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Prise en charge du mode de vie et des facteurs de risque

2017 MISE À JOUR
octobre 2017

Remarque : Ces recommandations s’appliquent à l’AVC d’origine ischémique et hémorragique, sauf indication contraire.

2.0 Évaluation des facteurs de risque :

  1. Les personnes à risque d’AVC et les patients ayant eu un AVC devraient être évalués afin d’identifier les facteurs de risque vasculaire, cerner les enjeux entourant leur mode de vie (alimentation, apport sodé, exercice, poids, consommation d’alcool, tabagisme, utilisation de contraceptifs ou traitement hormonal substitutif) [niveau de preuve B].
  2. Les personnes à risque d’AVC devraient recevoir des renseignements et des conseils personnalisés sur les stratégies qu’elles pourraient adopter pour changer leur mode de vie et maîtriser leurs facteurs de risque [niveau de preuve B].
  3. Les patients devraient être orientés vers les spécialistes appropriés, le cas échéant [niveau de preuve B].
    1. Les spécialistes peuvent fournir des évaluations plus complètes et des programmes structurés pour prendre en charge les facteurs de risque spécifiques [niveau de preuve B].

2.1 Alimentation saine et équilibrée

  1. Conseiller et encourager les personnes victimes d’AVC ou d’AIT à avoir une alimentation saine et équilibrée incluant :
    1. un grand nombre d’aliments naturels/complets à chaque repas [niveau de preuve B].
    2. moins d’aliments transformés, y compris les friandises, boissons sucrées, viandes transformées et collations [niveau de preuve B].
    3. un régime alimentaire riche en légumes et en fruits ; encourager les patients à choisir des fruits frais ou surgelés non sucrés, ou des fruits en conserve dans de l’eau sans sucres ajoutés/libres ni édulcorants artificiels/non caloriques, des légumes frais ou surgelés sans sauce, ou des légumes en conserve sans sel ajouté [niveau de preuve B].
    4. du lait écrémé et des alternatives, et des fibres alimentaires solubles [niveau de preuve B].
    5. des viandes maigres, des céréales complètes et des protéines végétales pauvres en acides gras trans et saturés, pauvres en cholestérol (< 200 mg par jour pour les patients plus exposés au risque de maladies cardiovasculaires) et pauvres en sodium [niveau de preuve B].
  2. Fournir aux personnes avec AIT ou AVC des conseils et une éducation relatifs à l’adoption d’un régime méditerranéen riche en légumes, fruits, céréales complètes, poisson, noix et huile d’olive, et pauvre en viande rouge [niveau de preuve B].
  3. Fournir aux personnes avec AIT ou AVC des conseils et une éducation relatifs à l’adoption d’un régime alimentaire où la quantité quotidienne de sucres libres absorbée ne dépasse pas 10 % de l’apport calorique total quotidien (énergie) [niveau de preuve B].

Remarque : La quantité de sucre présente dans notre régime alimentaire est problématique, mais le sucre que l’on retrouve dans les boissons est pire encore. Les boissons sucrées (comme les boissons gazeuses, les jus de fruits, les eaux vitaminées, les boissons énergétiques, etc.) sont considérées comme riches en énergie, mais pauvres en nutriments en raison de la grande quantité de calories qu’elles renferment et de leur faible valeur nutritive. Énoncé de position 2016 de Cœur + AVC sur les boissons sucrées.

2.2 Apport en sodium

  1. Fournir aux personnes avec AVC ou AIT des conseils et une éducation relatifs à un apport quotidien en sodium de toutes les sources de maximum 2 000 mg [niveau de preuve A]. Pour en savoir plus, veuillez vous référer au programme d’alimentation – santé 2016 de l’Université de Cornell.

2.3 Exercice

  1. Fournir aux personnes avec AVC ou AIT des conseils et une éducation relatifs à une diminution des comportements sédentaires et à une augmentation des activités physiques, tant que l’évolution de leur rétablissement le permet [niveau de preuve B].
  2. Encourager les personnes avec AVC ou AIT à participer à des exercices dynamiques d’intensité modérée (comme la marche rapide, le jogging, la natation, le vélo) 4 à 7 jours par semaine, pour accumuler au moins 150 minutes d’épisodes de 10 minutes ou plus, en plus des activités de routine de la vie quotidienne (pour des informations supplémentaires, consultez les Directives canadiennes 2011 en matière d’activité physique de la SCPE et le programme d’alimentation-santé 2015 de l’Université de Cornell.) [niveau de preuve B].4
  3. La plupart des gens victimes d’AVC ou d’AIT devraient être encouragés à commencer un programme d’exercice régulier [niveau de preuve C].
    1. À l’amorce d’un programme d’exercices, les patients à haut risque de chutes ou de blessures et les patients qui présentent des comorbidités (p. ex., les patients cardiaques), qui peuvent les mettre davantage à risque de complications, devraient participer à des programmes d’exercices sous surveillance médicale (comme celle fournie par un physiothérapeute) [niveau de preuve C].

2.4 Poids

  1. Fournir aux personnes avec AVC ou AIT des conseils et une éducation relatifs au maintien d’un indice de masse corporelle (IMC) de 18,5 à 24,9 kg/m2 ; ou un tour de taille inférieur à 88 cm chez la femme et inférieur à 102 cm chez l’homme [niveau de preuve B]. (Remarque : ces cibles viennent de recherches actuelles portant principalement sur des patients de race blanche. Veuillez consulter les références pour connaître les valeurs de référence pour d’autres groupes ethniques).
  2. Offrir aux personnes victimes d’AVC ou d’AIT et aux personnes en surpoids des conseils et une éducation qui permettent de fixer des objectifs de perte de poids et de mettre au point des programmes individualisés [niveau de preuve B].
    1. L’orientation vers un diététicien doit être prise en considération [niveau de preuve B].

