OSA IS A RISK FACTOR FOR STROKE Our Lady Of Lourdes Stroke Center of Excellence Stroke Symposium 5.20.2011 Kevin R. Hargrave, MD; CNS Clinic Board Certified in Neurology and Sleep Medicine, Certified in Neuroimaging CNS Clinic is an AASM Accredited Sleep Center OSA is a risk factor for Stroke Kevin R. Hargrave, MD; CNS Clinic Our Lady Of Lourdes Stroke Center of Excellence 2 TOPICS, OBJECTIVES • CVA: definitions, mechanisms • OSA: definition, epidemiology • Expert Consensus Document from J Amer College of Cardiology • JCSM article • Risks factors for CVA which OSA causes or exacerbates – HTN – Hypertension – Diabetes – Dyslipidemia – Carotid stenosis – Atrial fibrillation – CHF/cardiomyopathy – Hypercoagulability/inflammation/endothelial dysfunction – Smoking • OSA treatment improves some of the above CLASSIFICATION BY MECHANISM Cryptogenic Cardio or aorto-embolic Carotid stenosis Intracranial large artery stenosis Lacunar/ small artery atherosclerosis 4 Types of Stroke 15% 85% Primary Hemorrhage Transient Ischemic Ischemic Stroke Attack Atherosclerotic Disease 20% Intraparenchymal Subarachnoid Hemorrhage Hemorrhage Lacunar (Small Vessel) 25% Other/Unknown 35% Cardioembolism 20% 5 Partial and complete airway obstruction resulting in hypopnea and apnea, respectively Somers, V. K. et al. J Am Coll Cardiol 2008;52:686-717 Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply. Stroke; cerebral infarct (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability Smoking Endothelial dysfunction OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events Obstructive Sleep Apnea (OSA) Stroke; cerebral infarct (CVA) exacerbates: Hypertension( ) Diabetes ( ) Dyslipidemia ( ) Carotid stenosis ( ) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation ( ) CHF( ) Hypercoagulability Atrial fibrillation CHF Hypercoagulability *Smoking Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events (CVA) Nonmodifiable Risk Factors: Family history Age Ethnicity (CVA) Nonmodifiable Risk Factors: Family history Age Ethnicity Treating your apnea will not relieve you of your family history, make you younger or make you tall dark or handsome… (but you might feel younger and more attractive and you may be able to tolerate your family better) PREVALENCE VS AWARENESS • % of pop w d.o. • HTN: • DM: • Afib: > 30% 8% 4-8% » (4% over 60yo; 8% over 80yo) • OSA 10-20% http://emedicine.medscape.com PREVALENCE • % of pop w d.o. VS AWARENESS % aware they have d.o. (ideally 100%) • HTN: • DM: • Afib: > 30% 8% ** 70% <70% <60% • OSA 10-20% 18% http://content.onlinejacc.org/cgi/content/full/52/8/686 Over 400 references OSA affects an estimated 15 million adult Americans and is present in a large proportion of patients with hypertension and in those with other cardiovascular disorders, including • coronary artery disease, • stroke, and • atrial fibrillation (1–14). However, >85% of patients with clinically significant and treatable OSA have never been diagnosed, and referral populations of OSA patients represent only the "tip of the iceberg" of OSA prevalence (42,43) Schematic outlining proposed pathophysiological components of OSA, activation of cardiovascular disease mechanisms, and consequent development of established cardiovascular disease Somers, V. K. et al. J Am Coll Cardiol 2008;52:686-717 Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply. • A blunted nocturnal BP decline has been associated with greater leukoaraiosis (white matter disease) (134). • In a cross-sectional study of Japanese men, brain MRI revealed silent brain infarction in – 25% of patients with moderate to severe OSA – 8% of patients with mild OSA – 6% of control subjects, suggesting that OSA may elicit early and asymptomatic cerebrovascular damage (88) • patients with drug-resistant HTN, defined as a BP of 140/90 mm Hg on 3 BP meds, Logan