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Sleep Apnea and the Cardiovascular System

Patrick J. Burns D.O. Sleep Medicine/Neurology The Sleep Medicine Center Kalispell,Mt.

References 1 2 3 4. 5 Some Epidemiological data on snoring and cardiocirculatory disturbances. Lugaresi et.al; Sleep et.al; 1980;3:221-24 1980;3:221Snoring as a risk factor for hypertension and angina pectoris. Koskenvuo et.al; Lancet 1985;i:893-96 pectoris. et.al; 1985;i:893Snoring and Cerebral Infarction. Partinen & Palomaki; Lancet 1985;1325-1326 Palomaki; 1985;1325_____________________________________________________ ___________________ __________________________________ Sleep and Hypertension: V.K. Somers; Minerva Medicine, Vol.95,n4 ,p281-290 ; Excellent review ,p281article with references to all topics Sleep Disordered Breathing and Cardiovascular Disease: Sleep Heart Health Study Group; Am. J. Respir. Crit. Care Med., vol. 163,no.1, Jan. 2001, p19-25 ; large data base (6,424) showing effects Respir. Crit. p19on heterogeneous manifestations of CVD within a range of AHI values that are considered normal or values mildly abnormal Obstructive Sleep Apnea and Cardiovascular Disease: Mayo Clinic Proc., Aug. 2004;79(8),p.1036-1046; Mayo 2004;79(8),p.1036Excellent Review Sleep Apnea and Heart Failure Part I & II: Circulation 2003; 107: p. 1671-1678 and 1822-1826 16711822Effects of Nasal Continuous Airway Pressure Treatment on Blood Pressure in Patients With Obstructive Sleep Apnea: Circulation 2003; 7;107(1):68-73 7;107(1):68High Prevalence of Obstructive Sleep Apnea in Drug Resistant Hypertension: J. Hypertension Resistant 2001;Dec.;19(12):2271-2277 2001;Dec.;19(12):2271Obstructive Sleep Apnea Syndrome: More Insights on Structural and Functional Cardiac Alterations, Structural and the Effects of Treatment with CPAP: Journal of the American College of Cardiology 2006;Vol.47,No.7,1435-1439 2006;Vol.47,No.7,1435Obstructive Sleep Apnea as a risk factor for stroke and death: NEJM 2005; 352: 2034-2041 2034Association of sleep-disorder breathing and the occurrence of stroke: Am J Resp Crit Care Med. 2005; sleep172: 1447-1451 1447_____________________________________________________ _____________________________________________________ Sleep-Disordered Breathing and Cardiovascular Risk: SLEEP 2007;30(3):291-304 Sleep2007;30(3):291Decreased Right and Left Myocardial Performance in Obstructive Sleep Apnea: Chest Oct. 1, 2007 Obstructive Effect of Nocturnal Nasal CPAP on Blood Pressure in OSA: Hypertension 2007 OSA: Beneficial Effect of Bilevel Positive Airway Pressure on Left Ventricular Function in Ambulatory Patients Ambulatory With Idiopathic Dilated Cardiomyopathy and Central Sleep Apnea-Hypopnea A Preliminary Study: ApneaChest Vol 131, Issue 6, June 2007 Efficacy of Adaptive Servoventilation in Treatment of Complex and Central Sleep Apnea Syndromes: Chest 2007, 132:1839-1846 132:1839-

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The Essentials For Life

Eat

Drink

Life

Sleep

Breathe

Sleep-Disordered Breathing and Cardiovascular Risk. SLEEP, Vol.30, No.3,2007, 291-303: Division of Pulmonary and Critical Care Medicine; Division of Cardiovascular Disease; Division of Hypertension, Mayo Clinic College of Medicine; Somers, et al.

" There is abundant physiologic evidence

implicating OSA in perpetuating, if not inciting, heart failure."

" Collectively, the data are compelling to implicate OSA not only in acute increases in nocturnal blood pressure, but also in sustained daytime hypertension as well"

Outline

Definition of terms Physiological effects of "Flow Limitation" Biochemical studies in SRBD (Sleep Related Breathing Disorder)

­ ­ ­ ­ Vascular/Endothelial Inflamatory Metabolic/Sympathetic Cardiogenic/Neurogenic

Clinical studies in SRBD

­ Hypertensive/Vascular ­ Cardiac

Central Sleep Apnea,CHF,& and Adaptive Servo-Ventilatio (ASV) Overview of interactions of Sleep Related Breathing Disorder and Health

Definition of terms

Snoring: A form of flow limitation not ass. with physiologic event but potentially ass. with tiredness or cognitive/behavioral abnormalities Flow Limitation: Evidence of flattening of pressure transducer <30% with ass. physiologic event (i.e. arousal, CAP complex, paradoxical breathing, pulse transit time, RR ) Hypopnea: Decrease in amplitude of pressure transducer >30% for >10sec. And an arousal or 4% desat Apnea: Cessation of breathing for >10 sec. (Obstructive/Central/Complex) Sleep Related Breathing Disorder: Any or all of the above AHI: Apnea Hypopnea Index (5-15;15-30;>30) RDI: Respiratory Disturbance Index (AHI + Flow Limitations)

