstimulated) mean blood pressure that lasts for several weeks after cessation of the daily cyclic hypoxia. Carotid body denervation, sympathetic nerve ablation, renal sympathectomy, adrenal medullectomy, and angiotensin II receptor blockade block the blood pressure increase. It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.

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The effect of antihypertensive therapy and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea syndrome in association with arterial hypertension

Systemic Hypertension ◽

10.26442/sg29171 ◽

2017 ◽

Vol 14 (1) ◽

pp. 37-40

Author(s):

E M Elfimova ◽

A V Rvacheva ◽

M I Tripoten ◽

O V Pogorelova ◽

T V Balakhonova ◽

...

Keyword(s):

Blood Pressure ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Endothelial Dysfunction ◽

Arterial Hypertension ◽

Antihypertensive Therapy ◽

Adhesion Molecule ◽

Severe Obstructive Sleep Apnea ◽

Cpap Therapy ◽

Obstructive Sleep

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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