et al noted the prevalence of OSA (AHI >10), was 83% (145). • The weight of evidence has led the most recent Joint National Committee on the Detection and Management of Hypertension to identify OSA as an important identifiable cause of hypertension (149). Recent 10-year follow-up data of patients with stroke show an increased risk of death in those patients with OSA (adj OR, 1.76) that is independent of age, sex, BMI, smoking, hypertension, diabetes mellitus, atrial fibrillation, Mini-Mental State Examination Score, and Barthel Index. Treatment Options in OSA. Obesity is the single most important cause of OSA. Weight loss can lead to a decrease in AHI, improved sleep efficiency, decreased snoring, and improved oxygenation. The most dramatic results have been reported with surgical weight loss (312–314). • In addition, apnea often is worse in the supine posture, with some patients having OSA only in that position (315,316). • For patients with "positional apnea," behavioral techniques aimed at keeping the patient in the lateral posture during sleep (an uncomfortable object sewn into the back of the nightshirt or positional alarms) may offer benefit. CPAP, applied via a nasal mask, continues to be the primary therapy for patients with OSA (59,60). The device consists of a mask connected to a blower that maintains positive airway pressure at the desired level, acting as a pneumatic splint for the pharyngeal airway (317,318). The prescribed CPAP pressure is generally determined in the sleep laboratory as that pressure required to eliminate all snoring, apneas, and hypopneas during all sleep stages and in all body positions. There is evidence supporting improvements in measures of OSA, daytime sleepiness, and neurocognitive function with nasal CPAP (319–324). Despite the effectiveness of CPAP in treating OSA, adherence to therapy continues to be a major problem (325,326). This relates primarily to the facial interface (mask) and the pressure required to prevent airway collapse, with some patients finding CPAP intolerable. Most evidence suggests that proper introduction of and education regarding CPAP, in both the sleep laboratory and the physician's office, are important. Proper humidification of the inspired air, careful selection of the appropriate mask, and the addition of a pressure ramp all may improve compliance. The use of bilevel positive airway pressure (higher pressure on inspiration than expiration) or a constantly adjusting, autotitrating device may improve patient acceptance. *** Obstructive Sleep Apnea (OSA) exacerbates: Hypertension (Bixler, Hoffstein, Jelic, Lavie, Nieto, Lindbergh, Pancow, Peppard, Suzuki, Vgontzas, Waller, Wilcox, Young, Hoffstein,) Stroke; cerebral infarct (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events SLEEP HEART HEALTH STUDY 1995-98; 6,132 pt’s unattended home PSG’s OR for HTN if OSA present 1.37 (Comparing an AHI of >30 to <1.5) Similar results seen if use desats <90 HTN and AHI correlated even when BMI, ETOH, ethnicity, and age are adjusted for, but association less tight after adjusting for BMI Nieto et al. (Sleep Heart Health Study) JAMA 2000;283:1829-36 TORONTO STUDY 2,677 pt’s with PSG Each 1 unit increase in AHI increased risk of HTN by 1% Also, for each 10% dec in O2 sat, inc HTN risk by 13% Lavie et al. BMJ 2000;320:479-82. WISCONSIN SLEEP COHORT • • • • 1993 N=602 OSA: 24% of men, 9% of women 100 publications have stemmed from the WSC • Nocturnal non-dipping of BP in apneics, with severity gradation Hla et al. Sleep 2008 WISCONSIN SLEEP COHORT STUDY 709 pt’s PSG After 4 yrs OR of HTN 2.89 if had AHI >15 Peppard et al (Wisconsin Sleep Cohort Study) NEJM 2000;342:1378-84 HYPERTENSION A study of over 16,000 men and women 1,700 of which underwent PSG after screening (sleep lab phase) mean age 47yo; mean BMI 27 No SDB SDB (controls) OR 1.0 HTN Snoring only Mild SDB Mod –severe (AHI of 0.0) (AHI of 1-14.9) (AHI>,=15) 1.6 2.3 6.8 36-37 47-52 % w/ HTN 25-29 Bixler, et al., Arch Int Med 2000 Aug14/28160;2289-95 51-59 …the findings of this study add further support to the hypothesis that SDB, including snoring, is an independent risk factor for hypertension (HTN)… Thus a physician should consider the possibility of HTN whenever any type of SDB is present and conversely should consider the possibility of SDB whenever HTN is present. Bixler, et al., Arch Int Med 2000 Aug14/28160;2289-95 HYPERTENSION Snoring and RR of HTN between 1.3 to 2.0 CAD between 1.3 to 2.0 CVA between 1.6 to 10.3 Waller and Bhopal, Lancet. 1989 Jan 21;1(8630):143-6; TREATING OSA CAN IMPROVE HTN • Suzuki et al. Sleep 1993:16;545-49 • Hoffstein et al. AM J of Med 1991:91;190-96 • Duran-Cantolla J, Aizpuru F, Martinez-Null C, Barbe-Illa F. Obstructive sleep apnea/hypopnea and systemic hypertension. Sleep Med Rev. 2009;13(5):323–31. • Giles TL, Lasserson TJ, Smith BJ, White J, Wright J, Cates CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006;(1):CD001106. • Lavie et al. BMJ 2000;320:479-82. • Pankow et al. NEJM 2000:343:966. • Robinson GV, Smith DM, Langford BA, Davies RJ, Stradling JR. Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients. Eur Respir J. 2006;27(6):1229–35. • Faccenda JF, Mackay TW, Boon NA, Douglas NJ. Randomized placebo-controlled trial of continuous positive airway pressure on blood pressure in the sleep apnea-hypopnea syndrome. Am J Respir Crit Care Med. 2001;163(2):344–8. • Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet. 2002;359(9302):204–10. • Wilcox et al.Sleep 1993;16:539-44 Obstructive Sleep Apnea infarct (OSA) exacerbates: Hypertension Diabetes (Dean, Vgontzas, Martins, Punjabi) Stroke; cerebral (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events OSA and Diabetes K Hargrave, MD Louisiana Academy of Sleep Medicine 2009 GLUCOSE DYNAMICS/DIABETES MELLITUS • OSA causes leptin and insulin resistance Journal of Internal Medicine Volume 254 Issue 1 Page 32 - July 2003 Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance Vgontzas AN, Bixler EO, Chrousos GP In conclusion, accumulating evidence provides support to our model of the bi-directional, feedforward, pernicious association between sleep apnea, sleepiness, inflammation and insulin resistance, all promoting atherosclerosis and cardiovascular disease. Sleep-disordered breathing and insulin resistance in middle-aged and overweight men. Multivariable linear regression analyses revealed that increasing AHI was associated with worsening insulin resistance independent of obesity. Thus, sleep-disordered breathing is a prevalent condition in mildly obese men and is independently associated with glucose intolerance and insulin resistance. Punjabi et al. Am J Respir Crit Care Med. 2002 Mar 1;165(5):677-82. CPAP not helpful for DM West, Coughlin, Czupryniak, Smurra, Ip, Stoohs, Cooper, Saini, Thorax 07 Eur Resp J 07 Sleep 05 Sleep Med 01 Chest 2000 AJRCCM 96 Sleep 95 Horm Met Res 93 CPAP helpful Steiropoulos, Lindberg, Pallayova, Fahed, Sharafkhaneh, Babu, Hassabala, Harsch, CPAP may be helpful Oktay, Acta Clin Belg Schahin, Med Sci Monit Sleep Med 09 Sleep Med 06 Sleep Med 06 ATS mtg 06 ATS mtg 06 Arch Int Med 05 Sleep Breath 05 AJRCCM 04 Obstructive Sleep Apnea infarct (OSA) exacerbates: Hypertension Diabetes Dyslipidemia ( Barcelo, Robinson, She ) Stroke; cerebral (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events Circulating cardiovascular risk factors in obstructive sleep apnoea: data from randomised controlled trials. Levels of activated coagulation factors XIIa, VIIa, TAT and sP-sel were higher in OSA patients at baseline than in unmatched controls, but did not fall with 1 month of therapeutic CPAP treatment. The raised sP-sel levels correlated only with body mass index (p = 0.002). There was a trend towards a significant fall in total cholesterol with therapeutic CPAP (p = 0.06) compared with the control group. In the therapeutic group there was a clinically significant mean fall in total cholesterol of 0.28 mmol/l (95% confidence interval 0.11 to 0.45, p = 0.001) which may reduce cardiovascular risk by about 15%. Robinson et al Thorax. 