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Cardiovascular Consequences of

Cardiovascular Consequences of. Obstructive Sleep Apnea.

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Cardiovascular Consequences of

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  1. Cardiovascular Consequencesof Obstructive Sleep Apnea

  2. Ronald J. Green, MD, FCCP, FAASMDiplomate, American Board of Sleep MedicineSleep Medicine, Pulmonary Disease & Smoking Cessation, The Everett Clinic Associate Medical DirectorNorth Puget Sound Center for Sleep DisordersEverett, WA425-339-5410; www.ilikesleep.com

  3. Cardiovascular disease is • Common • Dangerous • Easily recognized • Treatable

  4. Obstructive Sleep Apnea Syndrome (OSAS) is • Common • Dangerous • Easily recognized • Treatable

  5. I hope to demonstrate to you today that OSAS is associated with the development ofcardiovascular disease

  6. OUTLINE • Overview of obstructive sleep apnea syndrome (OSAS) • OSAS & the cardiovascular system: pathophysiology • OSAS and • Hypertension • Myocardial ischemia and infarction • Congestive heart failure • Stroke • Cardiac dysrhythmias, particularly Atrial fibrillation • Effects of OSAS treatment on cardiovascular disease • Conclusions

  7. Overview of The obstructive sleep apnea syndrome

  8. What is the “apnea” in sleep apnea? • Apnea • Cessation of airflow > 10 seconds • Hypopnea • Decreased airflow > 10 seconds associated with: • Arousal from sleep • Oxyhemoglobin desaturation

  9. Measures of Sleep Apnea Frequency • Apnea Index • # apneas per hour of sleep • Apnea / Hypopnea Index (AHI) • # apneas + hypopneas per hour of sleep • > 5 considered abnormal in adults

  10. Pathophysiology of an obstructive apnea

  11. Awake: Small airway + neuromuscular compensation Loss of neuromuscular compensation SleepOnset Hyperventilate: connect hypoxia & hypercapnia + Decreased pharyngeal muscle activity Airway opens Airway collapses Pharyngeal muscle activity restored Apnea Arousal from sleep Hypoxia & Hypercapnia Increased ventilatory effort Pathophysiology of Obstructive Sleep Apnea

  12. Clinical Consequences Obstructive Sleep Apnea Sleep fragmentation, Hypoxia / Hypercapnia excessive daytime sleepiness cardiovascular & metabolic complications Morbidity Mortality

  13. Obstructive Sleep Apnea: Most common risk factors • Obesity • Increasing age • Male gender • Anatomic abnormalities of upper airway • Family history of OSAS • Alcohol or sedative use

  14. Diagnosis: History • Loud snoring (not all snore) • Nocturnal gasping and choking • Ask bed partner (witnessed apneas) • Automobile or work related accidents • Personality changes or cognitive problems • Risk factors • Excessive daytime sleepiness (often not recognized by patient) • Frequent nocturia Sleep Apnea: Is Your Patient at Risk? NIH Publication, No 95-3803.

  15. Diagnosis: Physical Examination • Upper body obesity / thick neck > 17” males > 16” females • Hypertension • Obvious airway abnormality

  16. Exam: Oropharynx

  17. Physical Examination Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978.

  18. Why Get a Sleep Study? • Signs and symptoms poorly predict disease severity • Appropriate therapy dependent on severity • Failure to treat leads to: • Increased morbidity • Motor vehicle crashes • Mortality • Help diagnose other causes of daytime sleepiness

  19. Polysomnography

  20. Treatment of Obstructive Sleep Apnea Syndrome

  21. Treatment Objectives Reduce mortality and morbidity Decrease cardiovascular complications Reduce sleepiness Improve metabolic derangements, including type 2 diabetes mellitus Improve quality of life

  22. Therapeutic Approach Risk counseling Motor vehicle crashes Job-related hazards Judgment impairment Apnea treatment Weight loss; avoidance of alcohol & sedatives CPAP Oral appliance Surgery (UPPP)

  23. Positive Airway Pressure

  24. Positive Airway Pressure

  25. Oral Appliance: Mechanics

  26. Uvulopalatopharyngoplasty (UPPP)

  27. Primary Care Management Risk counseling Behavior modification (weight loss, etc) Monitor symptoms and compliance Monitor weight and blood pressure Ask about recurrence of symptoms Evaluate CPAP use and side effects Sleep Apnea: Is Your Patient at Risk? NIH Publication No.95-3803.

  28. Cardiovascular ConsequencesofObstructive Sleep Apnea

  29. Effects of normal sleep on the cardiovascular system (vs wake) Decreased metabolic rate Decreased sympathetic nervous activity Decreased blood pressure Decreased heart rate Increased cardiac vagal tone Bradley & Floras, The Lancet, 2009. 373: 82-93.

  30. Effects of obstructive sleep apnea on the cardiovascular system (vs wake) Interruption of cardiovascular quiescence: Increased sympathetic nervous activity Increased blood pressure Increased heart rate Decreased parasympathetic nervous activity Bradley & Floras, The Lancet, 2009. 373: 82-93.

  31. OSA triggers a cascade of events effecting the cardiovascular system Bradley & Floras, The Lancet, 2009. 373: 82-93.

  32. OSA Impact on Cardiovascular System • Hypoxia • Increases metabolic demands on heart • Impairs cardiac contractility • Increases pulmonary artery pressures NOCTURNAL ISCHEMIA Leung AJRCCM 2001 NaughtonCirculation 1995

  33. OSA Impact on Cardiovascular System • Arousals from sleep • Surges in heart rate and blood pressure • Increases in sympathetic nervous activity REPETITIVE STRAIN Leung AJRCCM 2001 NaughtonCirculation 1995

  34. Effects of OSAS on sympathetic nerve activity and BP in OSA pt without HTN Somers, et al, J Clin Invest, 1995. 96: 1897-1904.

