sommeil et avc - ssvq.org · pfo-associated ischemic strokes115 and there is an increased reported...

Alex Desautels, MD, PhD Directeur, Clinique des troubles du sommeil, HSCM

Chef, Service de neurologie, CIUSSS NIM

Professeur adjoint de clinique, Université de Montréal

LE SOMMEIL

SOMMEIL ET AVC une relation bi-directionnelle

Conflits d’intérêts potentiels Octrois de recherche

 Novartis

 Jazz Pharma  Biron

 Flamel Ireland

Comité consultatif  UCB

Conférencier  Paladin

 UCB

Les honoraires sont versés aux étudiants gradués du CEAMS

Objectifs de la présentation

 Reconnaître les pathologies du sommeil comme facteur de risque de l’AVC

 Sélectionner les examens appropriés chez le patient somnolent suite à un AVC

 Comprendre les conséquences de l’AVC sur le sommeil et la vigilance

LE SOMMEIL

AVC ET APNÉE DU SOMMEIL

Négligeons-nous un facteur de risque vasculaire modifiable?

Dans quelle mesure devons-nous harceler les cliniques de sommeil pour enregistrer nos patients vasculopathes?

Types d’apnée Apnée obstructive   Réduction de ≧90% signal respiratoire durant

≧10sec associé à des efforts respiratoires

Hypopnée   Réduction ≧30% débit respiratoire durant 10sec

  Désaturation ≧3% OU Micro-éveil à l’EEG

Apnée centrale   Absence d’effort respiratoire

  Population et pathophysiologie distinctes de l’apnée obstructive

Indice d’apnées-hypopnées (IAH)   5-14/h léger

  15-29/h modéré

  ≧30/h sévère

AASM 2012

Incidence d’AVC chez les apnéiques

Études transversales  AHI ≧ 20 OR 4.33 (CI: 1,32-14.24)1

Études prospectives  AHI ≧ 20 HR 2,86 (CI: 1.1-7.4)2

 HR 1.97 (CI: 1,12-3,48)3

 Relation linéaire entre AHI et risque d’AVC

1Arzt et al., 2005 2 Redline et al., 2010 3Yaggi et al. 2005

Prévalence d’apnée dans l’AVC

Patients victimes d’AVC/ICT1

 AHI >5/h 72% des patients

 AHI >10/h 63% des patients

 AHI > 20/h 38% des patients

 Apnée centrale 7% des patients

1Johnson et al., 2010

134Journal of Clinical Sleep Medicine, Vol.6, No. 2, 2010

KG Johnson and DC Johnson

135

SDB was primarily obstructive in nature, with only 7% of pa-tients having primarily central apneas. SDB was more common in male patients, those with recurrent strokes and those with strokes of unknown etiology. SDB was less common among those with strokes of cardioembolic etiology. Other factors, in-cluding stroke event type, patient location, timing, and testing methods after stroke, did not affect the percentage of patients with OSA.

The SDB frequency was high in stroke patients despite a rel-atively low average BMI of 26.4 kg/m2. The frequency of OSA found in this study was very similar to rates found in a commu-nity-based study of adults with age greater than 65 (62% with AHI > 10)36; however, it was significantly higher than the rates of OSA found in younger adults.4 This meta-analysis found a trend toward increasing average age in the study population being associated with increasing rates of SDB. Several of the individual studies reported a significant relationship between increasing age and OSA frequency.9,13,14,15,35 There are no studies of the frequency of OSA in stroke patients broken down by age groups. However, it is likely that younger stroke patients would have a higher OSA frequency than a similar aged non-stroke population.

This analysis found no significant difference between the dif-ferent stroke types, although there was limited data on hemor-

tory of snoring (p < 0.001). The relative risk of snoring in SDB patients was 1.39.

DISCUSSION

This meta-analysis found that SDB is present in up to 72% of ischemic and hemorrhagic stroke and TIA patients. The

Table 2—Percentage of patients with SDB by AHI cut-off pointsStudy & Year > 5 > 10 > 20 > 30 > 40

Bassetti 1999 63Bassetti 2006 58 31 17Broadley 2007 58Brown 2008 73Cadhilac 2005 81 45 18 8Disler 2002 61Dziewas 2005 52Dziewas 2007 51Dziewas 2008 78Dyken 1996 83 71 46 42 29Harbison 2003 92 67 46Herman 2007 58Hsu 2006 50Hui 2002 67 49 31Iranzo 2002 62 46Kaneko 2003 72Martinez 2005 54Mohsenin 1995Nachtmann 2003 43 25NorAdina 2006 93 79 39Palombini 2006 76Parra 2000 72 47 28 11Rola 2007 66Sandberg 2001 77 55 37 21 8Selic 2005 69 29Siccolli 2008 55Turkington 2002 80 61 30Wessendorf 2000 61 43 22Wierzbicka 2006 63 40 21

Table 3—Percentage of stroke or TIA patients with SDB stratified by AHI

Cutpoint # Studies (# patients) % (95% CI)AHI > 5 9 (908) 72 (60–81)AHI > 10 24 (1980) 63 (58–68)AHI > 20 15 (1405) 38 (31–46)AHI > 30 10 (865) 29 (21–37)AHI > 40 3 (318) 14 (7–25)Central* 17 (1286) 7 (5–12)

*Percentage of patients who had primarily central apnea

0 50% 100%

Bassetti (1999) Bassetti (2006) Broadley (2007) Cadilhac (2005) Disler (2002) Dyken (2005) D iewas (2005) D iewas (2007) D iewas (2008) Harbison (2002) Hermann (2007) Hui (2002) Iran o (2001) Kaneko (2003) NorAdina (2006) Palombini (2006) Parra (2000) Sandberg (2001) Selic (2005) Siccoli (2008) Turkington (2002) Wessendorf (2000) Wier bicka (2006) All Studies

Stud

y (ye

ar)

Percentage with AHI > 10

Figure 1—Forest plot of percentage of patients with AHI > 10 with 95% confidence intervals.

Apnée et pronostic post AVC

Apnée obstructive comorbide

Durée de l’hospitalisation

Durée de réadaptation

Délirium

Récurrence AVC/ICT

Mortalité

Dysthymie

Pronostic fonctionnel Months

Cu

mu

lativ

e s

urv

iva

l

Menon et al., 2017

NIH

SS

Admission Discharge

OSA

No OSA

Apnée comme facteur de risque indépendant d’AVC  Hypertension  Non-dipping

 Activation système R-A-A

 Résistance à l’insuline

 Obésité

  leptine/ ghreline

 Arythmies (FA)  Prévalence accrue chez apnéiques

 Relation linéaire

 Survenue facilitée en REM

variability, and augmented blood pressure variability.102

There is extensive innervation of the cerebral vasculatureand the increased sympathetic nervous activity might perturbcerebral autoregulation and blood flow predisposing to cere-bral ischemia.103 In fact, increased sympathetic nervous ac-tivity in subjects after a stroke is an independent predictor ofpoor outcome at 12 months.104

Hypercoagulability. Hypercoagulability might predispose toacute thrombosis and subsequent cerebrovascular events.105

Altered hypercoagulability occurs by a variety of mecha-nisms in OSA106,107 and might peak during the night.108

Furthermore, treatment of OSA with CPAP is successful inreducing coagulation markers.109

Patent foramen ovale. Cryptogenic strokes occur morefrequently in those with patent foramen ovale (PFO).110 The

reported prevalence of PFO in OSA is variable (26.9%-68.8%), with 2 studies suggesting increased prevalencecompared with the general population.111,112 Most PFOs arebenign and not associated with shunting. In OSA the negativeintrathoracic pressure that occurs during apnea episodes leadsto increased venous return to the right heart which favoursright-to-left shunting.113 This is particularly evident in thosewith obstructive apneas of long duration112 and might beassociated with more severe nocturnal oxygen desaturation.The intermittent hypoxia associated with the obstructiveevents might also cause pulmonary vasoconstriction, whichacutely increases the systolic transmural pulmonary arterypressure, and contributes to right-to-left shunting.114 Theo-retically, the combination of a PFO and OSA might predis-pose to increased stroke risk, by potentially causing increasedright-to-left shunting and paradoxical embolism. It is recog-nized that wake-up strokes are independently associated withPFO-associated ischemic strokes115 and there is an increasedreported frequency of wake-up strokes in severe OSA115 giv-ing credence to the role of PFO in those with OSA.

Stroke and CSACSA has been observed in patients with acute stroke where

the reported prevalence is approximately 6%-24%.100,116 Thestroke location associated with hypercapnic CSA is the nu-cleus tractus solitarius region of the medulla responsible fordiaphragmatic function.117,118 Most recent studies have foundno relationship between the site, size or type of stroke, and thepresence of CSA.25,119 The CSA usually dissipates over timein most cases. The presence of underlying occult cardiacdysfunction might be present in a subset of patients.116 Theclinical significance of CSA in patients with stroke is unclear.

ConclusionsThe significant burden of stroke on the individual and so-

ciety is undisputed. SA is frequent within the general and post-stroke population. Current research provides a persuasiverationalization of the connection between stroke and SA.Ongoing research is imperative: (1) for the stratification andphenotyping of individuals at greatest risk from SA and those inwhom treatment will be most critical; (2) to determine thecorrect timing and modality of treatment; and (3) to under-stand the interplay between vascular remodelling, neuro-plasticity, and SA, particularly OSA. A more sophisticated,personalized approach is required. Although conceding thatthere are substantial knowledge gaps and further research isrequired, strategies for comprehensive acute, chronic, and pre-ventive care of stroke, should be complemented with evaluationand screening for OSA and consideration given to treatment.

DisclosuresThe authors have no conflicts of interest to disclose.

References

1. Feigin VL, Forouzanfar MH, Krishnamurthi R, et al. Global andregional burden of stroke during 1990-2010: findings from the GlobalBurden of Disease Study 2010. Lancet 2014;383:245-54.

Figure 3. Typical changes of mean arterial pressure (MAP) and cere-bral blood flow velocity (CBFV) during and after a 23-second apnea.The dashed line represents baseline values. PtcCO2, transcutaneouscarbon dioxide; SpO2, pulse oxygen saturation. Reproduced fromBålfors and Franklin48 with permission from the American ThoracicSociety. Copyright ª 1994 American Thoracic Society.

Lyons and Ryan 923Sleep Apnea and Stroke

variability, and augmented blood pressure variability.102

There is extensive innervation of the cerebral vasculatureand the increased sympathetic nervous activity might perturbcerebral autoregulation and blood flow predisposing to cere-bral ischemia.103 In fact, increased sympathetic nervous ac-tivity in subjects after a stroke is an independent predictor ofpoor outcome at 12 months.104

Hypercoagulability. Hypercoagulability might predispose toacute thrombosis and subsequent cerebrovascular events.105

Altered hypercoagulability occurs by a variety of mecha-nisms in OSA106,107 and might peak during the night.108

Furthermore, treatment of OSA with CPAP is successful inreducing coagulation markers.109

Patent foramen ovale. Cryptogenic strokes occur morefrequently in those with patent foramen ovale (PFO).110 The

reported prevalence of PFO in OSA is variable (26.9%-68.8%), with 2 studies suggesting increased prevalencecompared with the general population.111,112 Most PFOs arebenign and not associated with shunting. In OSA the negativeintrathoracic pressure that occurs during apnea episodes leadsto increased venous return to the right heart which favoursright-to-left shunting.113 This is particularly evident in thosewith obstructive apneas of long duration112 and might beassociated with more severe nocturnal oxygen desaturation.The intermittent hypoxia associated with the obstructiveevents might also cause pulmonary vasoconstriction, whichacutely increases the systolic transmural pulmonary arterypressure, and contributes to right-to-left shunting.114 Theo-retically, the combination of a PFO and OSA might predis-pose to increased stroke risk, by potentially causing increasedright-to-left shunting and paradoxical embolism. It is recog-nized that wake-up strokes are independently associated withPFO-associated ischemic strokes115 and there is an increasedreported frequency of wake-up strokes in severe OSA115 giv-ing credence to the role of PFO in those with OSA.

Stroke and CSACSA has been observed in patients with acute stroke where

the reported prevalence is approximately 6%-24%.100,116 Thestroke location associated with hypercapnic CSA is the nu-cleus tractus solitarius region of the medulla responsible fordiaphragmatic function.117,118 Most recent studies have foundno relationship between the site, size or type of stroke, and thepresence of CSA.25,119 The CSA usually dissipates over timein most cases. The presence of underlying occult cardiacdysfunction might be present in a subset of patients.116 Theclinical significance of CSA in patients with stroke is unclear.