2004 Sep;59(9):777-82. [Long-term follow-up of patients with obstructive sleep apnea syndrome treated with uvulopalatopharyngoplasty] UPPP can improve the hypoxemia of patients with OSAS, reduced the BP, FBG, BMI, improve the lipid metabolism. She W, et al. Zhonghua Er Bi Yan Hou Ke Za Zhi. 2001 Jun;36(3):227-30. Abnormal lipid peroxidation in patients with sleep apnoea. These results indicate that obstructive sleep apnoea syndrome is associated with abnormal lipid peroxidation and that this is improved by chronic use of Continuous positive airway pressure. Barcelo A, et al. Eur Respir J. 2000 Oct;16(4):644-7. Obstructive Sleep Apnea infarct (OSA) exacerbates: Hypertension Diabetes Dyslipidemia Carotid stenosis (Kaynak, Nachtmann, Silvestrini ) Stroke; cerebral (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events CAROTID STENOSIS retrospective study of 395 stroke pt’s severe OSA independently associated with carotid artery disease (OR 2.0) PVD (OR 6.7) ICA ds more strongly assoc with HTN than OSA PVD more strongly assoc with smoking than OSA Nachtmann et al. Athero. 169;2:Aug 03, 301-307. Is there a link between the severity of sleep-disordered breathing and atherosclerotic disease of the carotid arteries? The OSA groups had significantly higher IMT values compared with the habitual snoring group. Three groups were significantly different with regard to the presence of plaque. Age and body mass index were found to be significantly associated with IMT while age and RDI were found to be most probably predictive for plaque. Kaynak D, et al. Eur J Neurol. 2003 Sep;10(5):487-93. OSA AND CAROTID STENOSIS doppler of common carotid thickness 23 OSA pt’s; 23 controls (age and comorbid factors matched) • intima media thickness in OSA pt’s 1.43x that of controls Silvestrini et al. Stroke 02 July;33(7):1782-5. Obstructive Sleep Apnea infarct (OSA) Stroke; cerebral (CVA) exacerbates: Hypertension Diabetes Dyslipidemia Carotid stenosis Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation ( Mooe, Shamsuzzaman) Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events DYSRHYTHMIA/ATRIAL FIB • Even after adjustment for age, sex, BMI, and prevalent coronary artery disease, patients with SDB had increased likelihoods of atrial fib (OR 4.02), nonsustained ventricular tach (OR 3.40), and complex ventricular ectopy (OR 1.74) (231). OSA AND ARRYTHMIA • sinus brady and AV block • Atrial fibrillation • ventricular ectopy Mooe, et al. CAD 1996; 7:475-78. Shamsuzzaman et al. JAMA, Oct8, 2003-Vol 290, No. 14, 1906-1914. Obstructive Sleep Apnea infarct (OSA) Stroke; cerebral (CVA) exacerbates: Hypertension Diabetes Dyslipidemia Carotid stenosis Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF ( Garpestad, Leung, Nieto) Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events OSA AND CHF OSA is risk for CHF ^ heart chamber size AHI>11 OR2.4 for CHF Nieto et al. (Sleep Heart Health Study) JAMA 2000;283:1829-36 Garpestad et al. J Appl Phys. 1992;73:1743-48. OSA is risk for MI AHI >11 OR for CAD 1.3 Nieto et al. (Sleep Heart Health Study) JAMA 2000;283:1829-36 CHF and prior MI (especially subacute MI) are risks for stroke OSA AND CHF • OSA is risk for CHF ^ heart chamber size • OSA is risk for MI • CHF and prior MI (especially recent) are risks for stroke Obstructive Sleep Apnea infarct (OSA) Stroke; cerebral (CVA) exacerbates: Hypertension Diabetes Dyslipidemia Carotid stenosis Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability (Dean, Leung, Nobili, Wessendorf) Atrial fibrillation CHF Hypercoagulability Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events HYPERCOAGULABILITY OSA and blood viscosity 12 pt’s with OSA and 8 controls measures taken at 8pm then after awakening at 8 am controls showed no difference in 8p/8a • OSA pts showed increased Hct, Fibrinogen, and Whole Blood Viscosity in the am samples Nobili et al. Clin Hemorheol Microcirc. 