Effects of CPAP on systemic hypertension in OSAH: a monocentric, observational, cohort study.

Respir Med. 2012 Sep;106(9):1329-34.

Bottini P, Taranto-Montemurro L, Novali M, Bettinzoli M, Roca E, Andreoli C, Bentivoglio M, Corda L, Tantucci C.

Divisione di Medicina Interna, Laboratorio per le patologie sonno-correlate, Ospedale di Umbertide, Perugia, Italy.



Background: Obstructive sleep apnea-hypopnea (OSAH) is a risk factor for development of systemic arterial hypertension (SAH) and can worse the control of established SAH. We investigated the effects of long-term continuous positive airway pressure (CPAP) treatment in controlling and preventing SAH in a large cohort of subjects referred for sleep study for suspected OSAH.

Methods: In 495 subjects of whom 422 with OSAH and 73 without OSAH, the clinical history was obtained, arterial blood pressure was measured and the current anti-hypertensive drugs was recorded at diagnosis and/or at CPAP start. Subjects were interviewed after a follow-up period of (mean ± SD) 3.4 ± 2.2 yr (range 1-8 yr) and divided in patients with moderate-to-severe OSAH (n = 125) who referred to use CPAP regularly for at least 4 h every night (group 1), with moderate-to severe OSAH (n = 70) who refused or abandoned the CPAP treatment after few weeks (group 2), with mild OSAH (n = 227) with no CPAP indication (group 3) and simple snorers or normals (n = 73) (group 4). For each group clinical status, BMI, and changes in SAH therapy and occurrence of SAH were assessed at the follow-up.

Results: At the follow-up, a higher risk of increasing treatment for SAH was found for group 2 and group 3 versus group 1 (OR = 5, 95%CI 1-20, p<0.01 and OR = 3, 95%CI 1-10, p<0.05), respectively. The occurrence of SAH was lower (p<0.001) in the group 1 (1.9%), vs group 2 (35.9%), 3 (21.1%) and 4 (18.6%).



Obstructive Sleep Apnea-Hypopnea (OSAH) is an important public health care issue, is associated with an increased risk for cardiovascular diseases and overall mortality.1-3

Only 10% of OSAH patients is diagnosed and treated, so that diagnosis and treatment of this condition is far from being optimal.4

Several cross-sectional studies link OSAH to arterial hypertension, a major risk factor for fatal and nonfatal cardiovascular events.5-6

The pathophysiology of systemic hypertension in OSAH patients is complex: hypoxia induces modification of vasomotor control, directly or via altered chemoreceptor mechanisms7; the sympathoexitation generated by hypoxia is not  limited to the sleep state but extends to wakefulness.

The overall activation of the sympathetic nervous system is due to an increased chemoreceptive activity, to an altered central nervous processing of the chemosensory signal, or a combination of both.

Also baroreceptor function might be influenced by the intermittent blood pressure elevation, which occurs during apnea. Decreased baroreflex function has been observed during sleep in OSAH patients, and may contribute to sympathetic hyperactivity and increased blood pressure during sleep. Baroreceptor resetting has been suggested as a cause of hypertension.8

The intrathoracic pressure changes during obstructive apnea appear to affect mechanisms involved in volume regulation. Increased venous return induces a mechanical stress of the right atrium and an increased release of atrial natriuretic peptide (ANP). The failure of the compensatory ANP release in the patients with high AHI may lead to the development of hypertension.

Endothelial dysfunction could play a major role in pathogenesis of daytime SAH in OSAH.10 The hypoxia-oxygenation cycles occurring in OSAH disrupt endothelial cell function: there are a decreased bioavailability of nitric oxide, a potent vasodilator,11 an increased apopotosis of endothelial cell and low release of bone marrow-derived angiogenetic progenitors, an increased platelet aggregability.

Hormonal dysregulation could affect blood pressure in OSAH patients: increased angiotensin-II and aldosterone are found in untreated OSAH, mostly in patients with resistant SAH.12 Other hormones are affected by OSAH and may contribute to the pathogenesis of SAH, including the hypothalamic-pituitary-adrenal axis and cortisol.

Associated condition such as obesity significantly contribute to the pathogenesis of both OSAH and hypertension.

Short-term studies indicate that CPAP use is associated with a reduction in blood pressure in patients with hypertension and OSAH.9

Our study support previous reports that showed that OSAH appears to be a modifiable risk factor for new-onset and worsening of hypertension. The findings of study suggest that the severity of OSAH may be an important determinant of incident hypertension.

In conclusion, untreated OSAH is associated with an increased risk of new-onset and worsening of SAH, whereas treatment with CPAP therapy is associated with a significant, protective effect towards SAH development and SAH worsening in subjects with moderate-to-severe OSAH versus both untreated moderate-to-severe and mild OSAH.

Luciano Corda-1

Figure 1

Luciano Corda-2

Figure 2

Luciano Corda-3

Figure 3:



1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-1235.

2. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 2008;31(8):1071-1078.

3. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;353(19):2034-2041.

4. Young T, Evans L, Finn L, Palta M. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep 1997;20:705–6.

5. Carlson JT, Hedner JA, Ejnell H, Peterson LE. High prevalence of hypertension in sleep apnea patients independent of obesity. Am J Respir Crit Care Med. 1994;150(1):72-77.

6. Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000;283(14):1829-1836.

7. Hedner JA, Wilcox I, Laks L, Grunstein RR, Sullivan CE. A specific and potent pressor effect of hypoxia in patients with sleep apnea. Am Rev Respir Dis. 1992 Nov;146(5 Pt 1):1240-5.

8. Leuenberger UA, Jacob EM, Sweer LW, Zwillich CW, Sinoway LI. Hypoxiemia and surges of sympathetic activity mediate blood pressare oscillations in obstructive sleep apnea. Circulation.1992,86 (Suppl 1):637

9. Barbe´ F, Dura´ n-Cantolla J, Capote F, et al; Spanish Sleep and Breathing Group. Long-term effect of continuous positive airway pressure in hypertensive patients with sleep apnea. Am J Respir Crit Care Med. 2010;181(7):718-726.

10. Budhiraja R, Parthasarathy S, Quan SF. Endothelial dysfunction in obstructive sleep apnea. J Clin Sleep Med. 2007 Jun 15;3(4):409-15.

11. Kato M, Roberts-Thomson P, Phillips BG, Haynes WG, Winnicki M, Accurso V, Somers VK. Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea. Circulation. 2000 Nov 21;102(21):2607-10.

12. Pratt-Ubunama MN, Nishizaka MK, Boedefeld RL, Cofield SS, Harding SM, Calhoun DA. Plasma aldosterone is related to severity of obstructive sleep apnea in subjects with resistant hypertension. Chest. 2007 Feb;131(2):453-9.


Multiselect Ultimate Query Plugin by InoPlugs Web Design Vienna | Webdesign Wien and Juwelier SchönmannMultiselect Ultimate Query Plugin by InoPlugs Web Design Vienna | Webdesign Wien and Juwelier Schönmann