ConclusionsThe significant burden of stroke on the individual and so-

ciety is undisputed. SA is frequent within the general and post-stroke population. Current research provides a persuasiverationalization of the connection between stroke and SA.Ongoing research is imperative: (1) for the stratification andphenotyping of individuals at greatest risk from SA and those inwhom treatment will be most critical; (2) to determine thecorrect timing and modality of treatment; and (3) to under-stand the interplay between vascular remodelling, neuro-plasticity, and SA, particularly OSA. A more sophisticated,personalized approach is required. Although conceding thatthere are substantial knowledge gaps and further research isrequired, strategies for comprehensive acute, chronic, and pre-ventive care of stroke, should be complemented with evaluationand screening for OSA and consideration given to treatment.

DisclosuresThe authors have no conflicts of interest to disclose.

References

1. Feigin VL, Forouzanfar MH, Krishnamurthi R, et al. Global andregional burden of stroke during 1990-2010: findings from the GlobalBurden of Disease Study 2010. Lancet 2014;383:245-54.

Figure 3. Typical changes of mean arterial pressure (MAP) and cere-bral blood flow velocity (CBFV) during and after a 23-second apnea.The dashed line represents baseline values. PtcCO2, transcutaneouscarbon dioxide; SpO2, pulse oxygen saturation. Reproduced fromBålfors and Franklin48 with permission from the American ThoracicSociety. Copyright ª 1994 American Thoracic Society.

Lyons and Ryan 923Sleep Apnea and Stroke

Modifié de Balfors et al., 1994; Hendrikx et al., 2017

Ten patients had a previous diagnosis of atrial fibrillation and three were new diagnoses.Among patients with known atrial fibrillation, none had been treated with ablative therapy.

Atrial fibrillation occurred in 13 of 201 investigated patients (6.5%), and in 12 of 61 (20%)men aged 60 years and older. The prevalence of atrial fibrillation increased with the severity ofsleep apnea, p = 0.038 (Fig 1).

All the patients with atrial fibrillation were men and they all had sleep apnea. Only one of113 investigated patients younger than 60 had atrial fibrillation (0.9%), and 12 of 88 patientsolder than 60 had sleep apnea (14%), p<0.000. Atrial fibrillation occurred in six of 17 patients(35%) with concomitant central sleep apnea.

Table 1. Baseline characteristics.

Men [n, (%)] 138 (69)

Age [years, mean, SD] 56 ±12

Heart Failure [n, (%)] 9 (4.6)

Hypertension [n, (%)] 101 (51)

Diabetes mellitus [n, (%)] 20 (10)

Stroke/Transient Ischemic Attack [n, (%)] 6 (3.1)

Ischemic heart disease [n, (%)] 18 (9.2)

Body mass index [kg/m2, mean, SD] 30 ±5.4

Smoking [n, (%)] 16 (8.1)

doi:10.1371/journal.pone.0171575.t001

Fig 1. Prevalence of atrial fibrillation in relation to AHI. Prevalence of atrial fibrillation in relation to the severityof sleep apnea measured as the apnea-hypopnea index (AHI). (P = 0.038 for the trend).

doi:10.1371/journal.pone.0171575.g001

Atrial fibrillation in sleep apnea

PLOS ONE | DOI:10.1371/journal.pone.0171575 February 8, 2017 4 / 9

0

5

10

15

15-30 <5 5-15 >30 Pre

vale

nc

e o

f AF

(%)

AHI

Adapté de Lyon et 2015

CPAP chez les patients victimes d’AVC

Martinez-Garcia et al., 2012

Efficacité

 Études observationnelles et RC peu puissantes…

 Récupération à 1 mois

  Mortalité et morbidité

  Événements cardio-vasculaires

  Récurrence AVC/AIT1

 Étude observationnelle, N=189, suivi 7A

 AHI ≧ 20 HR=2,87 (CI: 1,11-7,11)

 NNT=4,9

Canadian Stroke Best Practice Recommendations: Mood, Cognition and FatigueFollowing Stroke practice guidelines, update 2015

Gail A. Eskes1, Krista L. Lanctôt2,3, Nathan Herrmann2,3, Patrice Lindsay3,4*, Mark Bayley3,5,Laurie Bouvier6, Deirdre Dawson7, Sandra Egi8, Elizabeth Gilchrist9, Theresa Green10,Gord Gubitz11, Michael D. Hill12, Tammy Hopper13, Aisha Khan14, Andrea King15, Adam Kirton16,Paige Moorhouse15, Eric E. Smith12, Janet Green1, Norine Foley17, Katherine Salter17, andRichard H. Swartz2,3 on behalf of the Heart Stroke Foundation Canada Canadian Stroke BestPractices Committees

Every year, approximately 62 000 people with stroke and tran-sient ischemic attack are treated in Canadian hospitals, andthe evidence suggests one-third or more will experiencevascular-cognitive impairment, and/or intractable fatigue,either alone or in combination. The 2015 update of the Cana-dian Stroke Best Practice Recommendations: Mood, Cognitionand Fatigue Module guideline is a comprehensive summary ofcurrent evidence-based recommendations for clinicians in arange of settings, who provide care to patients followingstroke. The three consequences of stroke that are the focus ofthe this guideline (poststroke depression, vascular cognitiveimpairment, and fatigue) have high incidence rates and signifi-cant impact on the lives of people who have had a stroke,impede recovery, and result in worse long-term outcomes.Significant practice variations and gaps in the research evi-dence have been reported for initial screening and in-depthassessment of stroke patients for these conditions. Also ofconcern, an increased number of family members and informalcaregivers may also experience depressive symptoms in thepoststroke recovery phase which further impact patient recov-ery. These factors emphasize the need for a system of care thatensures screening occurs as a standard and consistent compo-nent of clinical practice across settings as stroke patientstransition from acute care to active rehabilitation and reinte-gration into their community. Additionally, building systemcapacity to ensure access to appropriate specialists for treat-ment and ongoing management of stroke survivors with theseconditions is another great challenge.Key words: depression, fatigue, guidelines, stroke, transient ischemicattack, vascular cognitive impairment

Correspondence: Patrice Lindsay*, Heart and Stroke Foundation, 222Queen Street, Suite 1402, Ottawa, Ontario K1P 5V9, Canada.E-mail: [email protected] of Psychiatry, Psychology, & Neuroscience, Dalhousie Uni-versity, Halifax, Canada2Sunnybrook Health Sciences Centre, Toronto, Canada3University of Toronto, Toronto, Canada4Heart and Stroke Foundation, Ottawa, Canada5Toronto Rehabilitation Institute, University Health Network, Toronto,Canada6Moncton Hospital/Miramichi Regional Hospital, Miramichi, Canada7Department of Occupational Science & Occupational Therapy, & Gradu-ate Department of Rehabilitation Sciences, University of Toronto,Toronto, Canada8Riverview Health Centre, Winnipeg, Canada9Department of Psychology, Glenrose Hospital Stroke Program, Edmon-ton, Canada10Faculty of Nursing, University of Calgary, Calgary, Canada11Department of Neurology, Faculty of Medicine, Dalhousie University,Halifax, Canada12Department of Clinical Neurosciences, Calgary Stroke Program, Univer-sity of Calgary, Hotchkiss Brain Institute, Calgary, Canada13Faculty of Rehabilitation Medicine, University of Alberta, Edmonton,Canada14Stroke Department, Richardson Hospital and Montreal UniversityHealth Center, Royal Victoria Hospital, Montreal, Canada15Stroke Program Department, Queen Elizabeth II Health SciencesCentre, Capital District Health Authority, Halifax, Canada16Pediatrics and Clinical Neurosciences, Faculty of Medicine, University ofCalgary, Alberta Children’s Hospital Research Institute, Calgary, Canada17Western University, London, Canada

Received: 4 February 2015; Accepted: 19 May 2015; Published online 29June 2015

Conflict of interest: Dr. Gail A. Eskes (primary author): no conflicts ofinterest; Dr. Krista Lanctôt (co-primary author): research/travel support –AbbVie, Lundbeck, Pfizer, Hoffman-La Roche Ltd. Consultation fees –AbbVie; Dr. Richard Swartz: Heart and Stroke Foundation of Canada NewInvestigator Award and Henry Barnett Scholarship; Research support –CIHR, Heart and Stroke, Sunnybrook HSC AFP and Department ofMedicine, Hoffman-LaRoche Canada; Speaker: BMS Pfizer; Dr. NathanHerrmann: research support – Lundbeck, Pfizer, Roche, Transition Thera-peutics. Consultation fees – AbbVie, Eli Lilly; Dr. Mark Bayley: no conflictsof interest; Laurie Bouvier: no conflicts of interest; Dr. Deirdre Dawson:no conflicts of interest; Sandra Egi: no conflicts of interest; Dr. ElizabethGilchrist: no conflicts of interest; Dr. Theresa Green: no conflicts of inter-est; Dr. Gord Gubitz: Bayer, speaker; Boehringer Ingleheim, speaker; BMSPfizer, speaker; Dr. Michael D. Hill: Heart and Stroke Foundation ofAlberta Board Chair, salary award holder; Institute for Circulatory andRespiratory Health of CIHR Advisory Board member; Vernalis Group Ltdand Merck Ltd Consultant; Hoffmann-LaRoche Canada, provided drugfor clinical trial, consultancy and CME lecturer; Coviden, research grant

holder; Servier Canada, CME lecturer (funds donated to charity); BMSCanada, consultancy (funds donated to charity); Alberta Innovates HealthSolutions, salary award; Dr. Tammy Hopper: no conflicts of interest; AishaKhan: no conflicts of interest; Andrea King: no conflicts of interest; Dr.Adam Kirton: no conflicts of interest; Dr. Paige Moorhouse: no conflicts ofinterest; Dr. Eric E. Smith: no conflicts of interest; Janet Green, no conflictsof interest; Norine Foley: no conflicts of interest; Katherine Salter: noconflicts of interest; Dr. Patrice Lindsay (corresponding author): no con-flicts of interest.

Funding: The development of the Canadian Stroke Best Practice Recom-mendations is funded in their entirety by the Heart and Stroke Founda-tion, Canada. No funds for the development of these guidelines comefrom commercial interests, including pharmaceutical companies. Allmembers of the recommendation writing groups and external reviewersare volunteers and do not receive any remuneration for participation inguideline development, updates, and reviews. All participants complete aconflict of interest declaration prior to participation.

Specific references related to the best practice recommendations can beaccessed online at www.strokebestpractices.ca.

