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CONSEQUENCES OF SLEEP APNEA SYNDROME Yüksel Peker MD, PhD, Associate Professor

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CONSEQUENCES OF SLEEP APNEA SYNDROME Yüksel Peker MD, PhD, Associate Professor Sleep Medicine Unit, Skaraborg Hospital, Skövde & University of Gothenburg, Sweden. Wife stabbed snoring husband. rescued by thoracic surgeons. OSA (Asymptomatic OSA; “Non-sleepy sleep apnoeics”)

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slide1

CONSEQUENCES OF

SLEEP APNEA SYNDROME

Yüksel Peker

MD, PhD, Associate Professor

Sleep Medicine Unit, Skaraborg Hospital,

Skövde & University of Gothenburg, Sweden

slide2

Wife stabbed snoring husband

rescued by thoracic surgeons

slide4
OSA (Asymptomatic OSA; “Non-sleepy sleep apnoeics”)
  • OSAS (Symptomatic OSA; “Sleepy sleep-apnoeics”)
obstructive sleep apnea syndrome osas osa daytime sleepiness treatment indication
OBSTRUCTIVE SLEEP APNEA SYNDROME (OSAS) OSA + Daytime sleepinessTreatment indication
slide6

Prevalence (30-60 yrs) Men Women OSA 24 % 9 % OSAS 4 % 2 % The majority of the patients with OSA do not report daytime sleepiness

slide7

OSA increases by age

Eight-year follow-up AHI versus baseline AHI in the Wisconsin Sleep Cohort Study (n= 282) Young Tet al, AJRCCM 2002
slide9
OSA
  • Immediate changes
  • Long-term effects
slide11
OSA
  • Immediate changes
  • Long-term effects
slide14
Cardiovascular mechanisms (I)

Repeated nocturnal hypoxemia

Coccogna G et al, 1972; Podszus T et al, 1986

Sympathetic nervous activity

Fletcher EC et al, 1987; Hedner J et al, 1988;

Narkiewicz K & Somers VK 2003

Vascular endothelial dysfunction

Carlson J et al, 1996; Remsburg S et al, 1999;

Kraiczi H et al, 2000

slide15
Cardiovascular mechanisms (II)

Enhanced release of superoxide from polymorphonuclear neutrophils in OSA. Impact of CPAP.

Schulz Ret al, AJRCCM 2000

Plasma vascular endothelial growth factor in OSAS: Effects of CPAP.

Lavie L et al, AJRCCM 2002

Elevated levels of C-reactive protein and interleukin-6 in patients with OSAS are decreased by CPAP.

Yokoe Tet al, Circulation 2003

slide16

Pulse-oximetry

Oxygen

saturation %

Heart rate

50 %

Time

osa cvd
OSA & CVD
  • Immediate changes
  • Long-term effects
hypnogram
Hypnogram

Lights Out

MT

Normal

Wake

REM

S1

S2

S3

S4

00:00

02:00

04:00

06:00

08:00

OSA

Lights Out

MT

Wake

REM

S1

S2

S3

S4

00:00

01:00

02:00

03:00

04:00

05:00

06:00

07:00

long term complications
Long-term complications
  • Cognitive dysfunction
  • Cardiovascular dysfunction
slide24

AHI 30

AHI 30

AHI 30

AHI 30

AHI 30

AHI 30

long term complications1
Long-term complications
  • Cognitive dysfunction
  • Cardiovascular dysfunction
slide26
Clinical and epidemiological aspects

Obstructive sleep apnea is associated with

Hypertension

Coronary heart disease

Cardiac arrhythmias

Heart failure

Stroke

Diabetes and Insulin Resistance

Mortality

slide28

CVD

OSA

OSAS

slide30

CVD

OSA

Obesity

slide32
Prevalence of CAD in Sleep Clinic Cohorts

CAD in 25% of unselected patients with OSA

More common in severe OSA

Maekawa M et al, Psychiatry Clin Neurosci 1998

slide33

First author publ yr

n

AHI10

controls

De Olazabal 1982

Andreas 1996

Mooe 1996

Mooe 1996

Koehler 1996

Peker 1999

Moruzzi 1999

Sanner 2001

Mehra 2006

Takama 2007

Yumino 2007

17

50

142

102

74

62

22

49

104

65

89

76 %

50 %

37 %

30 %

35 %

31 %

9 %

27 %

66 %

45 %

57 %

yes

yes

yes

Total

776

42%

Prevalence of OSA in CAD clinic cohorts

slide35

Explanatory variables associated with CAD (multivariate analysis) _______________________________________________________________________________________Odds Ratio 95 % CI p values_______________________________________________________________________________________Current smoking 9.8 2.6-36.5 0.001Diabetes mellitus 4.2 1.1-17.1 0.045Obstructive sleep apnea 3.1 1.2-8.3 0.025_______________________________________________________________________________________

Peker et al, ERJ 1999

slide36
Prognosis of CAD with concomitant OSA is WORSE than the

prognosis of CAD patients without OSA

Peker et al, AJRCCM 2000

Mooe et al, AJRCCM 2001

Yumino et al, Am J Cardiol 2007

slide38
Prognosis of CAD after PCI in patients with

concomitant OSA

89 consecutive patients with acute coronary syndrome who were successfully treated with PCI

OSA in 51 patients (57%); follow-up period 6 months

Major cardiac event (cardiac death, reinfarction, revascularization)

