Systemic and Pulmonary HTN in OSA

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Systemic and Pulmonary HTN in OSA

• PAWAN CHAWLA, M.D.

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JNC 7

• ExpressSuccinct evidence-based recommendations.
  Published in JAMA May 21, 2003, and as a
  Government Printing Office publication.
• Full Reportcomprehensive justification and
  rationale (coming soon).

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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

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

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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

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Identifiable Causes of Hypertension

• Sleep apnea
• Drug-induced or related causes
• Chronic kidney disease
• Primary aldosteronism
• Renovascular disease
• Chronic steroid therapy and Cushings syndrome
• Pheochromocytoma
• Coarctation of the aorta
• Thyroid or parathyroid disease

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EVIDENCE FOR ASSOCIATION WITH SLEEP APNEA AND
HYPERTENSION
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Wisconsin Sleep Cohort Study

• A prospective, population-based study of the
  association between objectively measured
  sleep-disordered breathing and hypertension
• Hypertension is defined as a laboratory-measured
  blood pressure of at least 140/90 mm Hg or the
  use of antihypertensive medications.
• 709 subjects with follow up of 4 years
• Age 30 65 years

Peppard et al NEJM, 2000
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Peppard et al NEJM, 2000
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Sleep Heart Health Study

• 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

Nieto et al Jama, 2000
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Nieto et al Jama, 2000
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OR for HTN
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OSA HTN

• Gender ? Not Significant
• Race ? Not Significant
• Age ? Low risk Vs Not Significant
• BMI ? Increased OR with decreasing BMI

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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
• Abnormal upper airway resistance during sleep,
  often associated with snoring, can play a role in
  the development of hypertension

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OSA Diurnal Blood Pressure
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OSA/HTN CPAP

• Pepperell et al
• 118 patients with ODI of 17/hr on cpap Vs
  subtherapeutic cpap(1cm) x 4weeks
• Mean BP decreased by 2.4/3.4(sleep/wake) Vs an
  increase of 0.8
• Cpap gt 5 hours needed

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OSA/HTN CPAP

• Becker et al
• 32 patients on cpap Vs subtherapeutic cpap(1cm) x
  9 weeks
• SBP/DBP decreased by 10 mm Vs no change
• AHI decreased from 65 to 3 Vs 65 to 33

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N768
Becker et al Circulation, 2003
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Systolic HF OSA

• Prevalence of 5 32
• Sleep heart health study ? OR of 2.5
• Rx with cpap improves EF
• EF predicts survival

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Diastolic HF OSA

• OSA ? increase left ventricular mass ? left
  ventricular hypertrophy ? Diastolic dysfunction
• Cpap improves Diastolic dysfunction

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Arrhythmias OSA
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• Bradyarrhythmias ? complete heart block, asystole
• Ventricular arrhythmias
• Atrial fibrillation ? increase recurrence rate

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PHTN OSA

• Incidence 15-70
• Usually mild
• Chaouat et al
• 220 consecutive French patients with AHI gt 20/hr
• 17 had mean PAP gt20 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

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• Laks et al
• 100 consecutive Australian patients with AHI
  gt20/hr
• 42 had mean PAP gt 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

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• Sanner et al
• 92 consecutive German patients with OSA and AHI gt
  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 lt90 saturation were independent
  predictors of PAH

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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

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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 gt 5 hours

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Cardiovascular effects of SRDS
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Negative ITP