DOI: 10.1111/ijs.12557

Guidelines

© 2015 World Stroke Organization1130 Vol 10, October 2015, 1130–1140

Canadian Stroke Best Practice Recommendations: Mood, Cognition and FatigueFollowing Stroke practice guidelines, update 2015

Gail A. Eskes1, Krista L. Lanctôt2,3, Nathan Herrmann2,3, Patrice Lindsay3,4*, Mark Bayley3,5,Laurie Bouvier6, Deirdre Dawson7, Sandra Egi8, Elizabeth Gilchrist9, Theresa Green10,Gord Gubitz11, Michael D. Hill12, Tammy Hopper13, Aisha Khan14, Andrea King15, Adam Kirton16,Paige Moorhouse15, Eric E. Smith12, Janet Green1, Norine Foley17, Katherine Salter17, andRichard H. Swartz2,3 on behalf of the Heart Stroke Foundation Canada Canadian Stroke BestPractices Committees

Every year, approximately 62 000 people with stroke and tran-sient ischemic attack are treated in Canadian hospitals, andthe evidence suggests one-third or more will experiencevascular-cognitive impairment, and/or intractable fatigue,either alone or in combination. The 2015 update of the Cana-dian Stroke Best Practice Recommendations: Mood, Cognitionand Fatigue Module guideline is a comprehensive summary ofcurrent evidence-based recommendations for clinicians in arange of settings, who provide care to patients followingstroke. The three consequences of stroke that are the focus ofthe this guideline (poststroke depression, vascular cognitiveimpairment, and fatigue) have high incidence rates and signifi-cant impact on the lives of people who have had a stroke,impede recovery, and result in worse long-term outcomes.Significant practice variations and gaps in the research evi-dence have been reported for initial screening and in-depthassessment of stroke patients for these conditions. Also ofconcern, an increased number of family members and informalcaregivers may also experience depressive symptoms in thepoststroke recovery phase which further impact patient recov-ery. These factors emphasize the need for a system of care thatensures screening occurs as a standard and consistent compo-nent of clinical practice across settings as stroke patientstransition from acute care to active rehabilitation and reinte-gration into their community. Additionally, building systemcapacity to ensure access to appropriate specialists for treat-ment and ongoing management of stroke survivors with theseconditions is another great challenge.Key words: depression, fatigue, guidelines, stroke, transient ischemicattack, vascular cognitive impairment

Correspondence: Patrice Lindsay*, Heart and Stroke Foundation, 222Queen Street, Suite 1402, Ottawa, Ontario K1P 5V9, Canada.E-mail: [email protected] of Psychiatry, Psychology, & Neuroscience, Dalhousie Uni-versity, Halifax, Canada2Sunnybrook Health Sciences Centre, Toronto, Canada3University of Toronto, Toronto, Canada4Heart and Stroke Foundation, Ottawa, Canada5Toronto Rehabilitation Institute, University Health Network, Toronto,Canada6Moncton Hospital/Miramichi Regional Hospital, Miramichi, Canada7Department of Occupational Science & Occupational Therapy, & Gradu-ate Department of Rehabilitation Sciences, University of Toronto,Toronto, Canada8Riverview Health Centre, Winnipeg, Canada9Department of Psychology, Glenrose Hospital Stroke Program, Edmon-ton, Canada10Faculty of Nursing, University of Calgary, Calgary, Canada11Department of Neurology, Faculty of Medicine, Dalhousie University,Halifax, Canada12Department of Clinical Neurosciences, Calgary Stroke Program, Univer-sity of Calgary, Hotchkiss Brain Institute, Calgary, Canada13Faculty of Rehabilitation Medicine, University of Alberta, Edmonton,Canada14Stroke Department, Richardson Hospital and Montreal UniversityHealth Center, Royal Victoria Hospital, Montreal, Canada15Stroke Program Department, Queen Elizabeth II Health SciencesCentre, Capital District Health Authority, Halifax, Canada16Pediatrics and Clinical Neurosciences, Faculty of Medicine, University ofCalgary, Alberta Children’s Hospital Research Institute, Calgary, Canada17Western University, London, Canada

Received: 4 February 2015; Accepted: 19 May 2015; Published online 29June 2015

Conflict of interest: Dr. Gail A. Eskes (primary author): no conflicts ofinterest; Dr. Krista Lanctôt (co-primary author): research/travel support –AbbVie, Lundbeck, Pfizer, Hoffman-La Roche Ltd. Consultation fees –AbbVie; Dr. Richard Swartz: Heart and Stroke Foundation of Canada NewInvestigator Award and Henry Barnett Scholarship; Research support –CIHR, Heart and Stroke, Sunnybrook HSC AFP and Department ofMedicine, Hoffman-LaRoche Canada; Speaker: BMS Pfizer; Dr. NathanHerrmann: research support – Lundbeck, Pfizer, Roche, Transition Thera-peutics. Consultation fees – AbbVie, Eli Lilly; Dr. Mark Bayley: no conflictsof interest; Laurie Bouvier: no conflicts of interest; Dr. Deirdre Dawson:no conflicts of interest; Sandra Egi: no conflicts of interest; Dr. ElizabethGilchrist: no conflicts of interest; Dr. Theresa Green: no conflicts of inter-est; Dr. Gord Gubitz: Bayer, speaker; Boehringer Ingleheim, speaker; BMSPfizer, speaker; Dr. Michael D. Hill: Heart and Stroke Foundation ofAlberta Board Chair, salary award holder; Institute for Circulatory andRespiratory Health of CIHR Advisory Board member; Vernalis Group Ltdand Merck Ltd Consultant; Hoffmann-LaRoche Canada, provided drugfor clinical trial, consultancy and CME lecturer; Coviden, research grant

holder; Servier Canada, CME lecturer (funds donated to charity); BMSCanada, consultancy (funds donated to charity); Alberta Innovates HealthSolutions, salary award; Dr. Tammy Hopper: no conflicts of interest; AishaKhan: no conflicts of interest; Andrea King: no conflicts of interest; Dr.Adam Kirton: no conflicts of interest; Dr. Paige Moorhouse: no conflicts ofinterest; Dr. Eric E. Smith: no conflicts of interest; Janet Green, no conflictsof interest; Norine Foley: no conflicts of interest; Katherine Salter: noconflicts of interest; Dr. Patrice Lindsay (corresponding author): no con-flicts of interest.

Funding: The development of the Canadian Stroke Best Practice Recom-mendations is funded in their entirety by the Heart and Stroke Founda-tion, Canada. No funds for the development of these guidelines comefrom commercial interests, including pharmaceutical companies. Allmembers of the recommendation writing groups and external reviewersare volunteers and do not receive any remuneration for participation inguideline development, updates, and reviews. All participants complete aconflict of interest declaration prior to participation.

Specific references related to the best practice recommendations can beaccessed online at www.strokebestpractices.ca.

DOI: 10.1111/ijs.12557

Guidelines

© 2015 World Stroke Organization1130 Vol 10, October 2015, 1130–1140

Dépistage  Dépister les symptômes d’apnée chez tous les patients avec

AVC/AIT (évidence B)

 Dépister l’apnée lors des visites de suivi avec les outils validés (évidence C)

 S’il existe des symptômes suggestifs d’apnée: référer à un spécialiste du sommeil (évidence C)

Prise en charge

 Éviter les sédatifs (évidence B)

 Thérapies positionnelles (évidence B)

 Perte de poids (évidence B)

 CPAP (évidence B)

 App. dentaires (évidence B)

2160

Each year in the United States, >690 000 adults experience an ischemic stroke.1 The enormous morbidity of ischemic

stroke is the result of interplay between the resulting neuro-logical impairment, the emotional and social consequences of

that impairment, and the high risk for recurrence. An addi-tional large number of US adults, estimated at 240 000, will experience a transient ischemic attack (TIA).2 Although a TIA leaves no immediate impairment, affected individuals have a

Abstract—The aim of this updated guideline is to provide comprehensive and timely evidence-based recommendations on the prevention of future stroke among survivors of ischemic stroke or transient ischemic attack. The guideline is addressed to all clinicians who manage secondary prevention for these patients. Evidence-based recommendations are provided for control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism, and antiplatelet therapy for noncardioembolic stroke. Recommendations are also provided for the prevention of recurrent stroke in a variety of specific circumstances, including aortic arch atherosclerosis, arterial dissection, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, antiphospholipid antibody syndrome, sickle cell disease, cerebral venous sinus thrombosis, and pregnancy. Special sections address use of antithrombotic and anticoagulation therapy after an intracranial hemorrhage and implementation of guidelines. (Stroke. 2014;45:2160-2236.)

Key Words: AHA Scientific Statements ◼ atrial fibrillation ◼ carotid stenosis ◼ hypertension ◼ ischemia ◼ ischemic attack, transient ◼ prevention ◼ stroke

Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack

A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association

The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists.

Endorsed by the American Association of Neurological Surgeons and Congress of Neurological Surgeons

Walter N. Kernan, MD, Chair; Bruce Ovbiagele, MD, MSc, MAS, Vice Chair; Henry R. Black, MD; Dawn M. Bravata, MD; Marc I. Chimowitz, MBChB, FAHA; Michael D. Ezekowitz, MBChB, PhD;

Margaret C. Fang, MD, MPH; Marc Fisher, MD, FAHA; Karen L. Furie, MD, MPH, FAHA; Donald V. Heck, MD; S. Claiborne (Clay) Johnston, MD, PhD; Scott E. Kasner, MD, FAHA;

Steven J. Kittner, MD, MPH, FAHA; Pamela H. Mitchell, PhD, RN, FAHA; Michael W. Rich, MD; DeJuran Richardson, PhD; Lee H. Schwamm, MD, FAHA; John A. Wilson, MD; on behalf of the

American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular Disease

The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.

This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on February 28, 2013. A copy of the document is available at http://my.americanheart.org/statements by selecting either the “By Topic” link or the “By Publication Date” link. To purchase additional reprints, call 843-216-2533 or e-mail [email protected].

The Executive Summary is available as an online-only Data Supplement with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STR.0000000000000024/-/DC1.

The American Heart Association requests that this document be cited as follows: Kernan WN, Ovbiagele B, Black HR, Bravata DM, Chimowitz MI, Ezekowitz MD, Fang MC, Fisher M, Furie KL, Heck DV, Johnston SC, Kasner SE, Kittner SJ, Mitchell PH, Rich MW, Richardson D, Schwamm LH, Wilson JA; on behalf of the American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular Disease. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:2160–2236.

Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://my.americanheart.org/statements and select the “Policies and Development” link.

Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-Permission-Guidelines_UCM_300404_Article.jsp. A link to the “Copyright Permissions Request Form” appears on the right side of the page.

© 2014 American Heart Association, Inc.

Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STR.0000000000000024

AHA/ASA Guideline

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2160

Each year in the United States, >690 000 adults experience an ischemic stroke.1 The enormous morbidity of ischemic

stroke is the result of interplay between the resulting neuro-logical impairment, the emotional and social consequences of

that impairment, and the high risk for recurrence. An addi-tional large number of US adults, estimated at 240 000, will experience a transient ischemic attack (TIA).2 Although a TIA leaves no immediate impairment, affected individuals have a

Abstract—The aim of this updated guideline is to provide comprehensive and timely evidence-based recommendations on the prevention of future stroke among survivors of ischemic stroke or transient ischemic attack. The guideline is addressed to all clinicians who manage secondary prevention for these patients. Evidence-based recommendations are provided for control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism, and antiplatelet therapy for noncardioembolic stroke. Recommendations are also provided for the prevention of recurrent stroke in a variety of specific circumstances, including aortic arch atherosclerosis, arterial dissection, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, antiphospholipid antibody syndrome, sickle cell disease, cerebral venous sinus thrombosis, and pregnancy. Special sections address use of antithrombotic and anticoagulation therapy after an intracranial hemorrhage and implementation of guidelines. (Stroke. 2014;45:2160-2236.)

Key Words: AHA Scientific Statements ◼ atrial fibrillation ◼ carotid stenosis ◼ hypertension ◼ ischemia ◼ ischemic attack, transient ◼ prevention ◼ stroke

Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack

A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association

The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists.

Endorsed by the American Association of Neurological Surgeons and Congress of Neurological Surgeons

Walter N. Kernan, MD, Chair; Bruce Ovbiagele, MD, MSc, MAS, Vice Chair; Henry R. Black, MD; Dawn M. Bravata, MD; Marc I. Chimowitz, MBChB, FAHA; Michael D. Ezekowitz, MBChB, PhD;

Margaret C. Fang, MD, MPH; Marc Fisher, MD, FAHA; Karen L. Furie, MD, MPH, FAHA; Donald V. Heck, MD; S. Claiborne (Clay) Johnston, MD, PhD; Scott E. Kasner, MD, FAHA;

Steven J. Kittner, MD, MPH, FAHA; Pamela H. Mitchell, PhD, RN, FAHA; Michael W. Rich, MD; DeJuran Richardson, PhD; Lee H. Schwamm, MD, FAHA; John A. Wilson, MD; on behalf of the

American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular Disease

The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.

This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on February 28, 2013. A copy of the document is available at http://my.americanheart.org/statements by selecting either the “By Topic” link or the “By Publication Date” link. To purchase additional reprints, call 843-216-2533 or e-mail [email protected].

The Executive Summary is available as an online-only Data Supplement with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STR.0000000000000024/-/DC1.

The American Heart Association requests that this document be cited as follows: Kernan WN, Ovbiagele B, Black HR, Bravata DM, Chimowitz MI, Ezekowitz MD, Fang MC, Fisher M, Furie KL, Heck DV, Johnston SC, Kasner SE, Kittner SJ, Mitchell PH, Rich MW, Richardson D, Schwamm LH, Wilson JA; on behalf of the American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular Disease. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:2160–2236.

Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://my.americanheart.org/statements and select the “Policies and Development” link.

Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-Permission-Guidelines_UCM_300404_Article.jsp. A link to the “Copyright Permissions Request Form” appears on the right side of the page.

