1 / 46

OBSTRUCTIVE SLEEP APNEA AS A CAUSE OF HYPERTENSION Yüksel Peker MD, PhD, Associate Professor

OBSTRUCTIVE SLEEP APNEA AS A CAUSE OF HYPERTENSION Yüksel Peker MD, PhD, Associate Professor Sleep Medicine Unit, Skaraborg Hospital, Skövde & University of Gothenburg, Sweden. ASSOCIATIONS. OSA. Hypertension. Hypertension. OSA. OSAS. Obesity. OSA. Hypertension.

crwys
Télécharger la présentation

OBSTRUCTIVE SLEEP APNEA AS A CAUSE OF HYPERTENSION Yüksel Peker MD, PhD, Associate Professor

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. OBSTRUCTIVE SLEEP APNEA AS A CAUSE OF HYPERTENSION Yüksel Peker MD, PhD, Associate Professor Sleep Medicine Unit, Skaraborg Hospital, Skövde & University of Gothenburg, Sweden

  2. ASSOCIATIONS

  3. OSA Hypertension

  4. Hypertension OSA OSAS

  5. Obesity OSA Hypertension

  6. Aging Hypertension OSA Gender Obesity

  7. OSA • Immediate changes • Long-term effects

  8. Grote L. et al., J. Cardiovasc. Pharmacol. 1994

  9. Cardiovascular mechanisms (I) Repeated nocturnal hypoxemia Coccogna G et al, 1972; Podszus T et al, 1986 Sympathetic nervous activity Fletcher EC et al, 1987; Hedner J et al, 1988; Narkiewicz K & Somers VK 2003 Vascular endothelial dysfunction Carlson J et al, 1996; Remsburg S et al, 1999; Kraiczi H et al, 2000

  10. Cardiovascular mechanisms (II) Enhanced release of superoxide from polymorphonuclear neutrophils in OSA. Impact of CPAP. Schulz Ret al, AJRCCM 2000 Plasma vascular endothelial growth factor in OSAS: Effects of CPAP. Lavie L et al, AJRCCM 2002 Elevated levels of C-reactive protein and interleukin-6 in patients with OSAS are decreased by CPAP. Yokoe Tet al, Circulation 2003

  11. OSA & Hypertension • Sleep clinic population • Hypertensive population • General population

  12. OSAS as a risk factor for hypertension (sleep-clinic population, n=2677) Lavie P et al; BMJ 2000;320:479-482

  13. OSA & Hypertension • Sleep clinic population • Hypertensive population • General population

  14. Prevalence of OSA in hypertension-clinic populations OSA 30% in unselected patients with hypertension Kales et al, 1984; Fletcher et al, 1985 OSA 56% in non-responding HT, 19% in responding HT Isaksson & Svanborg, 1991 All “non-dippers” (n=10) but none in “dippers” had OSA Portaluppi F et al, J Hypertension 1997

  15. OSA & Hypertension • Sleep clinic population • Hypertensive population • General population

  16. OSA & Hypertension (cross-sectional data) Adjusted OR for HT 1.37 (95% CI 1.03-1.83) (comparing AHI>30 vs AHI<1.5)

  17. CAUSAL RELATIONSHIP

  18. Causal relation • OSA causes hypertension? • Hypertension causes OSA?

  19. 50-60 apneas / h of sleep

  20. All normotensive at baseline AJRCCM 2002

  21. Ambulatory BP after therapeutic and subtherapeutic CPAP for OSA: a randomised parallel trial • Normotensive & Hypertensive • OSAS (n=118) • More BP-reduction in hypertensives • More BP-reduction in severe OSAS Pepperell J et al, LANCET 2001; 359: 204-210

  22. Effect of CPAP treatment on BP in patients with OSAS • Moderate to severe OSAS with HT (n=60) • Randomized to therapeutic vs subtherapeutic CPAP; follow-up 9 w • 32 subjects completed (16 in each group) • AHI reduction 95% versus 50% • BP reduction 10 mmHg versus no change (p=0.01) • Reduction in both systolic & diastolic BP, both daytime & at night • The drop in mean BP by 10mmHg would be predicted to reduce CAD-event risk by 37% and stroke risk by 56% Becker HF et al, Circulation 2003;107:68-73

  23. OSA & Hypertension (cross-sectional data) Adjusted OR for HT 1.37 (95% CI 1.03-1.83) (comparing AHI>30 vs AHI<1.5)

  24. n.s.? Gender differences? Nieto FJ et al, JAMA 2000; 283:1829-36

  25. OSA & Hypertension (cross-sectional data) • Gender differences in a population-based cohort • n=344 patients • 183 HT, 161 normotensives • Matched for age and gender • Ambulatory home PSG • Independent association between OSA and hypertension in men • Not identifiable in these essentially postmenopausal females • The contribution of OSA to hypertension risk may be sex-dependent and higher in males than in females

  26. Endothelial function during menstrual, follicular and luteal phase S-Estradiol: M phase: 122 pmol/L; F phase: 632 pmol/L; L phase: 534 pmol/L adapted from Hashimoto M et al, Circulation 1995; 92:3431-5

  27. GENDER AND HYPERTENSION Endothelial dysfunction Endothelial dysfunction starts in men a decade earlier than in women Celermajer DS et al, J Am Coll Cardiol 1994; 24:71-6 Age related impairment of endothelium-dependent vasodilatation is only observed after menopause Taddei S et al, Hypertension 1996; 28:576-82

  28. Influence of menopause on blood pressure Staessen JA et al, J Hum Hypertens 1998; 12:587-92

  29. Hormone Replacement Therapy and Longitudinal Changes in BP in Postmenopausal Women After 10 Years n=226 Normotensive at baseline Scuteri A et al, Ann Intern Med 2001;135:229-38

  30. Obesity causes hypertension? OSA causes hypertension?

  31. CONCLUSIONS (I) • Recurrent obstructive events during sleep, independently or in concert with other recognized risk factors, seem to have harmful effects on vascular structure and function • Development of hypertension in OSA is likely to depend on genotypic and phenotypic factors • Not only may OSA induce hypertension but also the events in themselves may worsen the response to antihypertensive medication

  32. CONCLUSIONS (II) • OSA should be considered among factors regarding the primary and secondary prevention models of hypertension • OSA should be treated not only to eliminate daytime sleepiness. Treatment may also have a beneficial prognostic impact by reducing blood pressure levels in hypertensive patients. • However, more RCT are necessary to address this impact in “non-sleepy” OSA subjects with hypertension

More Related