2000;22(1):21-7. HYPERCOAGULABILITY • ^ platelet aggregation; procoagulant • ^ blood viscosity • ^fibrinogen (positive correlation with RDI and negative correlation with O2 sats) Dean et al. Sleep 1993: 16:S15-S22. Wessendorf et al. AJRCCM 2000; 162:2039 Obstructive Sleep Apnea infarct (OSA) exacerbates: Hypertension( ) Diabetes ( ) Dyslipidemia ( ) Carotid stenosis ( ) Stroke; cerebral (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation ( ) CHF( ) Hypercoagulability Atrial fibrillation CHF Hypercoagulability *Smoking (Hoflstein, Kashyap, Blazejova) Smoking OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events Higher prevalence of smoking in patients diagnosed as having obstructive sleep apnea. The prevalence of smoking in patients with OSA was found to be 35%, whereas it was only 18% in patients without OSA. We conclude that cigarette smoke may be an independent risk factor for OSA in this referral population. Kashyap R, Hock LM, Bowman TJ. Sleep Breath. 2001 Dec;5(4):167-72. Relationship between smoking and sleep apnea in clinic population. We found that patients with AHI greater than 50 were heavier smokers than nonapneic controls (14+/-17 vs. 10+/-17 pack-years, respectively). Conversely, heavy smokers had higher AHI than nonsmokers (26.3+/-28.3 vs. 19.7+/-23.9, respectively). Hoflstein V. Sleep. 2002 Aug 1;25(5):519-24 Prevalence of obesity, hypertension and smoking in patients with the sleep apnea syndrome-comparison with the Czech population CONCLUSIONS: Higher prevalence of obesity, hypertension, and smoking were found in patients with SAS compared to non-selected Czech population. Blazejova K, et al. Cas Lek Cesk. (Czech) 2000 Jun 7;139(11):339-42. Obstructive Sleep Apnea cerebral infarct (OSA) Stroke; (CVA) exacerbates: Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Modifiable Risk Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation CHF Hypercoagulability Atrial fibrillation CHF Hypercoagulability Smoking Smoking Metabolic Syndrome (Coughlin) OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events OBSTRUCTIVE SLEEP APNOEA IS INDEPENDENTLY ASSOCIATED WITH AN INCREASED PREVALENCE OF METABOLIC SYNDROME. OSA was independently associated with increased systolic and diastolic blood pressure, higher fasting insulin and triglyceride concentrations, decreased HDL cholesterol, increased cholesterol:HDL ratio, and a trend towards higher HOMA values. Metabolic syndrome was 9.1 (95% confidence interval 2.6, 31.2: p<0.0001) times more likely to be present in subjects with OSA. Coughlin et al Eur Heart J. 2004 May;25(9):735-41. Obstructive Sleep Apnea infarct (OSA) exacerbates: Hypertension( ) Diabetes ( ) Dyslipidemia ( ) Carotid stenosis ( ) Stroke; cerebral (CVA) Modifiable Risk Factors: Hypertension Diabetes Dyslipidemia Carotid stenosis Atrial fibrillation ( ) CHF( ) Hypercoagulability *Smoking Metabolic Syndrome Endothelial dysfunction(Ng) Atrial fibrillation CHF Hypercoagulability Smoking Endothelial dysfunction OSA OSA is an independent risk factor for stroke TIA or stroke patients should be screened for OSA Conversely, stroke can cause or exacerbate OSA Treating OSA can prevent further strokes or other vascular events OSA AND ENDOTHELIAL DYSFUNCTION Women seem to be more susceptible to OSA induced endothelial dysfunction. Faulx et al. Sleep 2004; 27:1113-20. Ng DK, Kwok KL Am