© 2014 American Heart Association, Inc.

Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STR.0000000000000024

AHA/ASA Guideline



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Une étude de sommeil devrait être considérée pour les patients victime d’AIT ou AVC sur la foi de la prévalence élevée de l’apnée dans cette population (Classe IIb, Évidence B)

Un traitement avec CPAP devrait être considéré vu les évidence grandissantes démontrant l’amélioration du pronostic (Classe IIb, Évidence B)

Apnées obstructives du sommeil

Snoring

Tired

Observed

Apnea

Blood Pressure

BMI > 35 kg/m2

Age > 50 yo

Neck circumference F > 41cm M > 43cm

Gender Male

Questionnaire STOP-Bang

1Guilleminaut et al.,1977 2Habukawa et al., 2010, 3Gagnadoux et al., 2014

Risque SAOS élevé  STOP- Bang: ≥3  STOP: ≥2

Méthodes diagnostiques

Polysomnographie (PSG)

 Test en laboratoire

 Méthode de référence

 Quand le demander

 Suspicion ASO légère

 Suspicion d’autres troubles du sommeil

 Enfant

 1500$

Méthodes diagnostiques

Polygraphie cardiorespiratoire (PCRS)   Test fait à domicile

  Examen diagnostic simplifié

  Quand le demander

  Probabilité d’AOS modérée-élevée

  Pas recommandé   Comorbidité de sommeil ou affectant la SatO2

  Apnée centrale (IC, IRC)

  Suspicion AOS légère

  500$

Oxymétrie nocturne   Rôle limité dans l’évaluation de l’AOS

  Utilisation diagnostique non appuyée par l’AASM

LE SOMMEIL

AVC et mouvements périodiques des jambes au cours du sommeil

Négligeons-nous un facteur de risque

vasculaire modifiable?

Possiblement…

MPJS

  Fortement associés au SJSR… … mais non spécifique

 Trouble comportemental sommeil paradoxal

 Narcolepsie

 Apnées du sommeil

 Médication

 insomnie

 Sujets sains

  Marqueur d’une activité sympathique?

SLEEP, Vol. 29, No. 9, 2006 1185

compared with both the “30 to 39 years” and “40 to 49 years” age groups. The age-related distribution of the mean PLMW index (Figure 2) yet suggests a U-curve evolution.

Movement Periodicity as a Function of Age

The distribution of IMI was influenced by age. Figure 3 il-lustrates the mean of the individual distributions of PLMS IMI duration per age group. With advancing age, the PLMS interval histograms show a peak between 15 and 35 seconds;; no peak was observed in younger subjects. Figure 4 illustrates the mean of the individual distributions of PLMW IMI duration per age group. A pattern quite different from that of PLMS emerges. In fact, the PLMW interval histograms do not show a clear peak for any age group. The figure rather illustrates an important number of small IMI shorter than 15 seconds, especially in young subjects, which seems to reflect spontaneous motor activity rather than PLMW per se.

DISCUSSION

PLMS and PLMW Prevalence in Relationship With Age

Because the present study included a wide range of age groups, it allowed us to evaluate the evolution of PLMS from young chil-dren to older subjects. As expected, the PLMS index was signifi-cantly correlated with age. However, Figure 1 presents a more precise picture of PLMS evolution with age. In fact, the presence of PLMS was very rare before the age of 40, but then the index in-creased dramatically. These results are consistent with other stud-ies reporting a low prevalence of PLMS in children and a high prevalence in middle-aged and older subjects. 9-15 This increase in prevalence is probably associated with the decrease of D2 recep-tors, which is observed in healthy humans and animals with ad-vancing age.23-24 Wong and coworkers23 have indeed demonstrated a decrease in human D2 receptors more marked from about 35 to 40 years of age. Several studies excluded healthy subjects presenting a PLMS index higher than 5 or 10. In the present study, the mean PLMS index was higher than 10 for the “40 to 49 years”, “50 to 59 years” and “60 years and older” groups. We can thus wonder if it would

be more appropriate to determine different criteria based on the subjects’ age, especially because PLMS are not considered to in-fluence polysomnographic sleep parameters in healthy subjects3,10, 25,26 although this issue still remains controversial.27-29 During wakefulness, the PLMW index seems to be negatively correlated with age. However, when the mean index is plotted for each age group, a quite different pattern appears. The PLMW index was higher in younger subjects, lower in middle-aged sub-jects, and slightly increased again (although it failed to reach sta-tistical significance) in older subjects. This is consistent with 1 study published in an abstract form, reporting a higher PLMW index in healthy children than in teenagers.19 It should be noted, however, that PLMW were not studied very often in healthy sub-jects. On the other hand, a study conducted in RLS patients re-ported an increase of the PLMW index with age.18 It is possible that the evolution of PLMW with aging is different in healthy and RLS subjects. However, discrepancy may also result from differ-ences in samples. The mean age of RLS patients in that study was 51 ± 10.8 years;; consequently, there were probably no children, teenagers, or young adults in that sample. In the present study, the PLMW index was actually higher in older age groups. In fact, if only subjects older than 30 years are considered, the PLMW index would be found to increase significantly with age (r = 0.50;; p = .003).

IMI as a Function of Age

If we consider the IMI histograms, it is quite clear that PLMS do not show a preferential interval in younger groups. A clear peak in IMI becomes obvious only for the last 3 age groups, namely: 40 to 49 years, 50 to 59 years, and 60 years and older. These are the same groups presenting a mean PLMS index higher than 10, which is consistent with the conclusion that younger subjects do not present typical PLMS. In younger subjects, an important number of small IMI during sleep can be observed, which are not as apparent in older groups. It probably means that children and young adults move more often in their sleep. In addition, results of the present study show that movement duration during sleep decreases with age. Taken together, these results suggest that young healthy subjects present longer movements with small

PLM and Age in Healthy Subjects—Pennestri et al

5-9 10-19 20-29 30-39 40-49 50-59 > 60

Age groups

0

10

20

30

40

50

60

70

80

90

100

PLM

W index

Figure 2—Mean periodic leg movements during wakefulness (PLMW) index for healthy subjects according to 7 age groups (5-9 y, 10-19 y, 20-29 y, 30-39 y, 40-49 y, 50-59 y, and 60 y and older). Vertical bars represent the SEM.

5-9 10-19 20-29 30-39 40-49 50-59 > 60

Age groups

0

10

20

30

40

PLM

S index

Figure 1—Mean periodic leg movements during sleep (PLMS) in-dex for healthy subjects according to 7 age groups (5-9 y, 10-19 y, 20-29 y, 30-39 y, 40-49 y, 50-59 y, and 60 y and older). Vertical bars represent the SEM.

Pennestri et al. SLEEP 2003

increase of the amplitude of BP responses with ageand with the duration of RLS.

Our results show a significant increase in SBPand DBP in association with PLMS without conven-tionally defined MA. However, the magnitude of BPchanges was greater when PLMS were associatedwith MA, and increased with duration of MA, whileappearing independent of PLMS characteristics.This implies that the intensity of cardiovascular re-sponse might be related to the degree of central acti-vation and less to the somatomotor response. Thesefindings are congruent with the hypothesis that legmovements are part of the same periodic activationprocess that is responsible for cardiovascular andEEG changes during sleep.26 Furthermore, they arein agreement with the theory that there exists ahierarchically organized arousal response system, in-volving both central and autonomic functions in acontinuum, where higher levels of brainstem stimu-lation might lead to more intense cortical and auto-nomic responses.

Another factor influencing BP responses related toPLMS-noMA is the exercise pressor reflex. However,

in a subset of eight subjects, we observed BP changesassociated with PLMS-noMA to be greater thanthose associated with PLMW, i.e., in the absence ofarousal from sleep (figure 3). SBP increments associ-ated with PLMS-noMA were also greater than thoseevoked by 5 seconds of dynamic muscle passivestretches (2 mm Hg) or by active contractions (6 mmHg) in healthy subjects.27 Thus, the exercise pressorreflex, while potentially contributing to the cardio-vascular changes associated to PLMS, cannot ex-plain the overall phenomenon.

The magnitude of PLMS-related BP response in-creased with age. Aging is associated with complexchanges in the cardiovascular system and its auto-nomic regulation.28 These changes are reflected inenhanced basal central sympathetic drive,29 bluntedHR responsiveness,30 and enhanced arterial BP re-sponsiveness to sympathetic stimuli,31,32 to name afew. Previous studies have documented a greater BPreactivity elicited by mental stressors (in laboratoryand in response to daily life stimuli) in older vsyounger normal subjects,31,32 contrary to the HR re-sponse, which appears blunted.30 A previous study

Figure 1. Periodic leg movements dur-ing sleep–related beat-to-beat bloodpressure, electrocardiogram, and EEGsignals, presented in a compact window(A), and wider temporal window (B).The portion of signals shown in (B) rep-resents the temporal window used forthe analyses. (C) The correspondingmeasurements of systolic blood pres-sure, diastolic blood pressure, andheart rate.

April 10, 2007 NEUROLOGY 68 1215

Pennestri et al., 2007








Sujets atteints du SJSR

Impact cardiovasculaire des MPJS








Sujets atteints du SJSR

Pennestri et al., 2007


Gareau et al., Ann Neurol. 2017 (soumis)


LE SOMMEIL

VASCULOPATIES ET DURÉE DE SOMMEIL

Négligeons-nous un facteur de risque vasculaire modifiable?

Difficile à dire pour le moment…

Durée de sommeil et vasculopathies Short and long sleep duration are associated with prevalentcardiovascular disease in Australian adults

CHR I S TOPHER A . MAGEE 1 , L EONARD KR I THAR I DES 2 , JOHN ATT I A 3 ,P A TR I CK MCELDUFF 3 and EM I L Y BANKS 4

1School of Psychology and Centre for Health Initiatives, University of Wollongong, Wollongong, NSW, Australia, 2Department of Cardiology,Concord Repatriation General Hospital, The University of Sydney, Sydney, NSW, Australia, 3Centre for Clinical Epidemiology and Biostatistics,The University of Newcastle, Newcastle, NSW, Australia and 4National Centre for Epidemiology and Population Health, Australian NationalUniversity, Canberra, ACT, Australia

Keywordscardiovascular disease, diabetes, epidemiology,high blood pressure, long sleep, short sleep,sleep duration

CorrespondenceChristopher Magee, PhD, School of Psychologyand Centre for Health Initiatives, University ofWollongong, Wollongong, NSW 2522, Australia.Tel.: +61 2 4221 3617;fax: +61 2 4221 4163;e-mail: [email protected]

Accepted in revised form 25 October 2011;received 21 August 2011

DOI: 10.1111/j.1365-2869.2011.00993.x

SUMMARYA growing number of studies from a range of different countries haveobserved an association between sleep duration and cardiovasculardisease. The objective of this paper was to examine the associationsbetween sleep duration and prevalent cardiovascular disease in a largesample of Australian adults, and identify the sociodemographic andhealth-related factors moderating these associations. Participantsincluded 218 155 Australian adults aged 45 years and over. The resultsindicated that 6 h versus 7 h sleep was associated with increased oddsof heart disease [odds ratio (OR) = 1.11 (1.06–1.17)], diabetes[OR = 1.15 (1.09–1.22)], stroke [OR = 1.25 (1.14–1.38)] and high bloodpressure [OR = 1.08 (1.04–1.11)]. Long sleep (‡9 h sleep) was alsorelated to elevated odds of heart disease [OR = 1.14 (1.09–1.19)],diabetes [OR = 1.25 (1.19–1.31)], stroke [OR = 1.50 (1.38–1.62)] andhigh blood pressure [OR = 1.04 (1.01–1.08)] compared to 7 h sleep.Some of these relationships varied by age, and were not evident in adultsaged 75 years and over. The magnitude of some associations variedsignificantly by body mass index, smoking and physical activity. Thesefindings provide further insight into the nature of the relationship betweensleep and cardiovascular health.