  35. Effects of OSAS on sympathetic nerve activity and BP in OSA pt without HTN Somers, et al, J Clin Invest, 1995. 96: 1897-1904.

  36. Effects of OSAS on sympathetic nerve activity and BP in OSA pt without HTN Somers, et al, J Clin Invest, 1995. 96: 1897-1904.

  37. Repetitive apnea-induced hypoxia and CO2 retention cause Ineffective inspiratory effort increased negative intra-thoracic pressure  increased LV transmural pressure (increased afterload) which causes LV hypertrophy Increased negative intra-thoracic pressure increased RV preload (pulls blood into RV) Hypoxia causes pulmonary vasoconstriction leading to pulmonary HTN Bradley & Floras, The Lancet, 2009. 373: 82-93.

  38. Repetitive apnea-induced hypoxia and CO2 retention cause Pulmonary vasoconstrictionincreased RV afterload  RV distention impaired LV diastolic filling  decreased LV stroke volume Apnea cycles cause oscillations in sympathetically-mediated peripheral vasoconstriction which raises systemic BP Arousal from sleep which terminates the apnea results in increased sympathetic tone and decreased vagal tone  surge in heart rate and blood pressure Bradley & Floras, The Lancet, 2009. 373: 82-93.

  39. Repetitive apnea-induced hypoxia and CO2 retention Effects on blood pressure and heart rate can be sustained into wakefulness resulting in systemic HTN These changes are rapidly relieved with treatment of OSAS by CPAP Bradley & Floras, The Lancet, 2009. 373: 82-93.

  40. Vascular effects of OSAS Intermittent hypoxia  O2 free radicals  activation of inflammatory pathways  impaired vascular endothelial function & increased BP independent of sympathetic activation. Hypercoagulability from increased expression of adhesion molecules & vascular smooth muscle proliferation This could predispose to HTN & atherosclerosis Bradley & Floras, The Lancet, 2009. 373: 82-93.

  41. Vascular effects of OSAS Increased risk of thrombosis in OSAS increased platelet activation & aggregability Elevated morning fibrinogen levels Decreased plasminogen activator inhibitor type-1 activity Bradley & Floras, The Lancet, 2009. 373: 82-93.

  42. Given the pathophysiology just discussed, if you think there is an increased incidence of OSAS in pts with cardiovascular disease, you are right!

  43. Higher prevalence of OSAS in patients with cardiovascular disease Prevalence of OSAS in general population: 7-10% Hypertension: 30-83% Congestive heart failure: 12-53% Ischemic heart disease: 30-58% Stroke: 43-91% Note that confounding variables including obesity need to be taken into account so correlation does not prove causality You need to have HIGH index of suspicion for OSAS in these patient populations Bradley & Floras, The Lancet, 2009. 373: 82-93. Young, et al, N Engl J Med, 1993. 328: 1230-35.

  44. OSAS and hypertension OSA is one known cause of HTN Patients with OSA more likely to develop HTN OSA listed by Joint National Committee on the Detection & Management of HTN as important identifiable cause of HTN Possible mechanisms: Intermittent hypoxemia Chemoreceptor stimulation Sympathetic activation Renin-angiotensin system Chobanian JAMA 2003; Lesske J Hypertens 1997 Fletcher Hypertension 1992; Brooks J Clin Invest 1997

  45. Dose response effect of OSA severity and risk of HTN (adjusted for confounders) Adjusted Odds Ratio of developing HTN 0 0.1-4.9 5.0-14.9 >15.0 Baseline AHI PeppardNEJM 2000

  46. Experimental evidence: OSAS can raise blood pressure Dogs exposed to OSA developed HTN during sleep and wake which resolved on reversal of the OSA Rats exposed to intermittent hypoxia (mimicking OSA) developed HTN. This was prevented by sympathectomy or peripheral chemoreceptor denervation. Bradley & Floras, The Lancet, 2009. 373: 82-93.

  47. OSAS and medication-resistant hypertension OSAS is VERY common in medication-resistant HTN 3 observational studies: >70% of patients with difficult-to-treat or resistant HTN have sleep disordered breathing (versus its presence in <40% of patients with controlled HTN) Logan Eur Respir J 2003 Goncalves Chest 2007 Logan J Hypertens 2001

  48. OSAS and medication-resistant hypertension HTN in OSAS often associated with biochemical features of primary aldosteronism which in turn can lead to oxidative stressinflammation LV fibrosis and hypertrophy Bradley & Floras, The Lancet, 2009. 373: 82-93. Logan, J Hypertension, 2001. 19: 2271-77. Marney & Brown, Clin Sci (Lond), 2007. 113:267-78.

  49. OSAS and medication-resistant hypertension If your patient is on 3 or more anti-hypertensive medications, think OSAS Bradley & Floras, The Lancet, 2009. 373: 82-93. Logan, J Hypertension, 2001. 19: 2271-77. Marney & Brown, Clin Sci (Lond), 2007. 113:267-78.

  50. Risk of myocardial ischemia and infarction in OSAS Marin, et al: prospective study showed more fatal and non-fatal MI in severe, untreated OSAS vs control. No difference in rates in OSAS treated w/ CPAP vs control. In CAD patients, OSAS associated with higher mortality, more major cardiac events and higher restenosis rate after PTCA vs controls without OSAS. Case-control study: graded increase in odds of acute MI with increased sleep apnea severity. People with OSA more likely than those without to have family hx of premature death from CAD Somers, et al, Circ, 2008. 118: 1080-1111. Marin, et al, The Lancet, 2005. 365: 1046-53. Yumino, et al, Am J Cardiol, 2007. 99: 26-30.

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