Progression of Sleep disordered Breathing

Snoring Flow Limitation Hypopneas Apneas Sleep Apnea Hypopnea Syndrome

The Many Faces of OSA

SYMPTOMS

­ ­ ­ ­ ­ ­ ­ ­ ­ ­ ­ EDS/Fatigue Mood disorders/Moodiness Memory /Impaired Concentration Morning Headaches/Chronic Headaches Fragmented sleep/Awakenings Nocturia/Enuresis Impotence/Decreased libido Hypertension, Heart Disease, Cerebrovascular Disease Snoring/Apneas Sleep Related Choking/Gasping New Onset Adult Seizures

Physiologic Effects of Flow Limitation

Mueller maneuver Increase intra-thoracic pressure i) Increase R ventricle end diastolic volume ii) L Septal bulge; Decrease L ventricle end diastolic volume iii) Increase after load resistance iv) Decrease ejection fraction v) Decrease cardiac perfusion vi) Increase in ventricular transmural pressure vii) Increase Pulmonary artery pressure viii) Increase L ventricular end systolic volume/L atrial volume ix) Cardiac remolding and apoptosis

Physiologic Effects of Flow Limitation

Hypoxemia Fragmented sleep with altered sleep architecture Metabolic dysfunction Pro-inflammatory activation CNS Arousals Sympathetic surges/Increased Catacholamines Tachycardia Non-Dipping Blood Pressures Impaired Vagal tone Increase resting daytime heart rate and blood pressure

Biochemical Studies

Vacular/Endothelial Dysfunction

1. 2. 3. 1. 1.

Inflammatory

Nitric oxide/ Biothiol VCAM/ ICAM/ P-Selectin/ endothelin-1/ VEGF Homocysteine

Metabolic/Sympathetic

CRP, IL-6, Isoprostane, TNF-alpha, CD-40 CD-40Ligand, Leukotrienes, Neopterin, CD146(+) Annexin V (+)

Neurodegenerative/Cardiogenic

1. 2. 3. 4.

Adrenomedullin, Aldosterone, Adioponectin, Insulin resistance, leptin, gremlin, CPK, Uric Acid, IGF-1, catecholamine

S100B astrocytic protein Prostaglandin D synthase & Substance P Brain Naturetic Peptide Atrial Naturetic Peptide

Cardiovascular Studies

Hypertensive/Vascular

1. 2. 3. 4. 5. 6.

7. 8.

Decrease cerebro-vascular response to hypoxemia in OSA Incremental increase in aortic stiffness with OSA Impaired endothelial function and peripheral vasodilatation in OSA Increase prevalence of OSA in refractory hypertension Increase in stroke and death in OSA Wisconsin Sleep Cohort Study: The presence of OSA at initial evaluation was associated with a 3-fold increase risk for future development of hypertension, that was independent of confounding factors Increase ambulatory BP and IL-6 in children with OSA CPAP is effective therapy for many patients with OSA and co-morbidities

Cardiovascular Studies

Cardiac

LVH in OSA LV adaptations leading to Dilated Cardiomyopathy in OSA Increase in Pulmonary hypertension in OSA with associated abnormal LV Diastolic function Increase in Nocturnal Dysrythmias in OSA High prevalence in paced patients Higher risk cardiac surgical outcomes in OSA Adverse clinical and angiographic outcomes in patients with ACS and PCI OSA estimated to be prevalent in 30% CHF patients In The Sleep Heart Health Study, OSA was a stronger risk for CHF than CAD and HTN Treatment with CPAP improves cardiac function and decreases work load in most patients with OSA

Decreased Right and Left Ventricular Myocardial Performance in Obstructive Sleep Apnea: CHEST Oct. 2007, Mayo Clinic Group

of the right/left ventricle + Isovolumic relaxation time of right/left ventricle) / pulmonary/aortic ejection time )

Measured Myocardial Performance Index ( isovolumic contraction time

155 patients over 9 year period Exclusion criteria: EF < 45% + 10 other Final : 85 subjects, 27 controls, 18 patients with mild OSA, and 40 patients with moderate-to-severe OSA Results/Conclusion: "OSA, particularly when modeate-to-severe, is associated with impaired right and left ventricular functon and increased left atrial volume. These findings support the notion that OSA may contribute to the development of atrial fibrillation and CHF"

Cardiopulmonary Consequences of OSA

Cardiovascular

1. 2. 3. 4. 5. 6. 7.

Pulmonary

1. 2. 3. 4. 5.