INTRODUCTION

Cardiovascular disease (CVD) is one of the leading causes ofmorbidity and mortality in developed countries, and isexpected to become increasingly common (WHO, 2000).Smoking, obesity, high-fat diets and physical inactivity areestablished behavioural risk factors for CVD (WHO, 2000).Recent research has also identified relationships betweensleep duration and CVD, which may have implications forfurther understanding behavioural contributors to CVD. Shortsleep (i.e. £ 6 h sleep a night) has been associated withhypertension (Gangwisch et al., 2006; Gottlieb et al., 2006),stroke (Sabanayagam and Shankar, 2010), myocardialinfarction (Ayas et al., 2003; Sabanayagam and Shankar,2010), diabetes (Spiegel et al., 2005) and mortality fromcoronary heart disease (Ikehara et al., 2009; Shankar et al.,2008). Long sleep (‡9 h sleep a night) has also been linked

with a variety of cardiovascular outcomes including hyper-tension (Gangwisch et al., 2006), stroke (Sabanayagam andShankar, 2010) and cardiovascular mortality (Cappuccioet al., 2011).Existing studies have examined the associations between

sleep duration and CVD in a range of countries including theUnited States, Germany, the Netherlands, Singapore, Japan,and the United Kingdom (Cappuccio et al., 2011). However,there have been some inconsistencies in the results of thesestudies, perhaps reflecting lack of statistical power (espe-cially for outcomes such as stroke) or differences in the typesof confounding variables controlled. Furthermore, few studieshave examined in detail whether the associations betweensleep duration and cardiovascular conditions vary accordingto sociodemographic factors such as age and sex, obesity orhealth behaviours which are associated with sleep durationand CVD risk (Sabanayagam and Shankar, 2010). Thus, the

J. Sleep Res. (2011) 21, 441–447 Sleep duration and the heart

! 2011 European Sleep Research Society 441

Research Article

Short sleep duration is an independent predictor of stroke eventsin elderly hypertensive patients

Kazuo Eguchi, MD, PhDa,*, Satoshi Hoshide, MD, PhDa, Shizukiyo Ishikawa, MD, PhDb,Kazuyuki Shimada, MD, PhDa, and Kazuomi Kario, MD, PhDa

aDivision of Cardiovascular Medicine, Department of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan; andbDepartment of Family Medicine, Department of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan

Manuscript received July 13, 2010 and accepted September 2, 2010

Abstract

Data relating habitual sleep duration to the risk of silent or overt stroke are sparse. We tested the hypothesis that shortduration of sleep is associated with increased risk of silent cerebral infarct (SCI) and stroke events in hypertensive patients.We performed ambulatory BP monitoring in 1268 hypertensives (mean age: 70.4 years) and followed them for 50 months.Brain MRI was performed in 932 of these subjects for the assessment of SCI, and these subjects were analyzed in this study.Cox proportional hazard models were used to calculate the hazard ratios (HR) of sleep-duration-associated risk forcardiovascular events while controlling for significant covariates. In multivariable Cox regression analysis, a sleep duration<7.5 h was independently associated with the risk of stroke (HR ¼ 2.21; P ¼ 0.003). The presence of SCI was also associatedwith stroke events (HR ¼ 2.60; P ¼ 0.005). When the subjects were divided into an SCI(þ) group and SCI(#) group, theshort sleep duration was a significant predictor for incident stroke only in the SCI(þ) group (HR ¼ 2.52; P ¼ 0.001). Shortersleep duration was an independent risk for future incidence of stroke events in hypertensive patients, especially those withSCIs. J Am Soc Hypertens 2010;4(5):255–262. ! 2010 American Society of Hypertension. All rights reserved.Keywords: Sleep; duration of sleep; stroke; hypertension; silent cerebral infarct.

Introduction

Sleep disorders have been shown to be related to varioustypes of diseases. Self-reported sleep time, especially shortsleep duration, has been shown to be associated withcardiovascular risk factors, such as hypertension,1 dia-betes,2 obesity,3 and metabolic syndrome.4 Short sleepduration has also been associated with coronary events5–8

and cardiovascular events.9 In contrast, long duration ofsleep has been reported to be associated with coronaryevents,6 stroke events,5,10 and death from stroke.8 However,

it is not established whether short or long duration of sleepis associated with future incidence of stroke, and in general,the mechanisms of the above associations are not wellunderstood.

Recently, we have shown that short duration of sleep wasassociated with cardiovascular events, and the combinationof a riser pattern (in which the average nighttime bloodpressure exceeds the daytime blood pressure) and shortduration of sleep was strongly predictive of future cardio-vascular disease (CVD), independent of ambulatory BPlevels.9 However, in this article and others, the extent oftarget organ damage was not taken into account becauseof the epidemiological nature of the study design. Silentcerebral infarct (SCI) is an established risk for future inci-dence of stroke,11 but its relationship with sleep durationhas never been studied. Our hypotheses in the present studywere that short sleep duration is associated with incidentstroke, and the presence of SCI has some interaction withsleep duration and the incidence of stroke. We performedthis study to clarify these issues.

Funding/support: There is no financial support to disclose.Conflict of interest: none*Corresponding author: Kazuo Eguchi, MD, PhD, Division of

Cardiovascular Medicine, Department of Medicine, Jichi MedicalUniversity School of Medicine, 3311–1 Yakushiji, Shimotsuke,Tochigi, Japan. Tel: þ81-285-58-7344; fax: þ81-285-44-5317.

E-mail: [email protected]

1933-1711/$ - see front matter ! 2010 American Society of Hypertension. All rights reserved.doi:10.1016/j.jash.2010.09.001

Journal of the American Society of Hypertension 4(5) (2010) 255–262

Research Article

Short sleep duration is an independent predictor of stroke eventsin elderly hypertensive patients

Kazuo Eguchi, MD, PhDa,*, Satoshi Hoshide, MD, PhDa, Shizukiyo Ishikawa, MD, PhDb,Kazuyuki Shimada, MD, PhDa, and Kazuomi Kario, MD, PhDa

aDivision of Cardiovascular Medicine, Department of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan; andbDepartment of Family Medicine, Department of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan

Manuscript received July 13, 2010 and accepted September 2, 2010

Abstract

Data relating habitual sleep duration to the risk of silent or overt stroke are sparse. We tested the hypothesis that shortduration of sleep is associated with increased risk of silent cerebral infarct (SCI) and stroke events in hypertensive patients.We performed ambulatory BP monitoring in 1268 hypertensives (mean age: 70.4 years) and followed them for 50 months.Brain MRI was performed in 932 of these subjects for the assessment of SCI, and these subjects were analyzed in this study.Cox proportional hazard models were used to calculate the hazard ratios (HR) of sleep-duration-associated risk forcardiovascular events while controlling for significant covariates. In multivariable Cox regression analysis, a sleep duration<7.5 h was independently associated with the risk of stroke (HR ¼ 2.21; P ¼ 0.003). The presence of SCI was also associatedwith stroke events (HR ¼ 2.60; P ¼ 0.005). When the subjects were divided into an SCI(þ) group and SCI(#) group, theshort sleep duration was a significant predictor for incident stroke only in the SCI(þ) group (HR ¼ 2.52; P ¼ 0.001). Shortersleep duration was an independent risk for future incidence of stroke events in hypertensive patients, especially those withSCIs. J Am Soc Hypertens 2010;4(5):255–262. ! 2010 American Society of Hypertension. All rights reserved.Keywords: Sleep; duration of sleep; stroke; hypertension; silent cerebral infarct.

Introduction

Sleep disorders have been shown to be related to varioustypes of diseases. Self-reported sleep time, especially shortsleep duration, has been shown to be associated withcardiovascular risk factors, such as hypertension,1 dia-betes,2 obesity,3 and metabolic syndrome.4 Short sleepduration has also been associated with coronary events5–8

and cardiovascular events.9 In contrast, long duration ofsleep has been reported to be associated with coronaryevents,6 stroke events,5,10 and death from stroke.8 However,

it is not established whether short or long duration of sleepis associated with future incidence of stroke, and in general,the mechanisms of the above associations are not wellunderstood.

Recently, we have shown that short duration of sleep wasassociated with cardiovascular events, and the combinationof a riser pattern (in which the average nighttime bloodpressure exceeds the daytime blood pressure) and shortduration of sleep was strongly predictive of future cardio-vascular disease (CVD), independent of ambulatory BPlevels.9 However, in this article and others, the extent oftarget organ damage was not taken into account becauseof the epidemiological nature of the study design. Silentcerebral infarct (SCI) is an established risk for future inci-dence of stroke,11 but its relationship with sleep durationhas never been studied. Our hypotheses in the present studywere that short sleep duration is associated with incidentstroke, and the presence of SCI has some interaction withsleep duration and the incidence of stroke. We performedthis study to clarify these issues.

Funding/support: There is no financial support to disclose.Conflict of interest: none*Corresponding author: Kazuo Eguchi, MD, PhD, Division of

Cardiovascular Medicine, Department of Medicine, Jichi MedicalUniversity School of Medicine, 3311–1 Yakushiji, Shimotsuke,Tochigi, Japan. Tel: þ81-285-58-7344; fax: þ81-285-44-5317.

E-mail: [email protected]

1933-1711/$ - see front matter ! 2010 American Society of Hypertension. All rights reserved.doi:10.1016/j.jash.2010.09.001

Journal of the American Society of Hypertension 4(5) (2010) 255–262

CLINICAL REVIEW

Sleep duration and risk of all-cause mortality: A flexible, non-linear,meta-regression of 40 prospective cohort studies

Tong-Zu Liu a, b, *, 1, Chang Xu a, c, Matteo Rota d, 1, Hui Cai e, 1, Chao Zhang c, 1,Ming-Jun Shi f, Rui-Xia Yuan g, Hong Weng a, Xiang-Yu Meng b, Joey S.W. Kwong h, c, **,Xin Sun h, ***

a Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Chinab Center for Evidence-Based Medicine, Wuhan University, Wuhan, Chinac Center for Evidence-based Medicine and Clinical Research, Taihe Hospital, Hubei University of Medicine, Shiyan, Chinad Department of Epidemiology, IRCCS e Istituto di Ricerche Farmacologiche Mario Negri, Via G. La Masa 19, 20156 Milan, Italye Vanderbilt Epidemiology Center, Department of Medicine and Vanderbilt-Ingram Cancer Center, Nashville, United Statesf The French National Center for Scientific Research, UMR 144, Institute Curie, 75248 Paris, Franceg Department of Epidemiology and biostatistics, School of public health, Wuhan University and global health institute, Wuhan University, Wuhan, Chinah Chinese Evidence-Based Medicine Center, Chinese Cochrane Center, West China Hospital, Sichuan University, Chengdu, China

a r t i c l e i n f o

Article history:Received 29 July 2015Received in revised form22 January 2016Accepted 10 February 2016Available online 3 March 2016

Keywords:Sleep durationAll-cause mortalityDoseeresponse relationshipMeta-analysis

s u m m a r y

Approximately 27e37% of the general population experience prolonged sleep duration and 12e16%report shortened sleep duration. However, prolonged or shortened sleep duration may be associatedwith serious health problems.

A comprehensive, flexible, non-linear meta-regression with restricted cubic spline (RCS) was used toinvestigate the doseeresponse relationship between sleep duration and all-cause mortality in adults.

Medline (Ovid), Embase, EBSCOhostdPsycINFO, and EBSCOhostdCINAHL Plus databases, referencelists of relevant review articles, and included studies were searched up to Nov. 29, 2015. Prospectivecohort studies investigating the association between sleep duration and all-cause mortality in adultswith at least three categories of sleep duration were eligible for inclusion.

We eventually included in our study 40 cohort studies enrolling 2,200,425 participants with 271,507deaths. A J-shaped association between sleep duration and all-cause mortality was present: comparedwith 7 h of sleep (reference for 24-h sleep duration), both shortened and prolonged sleep durations wereassociated with increased risk of all-cause mortality (4 h: relative risk [RR] ¼ 1.05; 95% confidence in-terval [CI] ¼ 1.02e1.07; 5 h: RR ¼ 1.06; 95% CI ¼ 1.03e1.09; 6 h: RR ¼ 1.04; 95% CI ¼ 1.03e1.06; 8 h:RR ¼ 1.03; 95% CI ¼ 1.02e1.05; 9 h: RR ¼ 1.13; 95% CI ¼ 1.10e1.16; 10 h: RR ¼ 1.25; 95% CI ¼ 1.22e1.28;11 h: RR ¼ 1.38; 95% CI ¼ 1.33e1.44; n ¼ 29; P < 0.01 for non-linear test). With regard to the night-sleepduration, prolonged night-sleep duration was associated with increased all-cause mortality (8 h:RR ¼ 1.01; 95% CI ¼ 0.99e1.02; 9 h: RR ¼ 1.08; 95% CI ¼ 1.05e1.11; 10 h: RR ¼ 1.24; 95% CI ¼ 1.21e1.28;n ¼ 13; P < 0.01 for non-linear test). Subgroup analysis showed females with short sleep duration a day(<7 h) were at high risk of all-cause mortality (4 h: RR ¼ 1.07; 95% CI ¼ 1.02e1.13; 5 h: RR ¼ 1.08; 95%CI ¼ 1.03e1.14; 6 h: RR ¼ 1.05; 95% CI ¼ 1.02e1.09), but males were not (4 h: RR ¼ 1.01; 95% CI ¼ 0.96e1.06; 5 h: RR ¼ 1.02; 95% CI ¼ 0.97e1.08; 6 h: RR ¼ 1.02; 95% CI ¼ 0.98e1.06).

