Systemic and Pulmonary HTN in OSA

1. Systemic and Pulmonary HTN in OSA PAWAN CHAWLA, M.D.

2. JNC 7 • Express—Succinct evidence-based recommendations. Published in JAMA May 21, 2003, and as a Government Printing Office publication. • Full Report—comprehensive justification and rationale (coming soon).

3. HYPERTENSION • HTN prevalence ~ 50 million people in the United States • The BP relationship to risk of CVD is continuous, consistent, and independent of other risk factors • Each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range starting from 115/75 mmHg

4. Blood Pressure Classification 7Th Joint National Committee on High Blood Pressure

5. Benefits of Lowering BP 7Th Joint National Committee on High Blood Pressure

6. Benefits of Lowering BP In stage 1 HTN and additional CVD risk factors, achieving a sustained 12 mmHg reduction in SBP over 10 years will prevent 1 death for every 11 patients treated

7. Patient Evaluation • Evaluation of patients with documented HTN has three objectives: • Assess lifestyle and identify other CV risk factors or concomitant disorders that affects prognosis and guides treatment • Reveal identifiable causes of high BP • Assess the presence or absence of target organ damage and CVD

8. Identifiable Causes of Hypertension • Sleep apnea • Drug-induced or related causes • Chronic kidney disease • Primary aldosteronism • Renovascular disease • Chronic steroid therapy and Cushing’s syndrome • Pheochromocytoma • Coarctation of the aorta • Thyroid or parathyroid disease

9. EVIDENCE FOR ASSOCIATION WITH SLEEP APNEA AND HYPERTENSION

10. WisconsinSleep Cohort Study Peppard et al: NEJM, 2000 A prospective, population-based study of the association betweenobjectively measured sleep-disordered breathing and hypertension Hypertension is defined as a laboratory-measured blood pressure of at least140/90 mm Hg or the use of antihypertensive medications. 709 subjects with follow up of 4 years Age 30 – 65 years

11. Peppard et al: NEJM, 2000

12. Sleep Heart Health Study Nieto et al: Jama, 2000 Cross-sectional analyses of participants in the Sleep Heart Health Study, a community-based multicenter study conducted between November 1995 and January 1998 6132 subjects Age 40 – 97 years

13. Nieto et al: Jama, 2000

14. OR for HTN

15. OSA & HTN • Gender  Not Significant • Race  Not Significant • Age  Low risk Vs Not Significant • BMI  Increased OR with decreasing BMI

16. UARS and Snoring and HTN • Young et al: Sleep, 1996 • Population-based sample of 580 adults was analyzed • Simple snoring represents the beginning of the SDB severity spectrum and that simple snoring has a proportionately smaller but, nevertheless, significant, risk for elevated blood pressure and CVD • Upper Airway Resistance Syndrome, Nocturnal Blood Pressure Monitoring, and Borderline Hypertension: Guilleminault et al: Chest, 1996 • Abnormalupper airway resistance during sleep, often associated withsnoring, can play a role in the development of hypertension

17. OSA & Diurnal Blood Pressure

21. OSA/HTN + CPAP • Pepperell et al • 118 patients with ODI of 17/hr on cpap Vs subtherapeuticcpap(1cm) x 4weeks • Mean BP decreased by 2.4/3.4(sleep/wake) Vs an increase of 0.8 • Cpap > 5 hours needed

22. OSA/HTN + CPAP • Becker et al • 32 patients on cpap Vs subtherapeuticcpap(1cm) x 9 weeks • SBP/DBP decreased by 10 mm Vs no change • AHI decreased from 65 to 3 Vs 65 to 33

23. N=768 Becker et al: Circulation, 2003

24. Systolic HF & OSA • Prevalence of 5 – 32% • Sleep heart health study  OR of 2.5 • Rx with cpap improves EF • EF predicts survival

26. Diastolic HF & OSA • OSA  increase left ventricular mass  left ventricular hypertrophy  Diastolic dysfunction • Cpap improves Diastolic dysfunction

27. Arrhythmias & OSA

28. Bradyarrhythmias  complete heart block, asystole • Ventricular arrhythmias • Atrial fibrillation  increase recurrence rate

29. PHTN & OSA • Incidence 15-70% • Usually mild • Chaouat et al • 220 consecutive French patients with AHI > 20/hr • 17% had mean PAP >20 mm Hg • Patients with PAH had more severe OSA, higher Paco2 and BMI, lower Pao2, and more obstructive and restrictive defect • Paco2 and FEV1 were independent predictors of PAH

30. Laks et al • 100 consecutive Australian patients with AHI >20/hr • 42% had mean PAP > 20 mm Hg; range, 20 to 52 • Paco2, Pao2, and FEV1 accounted for 33% of variability in PAH • 6 patients with PAH had normal Pao2

31. Sanner et al • 92 consecutive German patients with OSA and AHI > 10/hr; range, 10-100/hr • COPD was an exclusion criterion • 20% had mild PAH; range, 20 to 25 mm Hg • 8 patients had increased PCWP; all had systemic hypertension • PCWP and time <90% saturation were independent predictors of PAH

32. Mechanism • Precapillary PAH • Hypoxemia • Hypercapnia • Changes in intrathoracic pressure • Endothelial dysfunction or remodeling • Capillary PAH • Loss of vascular surface area due to a cormorbid disorder, such as in COPD • Postcapillary PAH • LVH and diastolic dysfunction

33. Treatment • Motta et al • 6 patients, reduction of PAP with tracheostomy(45 to 22) • Alchanatis et al, Sforza et al, Sajkov et al • Reduction of PAP with cpap • Cpap required for > 5 hours

34. Cardiovascular effects of SRDS

35. Negative ITP