Hypertension Congestive Heart Failure Systolic and Diastolic Dysfunction/Cardiomypathy Atherosclerosis Stroke Pulmonary Hypertension/Cor Pulmonale Cardiac Dysrhythmia/Atrial Fibrillation Worsening of Asthma Worsening of COPD GERD Recurrent pneumonia CORE syndrome

Central Sleep Apnea in CHF

Cheyne-Stokes Breathing, Central Sleep Apnea, Complex Sleep Apnea Pathophysiology :

­ Pulmonary Edema Desaturation in Sleep Hypoxemia Hyperventilation Hypocarbia Alkalosis Central Apnea Destaurations etc. Respiratory

Treatments:

­ ­ ­ ­ ­ ­ Oxygen Therapy Acetazolamide Inhaled CO2 CPAP Bi-Level Adaptive Servo-Ventilation

Continuous Positive Airway Pressure for Central Sleep Apnea and Heart Failure: NEJM Nov.10,2005

258 patients with EF <24% (+/-) 7%, and CSA and AHI> 40+/- 16 128 patients ­ 130 controls 3 months of CPAP to fixed level 10 cm H2O Results: Patients had improved quality of life but not in mortality Conclusion: " Although CPAP attenuated central sleep apnea, improved nocturnal oxygenation, increased the ejection fraction, lowered norepinephrine levels, and increased the distance walked in six minutes, it did not affect survival. Our data do not support the use of CPAP to extend life in patients who have central sleep apnea and heart failure."

Benificial Effect of Bilevel Positive Airway Pressure on Left Ventricular Function in Ambulatory Patients With Idiopathic Dilated Cardomyopathy and Central Sleep Apnea-Hypopnea A Preliminary Study: CHEST June 2007

52 Consecutive patients with IDCM Excluded patients with OSA Patients with AHI >20 were ramdomized to either medical therapy alone or together with BPAP Results:

­ "LV end-diastolic pressure, pulmonary capillary wedge pressure, and plasma concentration of BNP were sigificantly greater, and LVEF was significantly lower in patients with an AHI> 20 than in those <20." ­ "LVEF and Plasma BNP were significantly increase and decreased respectively after treatment with BPAP for 3 months, whereas these parameters remained unchanged in the control subjects"

Conclusion:

­ " Treatment of co-existing central sleep apnea with BPAP improves LV function in ambulatory patients with IDCM."

Efficacy of Adaptive ServoVentilation in Treatment on Central and Complex Sleep Apnea Syndromes: CHEST 2007 pg. 1839-1846

Retrospective analysis of first 100 patients treated with ASV at Mayo Clinic for CSA or CompSAS CompSAS 63%, CSA 22%,Cheyne/Stokes 15% Median AHI 48 (24-62) Failed previous CPAP, Bilevel continuous or with Back up rate with either worsened AHI From baseline or continued AHI >15 Findings: ASV had dramatic improvement of AHI with a mean of 5/hr. ASV also improved sleep architecture with an increase in REM% Overall 64 patients responded to ASV with an AHI < 10/hr. On follow up survey 32 of 44 responders reported improvement in sleep quality Concluded ASV is effective treatment for CSA/CompSAS not responsive to CPAP or Bilevel therapy

Pathophysiologic Interactions between Sleep Related Breathing Disorder and Health Clinical

Flow Limitation Event

Sympathetic activation De-oxygenation Re-oxygenation

Hypertension Cardio-Cerebrovascular Disease Daytime Sleepiness Neurocognitive Dysfunction NeuroBehavioral Dysfunction Sudden Death

Increase ITP

Sleep Fragmentation

Intermediary

Interacting

Autonomic Dysautoregulation Inflammation Oxidative Stress Endothelial Dysfunction Metabolic Dysregulation Hypercoagulability

Obesity Male Gender Advanced Age Smoking Metabolic Syndrome Co-Morbid CV Disease Drugs

Conclusion

Sleep Disorder Breathing is a spectrum condition from Snoring to Obstructive Sleep Apnea. Sleep Related Breathing Disorder has been associated with various biochemical markers involved with endothelial function, inflammation, and insulin resistance, as well as being a risk factor for hypertension, heart disease, congestive heart failure, stroke, pulmonary dysfunction, and impaired neurocognitive and behavioral function Treatment of sleep apnea may improve, as well as prevent, cardiovascular disease Reversal with CPAP therapy is multifactorial depending on the stage at which treatment is started and the existence of other co-morbid disorders, but is more often than not beneficial In heart failure patients therapy is more complex and not always responsive to simple CPAP/Bilevel therapy if Central/CompSAS is a dominant feature ASV is superior to CPAP/Bilevel for Central/CompSAS The best therapy is early therapy before the development of hypertensive/cardiovascular disease Don't wait for Retinopathy to treat Diabetes!

THE END

Histograms

Heart rate from 90 to 60 with CPAP

Heart rate decreased due to CPAP

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