Abbreviations: BMI, body mass index; CIs, confidence intervals; HRs, hazard ratios; MOOSE, meta-analysis of observational studies in epidemiology; NOS, New-castleeOttawa Scale; RRs, relative risks; RCS, restricted cubic spline.* Corresponding author. Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China. Tel./fax: þ86 67813104.** Corresponding author. Chinese Evidence-Based Medicine Center, West China Hospital, Sichuan University, Chengdu 610041, China.*** Corresponding author. Chinese Evidence-Based Medicine Center, Chinese Cochrane Center, West China Hospital, Sichuan University, Chengdu 610041, China.

E-mail addresses: [email protected] (T.-Z. Liu), [email protected] (J.S.W. Kwong), [email protected] (X. Sun).1 The following authors contributed equally to this study: Chang Xu, Matteo Rota, Hui Cai, Chao Zhang.

Contents lists available at ScienceDirect

Sleep Medicine Reviews

journal homepage: www.elsevier .com/locate/smrv

http://dx.doi.org/10.1016/j.smrv.2016.02.0051087-0792/© 2016 Elsevier Ltd. All rights reserved.

Sleep Medicine Reviews 32 (2017) 28e36

CLINICAL REVIEW

Sleep duration and risk of all-cause mortality: A flexible, non-linear,meta-regression of 40 prospective cohort studies

Tong-Zu Liu a, b, *, 1, Chang Xu a, c, Matteo Rota d, 1, Hui Cai e, 1, Chao Zhang c, 1,Ming-Jun Shi f, Rui-Xia Yuan g, Hong Weng a, Xiang-Yu Meng b, Joey S.W. Kwong h, c, **,Xin Sun h, ***

a Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Chinab Center for Evidence-Based Medicine, Wuhan University, Wuhan, Chinac Center for Evidence-based Medicine and Clinical Research, Taihe Hospital, Hubei University of Medicine, Shiyan, Chinad Department of Epidemiology, IRCCS e Istituto di Ricerche Farmacologiche Mario Negri, Via G. La Masa 19, 20156 Milan, Italye Vanderbilt Epidemiology Center, Department of Medicine and Vanderbilt-Ingram Cancer Center, Nashville, United Statesf The French National Center for Scientific Research, UMR 144, Institute Curie, 75248 Paris, Franceg Department of Epidemiology and biostatistics, School of public health, Wuhan University and global health institute, Wuhan University, Wuhan, Chinah Chinese Evidence-Based Medicine Center, Chinese Cochrane Center, West China Hospital, Sichuan University, Chengdu, China


Article history:Received 29 July 2015Received in revised form22 January 2016Accepted 10 February 2016Available online 3 March 2016

Keywords:Sleep durationAll-cause mortalityDoseeresponse relationshipMeta-analysis

s u m m a r y

Approximately 27e37% of the general population experience prolonged sleep duration and 12e16%report shortened sleep duration. However, prolonged or shortened sleep duration may be associatedwith serious health problems.

A comprehensive, flexible, non-linear meta-regression with restricted cubic spline (RCS) was used toinvestigate the doseeresponse relationship between sleep duration and all-cause mortality in adults.

Medline (Ovid), Embase, EBSCOhostdPsycINFO, and EBSCOhostdCINAHL Plus databases, referencelists of relevant review articles, and included studies were searched up to Nov. 29, 2015. Prospectivecohort studies investigating the association between sleep duration and all-cause mortality in adultswith at least three categories of sleep duration were eligible for inclusion.

We eventually included in our study 40 cohort studies enrolling 2,200,425 participants with 271,507deaths. A J-shaped association between sleep duration and all-cause mortality was present: comparedwith 7 h of sleep (reference for 24-h sleep duration), both shortened and prolonged sleep durations wereassociated with increased risk of all-cause mortality (4 h: relative risk [RR] ¼ 1.05; 95% confidence in-terval [CI] ¼ 1.02e1.07; 5 h: RR ¼ 1.06; 95% CI ¼ 1.03e1.09; 6 h: RR ¼ 1.04; 95% CI ¼ 1.03e1.06; 8 h:RR ¼ 1.03; 95% CI ¼ 1.02e1.05; 9 h: RR ¼ 1.13; 95% CI ¼ 1.10e1.16; 10 h: RR ¼ 1.25; 95% CI ¼ 1.22e1.28;11 h: RR ¼ 1.38; 95% CI ¼ 1.33e1.44; n ¼ 29; P < 0.01 for non-linear test). With regard to the night-sleepduration, prolonged night-sleep duration was associated with increased all-cause mortality (8 h:RR ¼ 1.01; 95% CI ¼ 0.99e1.02; 9 h: RR ¼ 1.08; 95% CI ¼ 1.05e1.11; 10 h: RR ¼ 1.24; 95% CI ¼ 1.21e1.28;n ¼ 13; P < 0.01 for non-linear test). Subgroup analysis showed females with short sleep duration a day(<7 h) were at high risk of all-cause mortality (4 h: RR ¼ 1.07; 95% CI ¼ 1.02e1.13; 5 h: RR ¼ 1.08; 95%CI ¼ 1.03e1.14; 6 h: RR ¼ 1.05; 95% CI ¼ 1.02e1.09), but males were not (4 h: RR ¼ 1.01; 95% CI ¼ 0.96e1.06; 5 h: RR ¼ 1.02; 95% CI ¼ 0.97e1.08; 6 h: RR ¼ 1.02; 95% CI ¼ 0.98e1.06).

Abbreviations: BMI, body mass index; CIs, confidence intervals; HRs, hazard ratios; MOOSE, meta-analysis of observational studies in epidemiology; NOS, New-castleeOttawa Scale; RRs, relative risks; RCS, restricted cubic spline.* Corresponding author. Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China. Tel./fax: þ86 67813104.** Corresponding author. Chinese Evidence-Based Medicine Center, West China Hospital, Sichuan University, Chengdu 610041, China.*** Corresponding author. Chinese Evidence-Based Medicine Center, Chinese Cochrane Center, West China Hospital, Sichuan University, Chengdu 610041, China.

E-mail addresses: [email protected] (T.-Z. Liu), [email protected] (J.S.W. Kwong), [email protected] (X. Sun).1 The following authors contributed equally to this study: Chang Xu, Matteo Rota, Hui Cai, Chao Zhang.


Sleep Medicine Reviews

journal homepage: www.elsevier .com/locate/smrv

http://dx.doi.org/10.1016/j.smrv.2016.02.0051087-0792/© 2016 Elsevier Ltd. All rights reserved.

Sleep Medicine Reviews 32 (2017) 28e36Original Article

Sleep Duration and the Risk of Mortality From Stroke in Japan:The Takayama Cohort StudyToshiaki Kawachi1, Keiko Wada1, Kozue Nakamura2, Michiko Tsuji3,Takashi Tamura1, Kie Konishi1, and Chisato Nagata1

1Department of Epidemiology and Preventive Medicine, Gifu University Graduate School of Medicine, Gifu, Japan2Department of Food and Nutrition, Gifu City Women’s College, Gifu, Japan3Department of Food and Nutrition, Nagoya Women’s University, Nagoya, Japan

Received January 13, 2015; accepted June 30, 2015; released online October 31, 2015

Copyright © 2015 Toshiaki Kawachi et al. This is an open access article distributed under the terms of Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

ABSTRACT

Background: Few studies have assessed the associations between sleep duration and stroke subtypes. Weexamined whether sleep duration is associated with mortality from total stroke, ischemic stroke, and hemorrhagicstroke in a population-based cohort of Japanese men and women.Methods: Subjects included 12 875 men and 15 021 women aged 35 years or older in 1992, who were followeduntil 2008. The outcome variable was stroke death (ischemic stroke, hemorrhagic stroke, and total stroke).Results: During follow-up, 611 stroke deaths (354 from ischemic stroke, 217 from hemorrhagic stroke, and 40 fromundetermined stroke) were identified. Compared with 7 h of sleep, ≥9 h of sleep was significantly associated with anincreased risk of total stroke and ischemic stroke mortality after controlling for covariates. Hazard ratios (HRs) and95% confidence intervals (CIs) were 1.51 (95% CI, 1.16–1.97) and 1.65 (95% CI, 1.16–2.35) for total strokemortality and ischemic stroke mortality, respectively. Short sleep duration (≤6 h of sleep) was associated with adecreased risk of mortality from total stroke (HR 0.77; 95% CI, 0.59–1.01), although this association was ofborderline significance (P = 0.06). The trends for total stroke and ischemic stroke mortality were also significant(P < 0.0001 and P = 0.0002, respectively). There was a significant risk reduction of hemorrhagic stroke mortality for≤6 h of sleep as compared with 7 h of sleep (HR 0.64; 95% CI, 0.42–0.98; P for trend = 0.08). The risk reduction waspronounced for men (HR 0.31; 95% CI, 0.16–0.64).Conclusions: Data suggest that longer sleep duration is associated with increased mortality from total and ischemicstroke. Short sleep duration may be associated with a decreased risk of mortality from hemorrhagic stroke in men.

Key words: sleep duration; cardiovascular; stroke; ischemic stroke; cohort studies

INTRODUCTION

Stroke is one of the main causes of death in Western countriesand in the Asia-Pacific region, including Japan. In particular,ischemic stroke accounts for more than 70% of all stroke casesin Western countries and about 74% of cases in Japan.1

Compared with the incidence of myocardial infarction, theincidence of stroke is high in Japan,2 and stroke is a diseasethat causes many to become bedridden. Because it generates ahigh burden and societal cost, effective primary preventivestrategies are needed.3 Besides the established risk factors,such as age, hypertension,4,5 diabetes,6,7 dyslipidemia,8

smoking,9 and atrial fibrillation,10 environmental and lifestylefactors might play an important role in the etiology of strokes.

Several previous studies have suggested an associationbetween sleep duration and cardiovascular disease (CVD),including stroke.11–22 A meta-analysis by Cappuccio et al23

reported that both short and long sleep durations wereassociated with increased incidence or mortality of stroke;hazard ratios (HRs) were 1.15 (95% confidence interval [CI],1.00–1.37) for short sleep durations and 1.65 (95% CI,1.45–1.87) for long sleep durations. However, the number ofcomponent studies was small (n = 5). Furthermore, studieson the subtypes of stroke are also scarce.20,24,25

Therefore, we investigated whether sleep duration isassociated with total stroke and subtypes of stroke in acohort of Japanese men and women (the Takayama cohortstudy).26

Address for correspondence. Toshiaki Kawachi, Department of Epidemiology and Preventive Medicine, Gifu University Graduate School of Medicine, 1-1Yanagido, Gifu 501-1194, Japan (e-mail: [email protected]).