23.5 % in OSA, 5.3 % in non-OSA (p=0.020)

Odds ratio for OSA 11.6 (95% CI 2.2-62-2)

Yumino et al, Am J Cardiol 2007

slide42
Prognosis of CAD with concomitant OSA is

NOT WORSE than the prognosis for CAD patients

without OSA

50 CAD patients (25 OSA, 25 non-OSA)

Follow-up period 10 years

Cardiac death in 4 versus 5 patients (ns)

Hagenah et al, Respir Med 2006

slide43
Weak association between OSA & CAD

in a general population

Sleep Heart Health Study

Cross-sectional analysis (n=6,132)

Adjusted OR for OSA 1.27 (95% CI 0.99-1.62)

(AHI>11 versus AHI<1.4)

Shahar E et al, AJRCCM 2001

slide44
CAUSALITY

Incident CAD in OSA

Impact of treatment of the OSA on CAD

slide47

CAD incidence in a sleep-clinic cohort

at a 7-yr follow-up

%

Peker et al, ERJ 2006

slide48
Probability of CAD incidence estimated by Poisson modelStart age 49 yrs, Systolic BP 133 mmHg and Sat. min 86%

Peker et al, ERJ 2006

slide50

First author publ yr

n

AHI10

controls

Bassetti 1996

Dyken 1996

Bassetti 1999

Wessendorf 2000

Parra 2000

Iranzo 2002

Hui 2002

Turkington 2002

Kaneko 2003

Bassetti 2006

59

24

128

147

161

50

51

120

61

152

69 %

71 %

63 %

44 %

71 %

62 %

67 %

61 %

72 %

58 %

yes

yes

Total

953

67%

Prevalence of sleep apnea in acute stroke/TIA

slide51
Sleep apnea improves after the acute phase of stroke

Normalizing in 40% of the patients within 6 months

Bassetti CL et al, Stroke 2006; 37:967-972

slide52
Early neurologic worsening in acute stroke and

sleep apnea

50 patients with acute stroke underwent polysomnography (first night)

62% had AHI10

Early neurologic worsening occurred in 30%

Sleep apnea and serum glucose predicted early neurologic worsening

No difference in functional outcome after 6 months

Iranzo A et al, Neurology 2002; 58:911-916

slide53
Increased 6-month mortality (37%) in patients with

stroke and sleep apnea

120 patients enrolled

Turkington PM et al, Thorax 2004; 59: 367-371

slide55
OSA is a risk factor for death in patients with stroke

10-year follow-up

132 patients (1995-1997) were enrolled

Obstructive Sleep Apnea (AHI15) in 23

Central Sleep Apnea in 28

116 had died at follow-up

Adjusted OR for death was 1.76 (95% CI 1.05-2.95) for OSA

No correlation with central sleep apnea

Sahlin C et al, Arch Intern Med 2008; 168:297-301

slide56
Association between OSA & stroke in a general population

Sleep Heart Health Study

Cross-sectional analysis (n=6,132)

Adjusted OR for OSA 1.58 (95% CI 1.02-2.46)

(AHI>11 versus AHI<1.4)

Shahar E et al, AJRCCM 2001

slide57

PREVALENCE of STROKE

General population: 1475 subjects

Arzt M et al, AJRCCM 2005; 172:1447-1451

slide58

INCIDENT STROKE

General population: 1189 subjects - at 4-yr follow-up

Arzt M et al, AJRCCM 2005; 172:1447-1451

slide60
Long-term cardiovascular outcomes in men with OSA with or without treatment with CPAP: an observational study

Marin JM et al

Lancet 2005; 365:1046-53

slide61

Long-term cardiovascular outcomes in men with OSA with or without CPAP

  • Sleep clinic (1992-1994), PSG 1465
  • Simple snorers (n=377)
  • OSA (n=1071)
  • CPAP recommended (n=667)
  • CPAP accepted (n=426)
  • Untreated severe OSA (AHI>30, n=235)
  • Healthy controls (n=264) individually matched with the severe untreated OSA for age and BMI (AHI<5)
slide62

Cardiovascular events in men during 10 years

%

***

***

modified from Marin JM et al, Lancet 2005

slide63

Fully adjusted Odds Ratios for cardiovascular death associated with clinical variables

OR (95% CI) p

Age, yrs 1.09 (1.04-1.12) 0.001

Snoring 1.03 (0.31-1.84) 0.88

Mild OSA 1.15 (0.34-2.69) 0.71

Severe OSA 2.87 (1.17-7.51) 0.025

CPAP 1.05 (0.39-2.21) 0.74

Cardiovascular disease 2.54 (1.31-4.99) 0.005

Marin JM et al, Lancet 2005

conclusions i
CONCLUSIONS (I)
  • Recurrent obstructive events during sleep have harmful effects on daytime vigilance as well as on vascular structure and function
  • Epidemiological data suggest an independent association between OSA and CVD in the clinical cohorts while the association is weaker in the general population
  • Not only may OSA induce CVD but also the events in themselves may worsen the prognosis of an already existing CVD
conclusions ii
CONCLUSIONS (II)
  • OSA should be included among factors considered in the primary and secondary prevention models of CVD.
  • OSA should be treated not only to eliminate daytime sleepiness. Treatment may also have a beneficial prognostic impact by reducing cardiovascular morbidity in OSA.
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