J Respir Crit Care Med. 2004 Jul 15;170(2):197. Nieto et al. AJRCCM 2004; 169:354-60. OSA AND DIRECT RISK FOR STROKE 198 pt’s with OSA Group A tracheostomy as treatment Group B weight loss encouraged (no trach or CPAP) 7 years later… 2 pt’s with CVA or MI 15 pt’s with CVA or MI Partinen and Guilleminault. Chest 1990.97:27-32 OSA AND VASCULAR DS. Other possible stroke pathogenetic mechanisms: ^dysautonomia ^ inflammatory cytokines ^ homocysteine/ oxidative products ^alters cerebral blood flow velocity OSA AND VASCULAR DS. Other possible stroke pathogenetic mechanisms: ^dysautonomia ^ inflammatory cytokines ^ homocysteine/ oxidative products ^alters cerebral blood flow velocity OSA AND CEREBRAL BLOOD FLOW • monitored CBF in an 81 yo man with an MCA stroke • CBF through a moderate stenosis of MCA increased from 220 to 320cm/sec • can increase or decrease CBF Benhrens et al., Sleep Breath. 2002 Sep;6(3):111-4. Netzer et al. Stroke ‘98;29:87-93 OSA AND CEREBRAL BLOOD FLOW Normotensive apneics have a greater pressor response to hypoxia than controls Hedner et al. Am Review of Resp Ds. 1992:146:1240-5. Apneics do not vasodilate normally in hypoxia Remsburg et al. J Appl Physiol 1999: 87(3):1148-53. Apneas lead to increased vasoconstrictor tone Leung and Bradley. AJRCCM 2001:164:2147-60. just Snoring SNORING 44% of middle aged men; 28% women associated with HTN INDEPENDENT RISK FACTOR FOR STROKE OR 2-3.3 BMJ ‘87, J Sleep R ‘95, Stroke ‘89, Q J Med ‘92, Lancet ‘89, Sleep ’96, Neurology ’92 SNORING AND VASCULAR DISEASE 330 ER visits for vasc ds./330 controls • 48% vasc pt’s snored/ 30% controls Smirne et al, Eur Respir J. 1993 Oct;6(9):1357-61. SNORING AND VASCULAR DISEASE A logistic regression analysis, entering the variables in the following order: age, gender, body mass index, diabetes, dyslipidaemia, smoking, alcohol, hypertension, and habitual snoring, showed that habitual snoring carries a significant risk factor for stroke and myocardial infarction, even after adjusting for other factors. Smirne et al, Eur Respir J. 1993 Oct;6(9):1357-61. SNORING AND VASCULAR DISEASE Since habitual snoring carries a definite risk for acute vascular disease, we conclude that inquiring about it should become routine practice. Smirne et al, Eur Respir J. 1993 Oct;6(9):1357-61. Snoring as a risk factor for type II diabetes mellitus: a prospective study. …snoring is independently associated with elevated risk of type II diabetes. Al-Delaimy et al. Am J Epidemiol. 2002 Mar 1;155(5):387-93. OSA AFTER STROKE 70-95% acute stroke pt’s have OSA AHI >10 about a third have severe OSA AHI >20 interestingly, lacunar strokes are more likely to cause OSA than large strokes* Harbison et al. QJM 2002 Nov;95(11):741-7. treating OSA after the 1st stroke might help prevent the 2nd stroke Good et al. Stroke 1996; 27:252-59. Dyken et al. Stroke 1996: 27:401-07. Bassetti et al. Neurology 1996: 47:1167-73. TREATING OSA • decreases cardiac demand; decreases BP; decreases LV size • improves heart pump (helps heart failure to improve) – even better than medications (can Improve EF by 30%) • these decrease risk of heart attack and stroke TREATING OSA 24 pt’s with CHF underwent CPAP • reduced daytime SBP from 126 to 116 • reduced HR from 68 to 64 • reduced LV size (LVESD) from 5.5 to 5.2cm • CPAP improved EF from 25% to 34% Kaneko et al, NEJM 2003 Mar 27;348(13):1233-41 STROKE OUTCOMES BETTER • in non apneic patients Clarenbach and Wessendorf. Rev Neurol (Paris) 2001 Nov;157(11pt2):S46-52. OSA AND STROKE AWARENESS • mean latency of stroke/TIA and dx of OSA= 42 months • 31/2 years of untreated OSA! Shulz et al. Pneumologie 2000 Dec;54(12):575-9 OTHER SLEEP DISORDERS AND STROKE OR VASCULAR RISK Pt’s with EDS despite >8h of sleep had higher risk of CVA and CAD Qreshi et al. Neurology 1997; 48:904-910. PLM’s Ali et al. Sleep 1991. 