J Epidemiol 2016;26(3):123-130doi:10.2188/jea.JE20140272

123

Original Article

Sleep duration and risk of stroke: a doseeresponse meta-analysis ofprospective cohort studies

Qiao He a, b, Hao Sun a, b, Xiaomei Wu a, b, Peng Zhang a, b, Huixu Dai a, b, Cong Ai a, b,Jingpu Shi a, b, *a Department of Clinical Epidemiology, Institute of Cardiovascular Diseases and Center of Evidence Based Medicine, The First Affiliated Hospital, ChinaMedical University, Shenyang, Chinab Center of Evidence Based Medicine, Liaoning Province & China Medical University, Shenyang, China


Article history:Received 8 September 2016Received in revised form17 November 2016Accepted 5 December 2016Available online 23 December 2016

Keywords:StrokeSleep durationMeta-analysisProspective studies

a b s t r a c t

Objectives: Suboptimal sleep duration has been considered to increase the risk of stroke incidence. Thuswe aimed to conduct a doseeresponse meta-analysis to examine the association between sleep durationand stroke incidence.Methods: We searched PubMed, Web of science and the Cochrane Library to identify all prospectivestudies evaluating the association of sleep duration and nonfatal and/or fatal stroke incidence. Then,restricted cubic spline functions and piecewise linear functions were used to evaluate the nonlinear andlinear doseeresponse association between them.Results: We included a total of 16 prospective studies enrolling 528,653 participants with 12,193 strokeevents. Nonlinear doseeresponse meta-analysis showed a J-shaped association between sleep durationand total stroke with the lowest risk observed with sleeping for 7 h. Considering people sleeping for 7 has reference, long sleepers had a higher predicted risk of total stroke than short sleepers [the pooled riskratios (95% confidence intervals): 4 h: 1.17 (0.99e1.38); 5 h: 1.17 (1.00e1.37); 6 h: 1.10 (1.00e1.21); 8 h:1.17 (1.07e1.28); 9 h: 1.45 (1.23e1.70); 10 h: 1.64 (1.4e1.92); pnonlinearity<0.001]. Short sleep durationswere only significantly associated with nonfatal stroke and with total stroke in the subgroups ofstructured interview and non-Asian countries. Additionally, we found a slightly decreased risk ofischemic stroke among short sleepers. For piecewise linear trends, compared to 7 h, every 1-h incrementof sleep duration led to an increase of 13% [the pooled risk ratios (95% confidence intervals): 1.13 (1.07e1.20); p < 0.001] in risk of total stroke.Conclusion: Both in nonlinear and piecewise linear doseeresponse meta-analyses, long sleep durationsignificantly increased the risk of stroke incidence.

© 2016 Elsevier B.V. All rights reserved.

1. Introduction

Stroke is the second-leading cause of death and a leading causeof disability worldwide [1]. The Global Burden of Disease (GBD)2013 study showed that, in 2013, there were globally almost25.7million stroke survivors; over the 1990e2013 period, therewas a statistically significant increase in the absolute number ofdisability adjusted life years (DALYs) due to ischemic stroke (IS),

and deaths, survivors and incident events of as a result of both ISand hemorrhagic stroke [2]. Therefore, it is important to look forthe risk factors of stroke, especially those that can be amelioratedby modified lifestyles.

Sleep, an important role in human life, takes up approximatelyone-third of our lifetime. An optimal sleep duration (7e8 h) predictsfewer deaths [3]. In recent decades, suboptimal sleep duration waswidely demonstrated to be associated with bad health outcomessuch as obesity, diabetes, metabolic syndrome and hypertensionwhich are risk factors of stroke [4e7]. Thus, accumulating epide-miological studies have begun to investigate whether habitual sleepduration is related to stroke. Several primary studies have put for-ward a curvilinear relationship between sleep duration and stroke[8,9], where both short and long sleep duration led to an increase in

* Corresponding author. Department of Clinical Epidemiology, Institute ofCardiovascular Diseases and Center of Evidence Based Medicine, The First AffiliatedHospital, China Medical University, No. 155 Nanjing Bei Street, Heping District,Shenyang, Liaoning 110001, China.

E-mail address: [email protected] (J. Shi).


Sleep Medicine

journal homepage: www.elsevier .com/locate/s leep

http://dx.doi.org/10.1016/j.sleep.2016.12.0121389-9457/© 2016 Elsevier B.V. All rights reserved.

Sleep Medicine 32 (2017) 66e74

Original Article

Sleep duration and risk of stroke: a doseeresponse meta-analysis ofprospective cohort studies

Qiao He a, b, Hao Sun a, b, Xiaomei Wu a, b, Peng Zhang a, b, Huixu Dai a, b, Cong Ai a, b,Jingpu Shi a, b, *a Department of Clinical Epidemiology, Institute of Cardiovascular Diseases and Center of Evidence Based Medicine, The First Affiliated Hospital, ChinaMedical University, Shenyang, Chinab Center of Evidence Based Medicine, Liaoning Province & China Medical University, Shenyang, China


Article history:Received 8 September 2016Received in revised form17 November 2016Accepted 5 December 2016Available online 23 December 2016

Keywords:StrokeSleep durationMeta-analysisProspective studies

a b s t r a c t

Objectives: Suboptimal sleep duration has been considered to increase the risk of stroke incidence. Thuswe aimed to conduct a doseeresponse meta-analysis to examine the association between sleep durationand stroke incidence.Methods: We searched PubMed, Web of science and the Cochrane Library to identify all prospectivestudies evaluating the association of sleep duration and nonfatal and/or fatal stroke incidence. Then,restricted cubic spline functions and piecewise linear functions were used to evaluate the nonlinear andlinear doseeresponse association between them.Results: We included a total of 16 prospective studies enrolling 528,653 participants with 12,193 strokeevents. Nonlinear doseeresponse meta-analysis showed a J-shaped association between sleep durationand total stroke with the lowest risk observed with sleeping for 7 h. Considering people sleeping for 7 has reference, long sleepers had a higher predicted risk of total stroke than short sleepers [the pooled riskratios (95% confidence intervals): 4 h: 1.17 (0.99e1.38); 5 h: 1.17 (1.00e1.37); 6 h: 1.10 (1.00e1.21); 8 h:1.17 (1.07e1.28); 9 h: 1.45 (1.23e1.70); 10 h: 1.64 (1.4e1.92); pnonlinearity<0.001]. Short sleep durationswere only significantly associated with nonfatal stroke and with total stroke in the subgroups ofstructured interview and non-Asian countries. Additionally, we found a slightly decreased risk ofischemic stroke among short sleepers. For piecewise linear trends, compared to 7 h, every 1-h incrementof sleep duration led to an increase of 13% [the pooled risk ratios (95% confidence intervals): 1.13 (1.07e1.20); p < 0.001] in risk of total stroke.Conclusion: Both in nonlinear and piecewise linear doseeresponse meta-analyses, long sleep durationsignificantly increased the risk of stroke incidence.

© 2016 Elsevier B.V. All rights reserved.

1. Introduction

Stroke is the second-leading cause of death and a leading causeof disability worldwide [1]. The Global Burden of Disease (GBD)2013 study showed that, in 2013, there were globally almost25.7million stroke survivors; over the 1990e2013 period, therewas a statistically significant increase in the absolute number ofdisability adjusted life years (DALYs) due to ischemic stroke (IS),

and deaths, survivors and incident events of as a result of both ISand hemorrhagic stroke [2]. Therefore, it is important to look forthe risk factors of stroke, especially those that can be amelioratedby modified lifestyles.

Sleep, an important role in human life, takes up approximatelyone-third of our lifetime. An optimal sleep duration (7e8 h) predictsfewer deaths [3]. In recent decades, suboptimal sleep duration waswidely demonstrated to be associated with bad health outcomessuch as obesity, diabetes, metabolic syndrome and hypertensionwhich are risk factors of stroke [4e7]. Thus, accumulating epide-miological studies have begun to investigate whether habitual sleepduration is related to stroke. Several primary studies have put for-ward a curvilinear relationship between sleep duration and stroke[8,9], where both short and long sleep duration led to an increase in

* Corresponding author. Department of Clinical Epidemiology, Institute ofCardiovascular Diseases and Center of Evidence Based Medicine, The First AffiliatedHospital, China Medical University, No. 155 Nanjing Bei Street, Heping District,Shenyang, Liaoning 110001, China.

E-mail address: [email protected] (J. Shi).


Sleep Medicine

journal homepage: www.elsevier .com/locate/s leep

http://dx.doi.org/10.1016/j.sleep.2016.12.0121389-9457/© 2016 Elsevier B.V. All rights reserved.

Sleep Medicine 32 (2017) 66e74

Sleep duration and risk of stroke events and strokemortality: A systematicreview and meta-analysis of prospective cohort studies

Wenzhen Li a, Dongming Wang b,c, Shiyi Cao a, Xiaoxv Yin a, Yanhong Gong a, Yong Gan a,Yanfeng Zhou a, Zuxun Lu a,⁎a Department of Social Medicine and Health Management, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, Chinab Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, Chinac Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, Wuhan, Hubei 430030, China

a b s t r a c ta r t i c l e i n f o

Article history:Received 20 June 2016Accepted 19 August 2016Available online 24 August 2016

Background: Numerous studies have suggested the relationship between sleep duration and risks of strokemortality and morbidity, however, the effect estimates varied substantially across studies and it remainsunknown how many hours of habitual sleep are associated with the lowest risk of stroke outcomes. Therefore,we performed a dose–response meta-analysis of prospective cohort studies to evaluate the relation of sleepduration with risk of total mortality and stroke events.Methods: PubMed and Embase databases were searched through January 2016, and multivariate-adjustedrelative risks were pooled by using fixed-effects models. Semiparametric and dose–response methods wereused to assess the relationship of sleep duration and risk of stroke and stroke mortality.Results: Eleven articles with 16 independent reports were included in our meta-analysis. An approximateJ-shaped relationship was detected between sleep duration and risk of stroke and stroke mortality. No evidenceof a curve linear relationship was seen between sleep duration and risk of stroke or stroke mortality. Comparedwith 7-h sleep duration per day, the pooled relative risks for stroke events were 1.07 (95% CI 1.02–1.12) for each1-h shorter sleep duration among individuals who slept b7 h per day and 1.17 (1.14–1.20) for each 1-h increaseof sleep duration among individuals with longer sleep duration and the pooled RR for stroke mortality was 1.17(95% CI 1.13–1.20) per 1-h increase of sleep duration.Conclusions: Both short and long duration of sleep are predictors of stroke outcomes, and long sleep duration issignificant marker of stroke mortality.

© 2016 Elsevier Ireland Ltd. All rights reserved.

Keywords:Sleep durationStrokeSystematic review

1. Introduction

Stroke is the third commonest cause of death and a major public-health burden worldwide, which caused 3% of the world's disabilityburden in 1990. By 2020, stroke mortality will have almost doubled [1,2]. Stroke is also a main cause of death in developed countries, and itis expected to become a rising health problem in developing countriesas well. Given the severe consequences and accompanying burden,recognition of risk factors may have a significant role in preventingthe incidence of stroke, and sleep duration has long been consideredas a main contributing factor to the risk of stroke.

Increasing numbers of prospective studies have suggested that sleepduration are associated with stroke and a meta-analysis by Cappuccioet al. [3] reported that both short and long sleep durations were

associated with increased stroke events. However, the number ofincluded studies was small, and the dose–response analysis was notconducted. Since 2010, the number of prospective studies with enoughquantitative categories has rapid increased [4–14]. Therefore, weconducted a dose–response meta-analysis of prospective studies todescribe the relationship between sleep duration and risk of strokeevents and stroke mortality.

2. Methods

2.1. Search strategy and selection criteria

In accordance with the PRISMA guidelines [15], we identified published studiesthrough PubMed and Embase from inception to January 29, 2016, with the followingsearch terms without restriction: (cardiovascular diseases[MeSH] or stroke[MeSH]) andsleep. In addition,we searched the reference lists of all identified relevant original publica-tions and relevant reviews.

Studies were identified on the basis of predefined inclusion criteria: the study designwas prospective, the exposure of interest was sleep duration, the outcome was stroke orstroke mortality, and the investigators reported relative risks (RRs) with 95% CIs for atleast three quantitative categories of short sleep or long sleep duration. Additionally,

International Journal of Cardiology 223 (2016) 870–876

⁎ Corresponding author at: Department of Social Medicine and Health Management,School of Public Health, Tongji Medical College, Huazhong University of Science andTechnology, No.13 Hangkong Road, Wuhan, Hubei 430030, China.

E-mail address: [email protected] (Z. Lu).

http://dx.doi.org/10.1016/j.ijcard.2016.08.3020167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.


International Journal of Cardiology

j ourna l homepage: www.e lsev ie r .com/ locate / i j ca rd

Sleep duration and risk of stroke events and strokemortality: A systematicreview and meta-analysis of prospective cohort studies

Wenzhen Li a, Dongming Wang b,c, Shiyi Cao a, Xiaoxv Yin a, Yanhong Gong a, Yong Gan a,Yanfeng Zhou a, Zuxun Lu a,⁎a Department of Social Medicine and Health Management, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, Chinab Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, Chinac Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, Wuhan, Hubei 430030, China

a b s t r a c ta r t i c l e i n f o

Article history:Received 20 June 2016Accepted 19 August 2016Available online 24 August 2016

Background: Numerous studies have suggested the relationship between sleep duration and risks of strokemortality and morbidity, however, the effect estimates varied substantially across studies and it remainsunknown how many hours of habitual sleep are associated with the lowest risk of stroke outcomes. Therefore,we performed a dose–response meta-analysis of prospective cohort studies to evaluate the relation of sleepduration with risk of total mortality and stroke events.Methods: PubMed and Embase databases were searched through January 2016, and multivariate-adjustedrelative risks were pooled by using fixed-effects models. Semiparametric and dose–response methods wereused to assess the relationship of sleep duration and risk of stroke and stroke mortality.Results: Eleven articles with 16 independent reports were included in our meta-analysis. An approximateJ-shaped relationship was detected between sleep duration and risk of stroke and stroke mortality. No evidenceof a curve linear relationship was seen between sleep duration and risk of stroke or stroke mortality. Comparedwith 7-h sleep duration per day, the pooled relative risks for stroke events were 1.07 (95% CI 1.02–1.12) for each1-h shorter sleep duration among individuals who slept b7 h per day and 1.17 (1.14–1.20) for each 1-h increaseof sleep duration among individuals with longer sleep duration and the pooled RR for stroke mortality was 1.17(95% CI 1.13–1.20) per 1-h increase of sleep duration.Conclusions: Both short and long duration of sleep are predictors of stroke outcomes, and long sleep duration issignificant marker of stroke mortality.

© 2016 Elsevier Ireland Ltd. All rights reserved.

Keywords:Sleep durationStrokeSystematic review

1. Introduction

Stroke is the third commonest cause of death and a major public-health burden worldwide, which caused 3% of the world's disabilityburden in 1990. By 2020, stroke mortality will have almost doubled [1,2]. Stroke is also a main cause of death in developed countries, and itis expected to become a rising health problem in developing countriesas well. Given the severe consequences and accompanying burden,recognition of risk factors may have a significant role in preventingthe incidence of stroke, and sleep duration has long been consideredas a main contributing factor to the risk of stroke.

Increasing numbers of prospective studies have suggested that sleepduration are associated with stroke and a meta-analysis by Cappuccioet al. [3] reported that both short and long sleep durations were

associated with increased stroke events. However, the number ofincluded studies was small, and the dose–response analysis was notconducted. Since 2010, the number of prospective studies with enoughquantitative categories has rapid increased [4–14]. Therefore, weconducted a dose–response meta-analysis of prospective studies todescribe the relationship between sleep duration and risk of strokeevents and stroke mortality.

2. Methods

2.1. Search strategy and selection criteria

In accordance with the PRISMA guidelines [15], we identified published studiesthrough PubMed and Embase from inception to January 29, 2016, with the followingsearch terms without restriction: (cardiovascular diseases[MeSH] or stroke[MeSH]) andsleep. In addition,we searched the reference lists of all identified relevant original publica-tions and relevant reviews.

Studies were identified on the basis of predefined inclusion criteria: the study designwas prospective, the exposure of interest was sleep duration, the outcome was stroke orstroke mortality, and the investigators reported relative risks (RRs) with 95% CIs for atleast three quantitative categories of short sleep or long sleep duration. Additionally,

International Journal of Cardiology 223 (2016) 870–876

⁎ Corresponding author at: Department of Social Medicine and Health Management,School of Public Health, Tongji Medical College, Huazhong University of Science andTechnology, No.13 Hangkong Road, Wuhan, Hubei 430030, China.

E-mail address: [email protected] (Z. Lu).

http://dx.doi.org/10.1016/j.ijcard.2016.08.3020167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.


International Journal of Cardiology

j ourna l homepage: www.e lsev ie r .com/ locate / i j ca rd

August 2017 | Volume 8 | Article 3921

MINI REVIEWpublished: 08 August 2017

doi: 10.3389/fneur.2017.00392

Frontiers in Neurology | www.frontiersin.org

Edited by: Ayrton R. Massaro,

Hospital Sirio-Libanes, Brazil

Reviewed by: Shunya Takizawa,

Tokai University, Japan Fabien Chauveau,

Lyon Neuroscience Research Center (INSERM), France

*Correspondence:Chun Seng Phua

[email protected]; Tissa Wijeratne

[email protected]

Specialty section: This article was submitted to

Stroke, a section of the journal Frontiers in Neurology

Received: 28 May 2017Accepted: 24 July 2017

Published: 08 August 2017

Citation: Phua CS, Jayaram L and Wijeratne T

(2017) Relationship between Sleep Duration and Risk Factors for Stroke.

Front. Neurol. 8:392. doi: 10.3389/fneur.2017.00392

Relationship between Sleep Duration and Risk Factors for StrokeChun Seng Phua1,2*, Lata Jayaram1,3 and Tissa Wijeratne1,2,4,5*

1 Department of Medicine, Melbourne Clinical School, University of Melbourne, Melbourne, VIC, Australia, 2 Department of Neurology, Western Health, St. Albans, VIC, Australia, 3 Department of Respiratory and Sleep Medicine, Western Health, St. Albans, VIC, Australia, 4 Department of Medicine, University of Rajarata, Saliyapura, Anuradhapura, Sri Lanka, 5 Department of Psychology and Counselling, School of Psychology and Public Health, College of Science, Health and Engineering, La Trobe University, Melbourne, VIC, Australia

Stroke is a leading cause of death and disability worldwide. While various risk factors have been identified, sleep has only been considered a risk factor more recently. Various epidemiologic studies have associated stroke with sleep such as sleep duration, and laboratory and clinical studies have proposed various underlying mechanisms. The pathophysiology is multifactorial, especially considering sleep affects many common risk factors for stroke. This review aims to provide an outline of the effect of sleep duration on common stroke risk factors. Appropriate sleep duration, especially in patients who have stroke risk factors, and increasing awareness and screening for sleep quality may contribute to primary prevention of stroke.

Keywords: sleep, stroke, diabetes mellitus, hypertension, obesity, dyslipidemia, atrial fibrillation

INTRODUCTION

Every year, 15 million people worldwide suffer a stroke. Nearly six million die, and another five million are left permanently disabled (1). Stroke is defined by the World Health Organization as rapidly developing clinical signs of focal disturbance of cerebral function, lasting more than 24 h or leading to death with no apparent cause other than that of vascular origin (2). Stroke is the second leading cause of death and a leading cause of disability worldwide (3). Recently, it was estimated that the total financial cost of stroke in Australia is five billion dollars a year (4).

Numerous traditional risk factors have been identified for stroke, including hypertension, hypercholesterolemia, cigarette smoking, obesity, dyslipidemia, previous stroke(s) or transient ischemic attack, advanced age, diabetes mellitus, and atrial fibrillation (AF) (5–7). Yet, sleep has been associated with stroke only more recently. Various aspects of sleep have been explored, such as sleep duration, sleep quality, and sleep-related breathing disorders, with some being more heavily implicated than others. For example, sleep-related breathing disorders such as obstructive sleep apnea are significantly associated with wake-up stroke. This may be explained by nocturnal hypox-emia, AF secondary to hypoxemia, and right-to-left shunt triggered by apnea events in patients with patent foramen ovale (8, 9).

While the consensus is the ideal amount of sleep for adults is 7 or more hours per night on a regular basis to promote optimal health (10), recent results from the 2016 Sleep Health Foundation national survey showed 12% of Australians sleep less than 5.5 h and 8% over 9 h (11). Studies have shown that insufficient or excessive sleep can be detrimental. In animal studies, sustained sleep deprivation was shown to reduce plasma thyroid hormone to severely low levels, reduce resistance to infection, cause a deep negative energy balance, and decrease cerebral function (12, 13). In clinical studies, insufficient and excessive sleep is associated with increased cardiovascular events, including stroke

August 2017 | Volume 8 | Article 3921

MINI REVIEWpublished: 08 August 2017

doi: 10.3389/fneur.2017.00392

Frontiers in Neurology | www.frontiersin.org

Edited by: Ayrton R. Massaro,

Hospital Sirio-Libanes, Brazil

Reviewed by: Shunya Takizawa,

Tokai University, Japan Fabien Chauveau,

Lyon Neuroscience Research Center (INSERM), France

*Correspondence:Chun Seng Phua

[email protected]; Tissa Wijeratne

[email protected]

Specialty section: This article was submitted to

Stroke, a section of the journal Frontiers in Neurology

Received: 28 May 2017Accepted: 24 July 2017

Published: 08 August 2017

Citation: Phua CS, Jayaram L and Wijeratne T

(2017) Relationship between Sleep Duration and Risk Factors for Stroke.

Front. Neurol. 8:392. doi: 10.3389/fneur.2017.00392

Relationship between Sleep Duration and Risk Factors for StrokeChun Seng Phua1,2*, Lata Jayaram1,3 and Tissa Wijeratne1,2,4,5*

1 Department of Medicine, Melbourne Clinical School, University of Melbourne, Melbourne, VIC, Australia, 2 Department of Neurology, Western Health, St. Albans, VIC, Australia, 3 Department of Respiratory and Sleep Medicine, Western Health, St. Albans, VIC, Australia, 4 Department of Medicine, University of Rajarata, Saliyapura, Anuradhapura, Sri Lanka, 5 Department of Psychology and Counselling, School of Psychology and Public Health, College of Science, Health and Engineering, La Trobe University, Melbourne, VIC, Australia

Stroke is a leading cause of death and disability worldwide. While various risk factors have been identified, sleep has only been considered a risk factor more recently. Various epidemiologic studies have associated stroke with sleep such as sleep duration, and laboratory and clinical studies have proposed various underlying mechanisms. The pathophysiology is multifactorial, especially considering sleep affects many common risk factors for stroke. This review aims to provide an outline of the effect of sleep duration on common stroke risk factors. Appropriate sleep duration, especially in patients who have stroke risk factors, and increasing awareness and screening for sleep quality may contribute to primary prevention of stroke.

Keywords: sleep, stroke, diabetes mellitus, hypertension, obesity, dyslipidemia, atrial fibrillation

INTRODUCTION

Every year, 15 million people worldwide suffer a stroke. Nearly six million die, and another five million are left permanently disabled (1). Stroke is defined by the World Health Organization as rapidly developing clinical signs of focal disturbance of cerebral function, lasting more than 24 h or leading to death with no apparent cause other than that of vascular origin (2). Stroke is the second leading cause of death and a leading cause of disability worldwide (3). Recently, it was estimated that the total financial cost of stroke in Australia is five billion dollars a year (4).

Numerous traditional risk factors have been identified for stroke, including hypertension, hypercholesterolemia, cigarette smoking, obesity, dyslipidemia, previous stroke(s) or transient ischemic attack, advanced age, diabetes mellitus, and atrial fibrillation (AF) (5–7). Yet, sleep has been associated with stroke only more recently. Various aspects of sleep have been explored, such as sleep duration, sleep quality, and sleep-related breathing disorders, with some being more heavily implicated than others. For example, sleep-related breathing disorders such as obstructive sleep apnea are significantly associated with wake-up stroke. This may be explained by nocturnal hypox-emia, AF secondary to hypoxemia, and right-to-left shunt triggered by apnea events in patients with patent foramen ovale (8, 9).

While the consensus is the ideal amount of sleep for adults is 7 or more hours per night on a regular basis to promote optimal health (10), recent results from the 2016 Sleep Health Foundation national survey showed 12% of Australians sleep less than 5.5 h and 8% over 9 h (11). Studies have shown that insufficient or excessive sleep can be detrimental. In animal studies, sustained sleep deprivation was shown to reduce plasma thyroid hormone to severely low levels, reduce resistance to infection, cause a deep negative energy balance, and decrease cerebral function (12, 13). In clinical studies, insufficient and excessive sleep is associated with increased cardiovascular events, including stroke

Limitations majeures!

 Durée de sommeil auto-rapportée

 Comorbidités sous-estimation du temps de sommeil

 Bons dormeurs sur-estimation du temps de sommeil

 Durée du sommeil quelque peu réducteur  Durée vs qualité du sommeil

 Besoins de sommeil: différences interindividuelles importantes  Courts vs longs dormeurs

Questions

sommeil et avc - ssvq.org · pfo-associated ischemic strokes115 and there is an increased reported...

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