14:163-165. ; Espinar-Sierra et al. Neuroscience 1997: 51:103-107. or sleep disruption of any etiology Horner et al. Sleep 1996. 19:S193-195. may lead to HTN and inc vasc ds. Screening for, and treating, OSA [or other sleep disorders] may improve a person’s quality of life, as well as prevent accidental death (MVA), vascular death (MI). or vascular disability (CVA). Thanks for your attention, KRH OSA TREATMENT • • • • CPAP continuous positive airway pressure a breathing mask that blows room air stops snoring improves nightime breathing and oxygenation (without O2 supplementation) TREATING OSA • helps improve sleep quality (deeper sleep) • decreases nighttime awakenings • decreases nighttime trips to urinate (improved sleep quality and decreased nocturnal urinary production) • data to support that it improves insulin sensitivity OSA AND STROKE AWARENESS • mean latency of stroke/TIA and dx of OSA= 42 months • 31/2 years of untreated OSA! Shulz et al. Pneumologie 2000 Dec;54(12):575-9 Screening for, and treating, OSA may improve a person’s quality of life, as well as prevent accidental death (MVA) or vascular disability (CVA) or death (MI). Thanks for your attention, KRH 41 yo 6’ 138#, ‘girlfr has to punch him to breathe’, ESS 16 REFERENCES Artz, et al AJRCC 2005 Al-Delaimy et al. Am J Epidemiol. 2002 Mar 1;155(5):387-93. Barcelo A, et al. Eur Respir J. 2000 Oct;16(4):644-7. Bassetti et al. Neurology 1996: 47:1167-73. Benhrens et al., Sleep Breath. 2002 Sep;6(3):111-4. Bixler, et al., Arch Int Med 2000 Aug14/28160;2289-95. Blazejova K, et al. Cas Lek Cesk. (Czech) 2000 Jun 7;139(11):339-42. Budhiraja Resp Care 2010 Clarenbach and Wessendorf. Rev Neurol (Paris) 2001 Nov;157(11pt2):S46 Coughlin et al Eur Heart J. 2004 May;25(9):735-41. Dean et al. Sleep 1993: 16:S15-S22. Dyken et al. Stroke 1996: 27:401-07. Garpestad et al. J Appl Phys. 1992;73:1743-48. Good et al. Stroke 1996; 27:252-59. Harbison et al. QJM 2002 Nov;95(11):741-7. Hoffstein et al. AM J of Med 1991:91;190-96 Jelic et al. Sleep 2002. 25(8):850-55. Johnson and Johnson JCSM 2010 . REFERENCES, PAGE 2 Kashyap R, et al. Sleep Breath. 2001 Dec;5(4):167-72. Kaynak D, et al. Eur J Neurol. 2003 Sep;10(5):487-93. Kaneko et al. NEJM 2003 Mar 27;348(13):1233-41. Koskenvuo et al. BMJ 1987; 294:16-19 Lavie et al. BMJ 2000;320:47982. Leung and Bradley. AJRCCM 2001:164:2147-60. Lindbergh et al. Eur Resp J 1998;11:884-89 Mohsehnin V. Stroke 2001:32:1271-78. Mooe, et al. CAD 1996; 7:475-78. Nachtmann et al. Athero. 169;2:Aug 03, 301-307 Netzer et al. Stroke ‘98;29:87-93 Ng DK, Kwok KL Am J Respir Crit Care Med. 2004 Jul 15;170(2):197. Nieto et al. (Sleep Heart Health Study) JAMA 2000;283:1829-36 Nobili et al. Clin Hemorheol Microcirc. 2000;22(1):21-7. Palomaki et al. Neurology 1992. Pankow et al. NEJM 2000:343:966. Partinen and Guilleminault. Chest 1990.97:27-32 Partinen and Palomaki. Lancet 1985;2:1325-26. REFERENCES, PAGE 3 Peppard et al (Wisconsin Sleep Cohort Study) NEJM 2000;342:1378-84 Pepperell et al. Lancet 2002;359:204-210. Qreshi et al. Neurology 1997; 48:904-910. Remsburg et al. J Appl Physiol 1999: 87(3):1148-53. Robinson et al Thorax. 2004 Sep;59(9):777-82. Shahar et al. AM J Resp Crit Care Med 1999:163;19-25 Shamsuzzaman et al. JAMA, Oct8, 2003-Vol 290, No. 14, 1906-1914. She W, et al. Zhonghua Er Bi Yan Hou Ke Za Zhi (chinese). 2001 Jun;36(3):227-30. Shulz et al. Pneumologie 2000 Dec;54(12):575-9. Silvestrini et al. Stroke 02 July;33(7):1782-5. Smirne et al, Eur Respir J. 1993 Oct;6(9):1357-61. Suzuki et al. Sleep 1993:16;545-49 Young et al. Arch Int Med. 1997:1746-52. Vgontzas AN, Bixler EO, Chrousos GP Journal of Internal Medicine. 2003; 254,32 Vgontzas et al. J of Clin Endoc and Metab 2000 85:1151-58. Waller and Bhopal, Lancet. 1989 Jan 21;1(8630):143-6. Wessendorf et al. AJRCCM 2000; 162:2039 Wilcox et al.Sleep 1993;16:539-44.