2.5 Consommation d’alcool

  1. Inciter les victimes d’AIT ou d’AVC à éviter la consommation élevée d’alcool, car la consommation excessive d’alcool augmente le risque d’AVC ischémique et d’hémorragie intracrânienne [niveau de preuve B].
  2. Encourager et aider les personnes victimes d’AIT ou d’AVC à suivre les Directives de consommation d’alcool à faible risque du Canada (2011) : Pour les femmes, pas plus de 10 consommations par semaine et pas plus de 2 consommations par jour la plupart des jours, sans jamais dépasser 3 consommations d’affilée ; pour les hommes, pas plus de 15 consommations par semaine et pas plus de 3 consommations par jour, sans jamais dépasser 4 consommations d’affilée [niveau de preuve C].

Remarque : Un verre normal contient 13,6 g ou 17,2 ml d’éthanol, ou environ 44 ml de spiritueux à 40 %, 355 ml de bière à 5 % ou 148 ml de vin à 12 %.

2.6 Contraceptifs oraux et traitement hormonal substitutif

  1. Les contraceptifs oraux contenant des œstrogènes ou le traitement hormonal substitutif devrait être supprimé chez les patientes avec AIT ou AVC ischémique [niveau de preuve B]. D’autres choix de prise en charge devraient être envisagés pour ces patientes [niveau de preuve C].

2.7 Consommation de drogue à usage récréatif

  1. Les personnes ayant eu un AVC et consommant des drogues à usage récréatif pouvant augmenter le risque d’AVC (comme la cocaïne, les amphétamines) doivent être encouragées à stopper leur usage si elles n’ont pas été prescrites pour des raisons médicales [niveau de preuve C] et devraient recevoir un soutien approprié et être orientées vers des services et des ressources spécialisés dans la toxicomanie et la rééducation [niveau de preuve B].

2.8 Abandon du tabac

Remarque : Le terme « tabac » dans les présentes Recommandations englobe aussi bien le tabac que d’autres substances inhalées. Elles s’appliquent à l’AVC d’origine ischémique et hémorragique.

  1. Quel que soit le contexte médical dans le continuum des soins de l’AVC (soins actifs, consultations externes ou milieu extrahospitalier), la consommation de tabac par le patient devrait être déterminée, évaluée et documentée [niveau de preuve A].
  2. Des conseils sans ambiguïté, sans jugement et personnalisés sur l’importance d’arrêter de fumer doivent être prodigués à tous les fumeurs [niveau de preuve B] et aux personnes qui vivent avec eux.
  3. Une aide devrait être proposée afin de faire une tentative d’abandon du tabac – soit directement, soit par l’aiguillage vers des ressources appropriées [niveau de preuve A].
  4. Il faudrait offrir une intervention comportementale motivationnelle aux personnes qui ne sont pas prêtes à abandonner le tabac afin de rehausser leur état de préparation en vue d’arrêter de fumer [niveau de preuve B]. Voir les ressources de mises en œuvre ci-dessous pour des outils motivationnels d’entrevue.
  5. Il faudrait envisager une combinaison de pharmacothérapie et de thérapie comportementale dans tous les programmes d’abandon du tabac et toutes les interventions à ce sujet [niveau de preuve A].
  6. À titre de thérapie en première ligne, il faudrait envisager les trois catégories d’agents pharmacologiques suivantes : Une thérapie de remplacement de la nicotine, la varénicline et le bupropion [niveau de preuve A].
    1. Le choix de la pharmacothérapie appropriée devrait tenir compte de la stabilité de l’état de santé, des besoins cliniques, d’autres facteurs médicaux et des préférences du patient [niveau de preuve C]. Voir Annexe 2 : La pharmacothérapie dans le traitement pour arrêter de fumer.
  7. Des protocoles devraient prévoir le sevrage de la nicotine durant l’hospitalisation de patients victimes d’AVC et fumeurs [niveau de preuve B]. Voir les ressources de mise en œuvre ci-dessous pour le modèle d’Ottawa en tant qu’exemple d’outil de protocole.
  8. Les membres de l’équipe interprofessionnelle devraient prodiguer des conseils au patient, à sa famille et aux aidants en ce qui a trait aux effets néfastes de l’exposition à la fumée environnementale secondaire [niveau de preuve B].

2.9 Adhésion aux programmes de prévention individuels

  1. Lors de chaque visite de prévention de l’AVC avec les membres de l’équipe soignante, évaluer l’adhésion des patients aux programmes de prévention secondaire personnalisés (pharmacothérapie et changements dans le mode de vie) [niveau de preuve C].

Remarque : L’adhésion comprend l’observance thérapeutique, la gestion de l’équilibre alimentaire, le traitement de réadaptation et/ou la participation à une activité physique et d’autres domaines spécifiques du patient.

La version définitive de cet article a été publiée dans l’International Journal of Stroke par SAGE Publications Ltd. © World Stroke Organization, 2017.
http://journals.sagepub.com/doi/suppl/10.1177/1747493017743062/suppl_file/supplementary_material.pdf

Justification

Un mode de vie sain réduit le risque d’un premier AVC et d’une récidive chez les patients qui ont été victimes d’un AVC. L’hypertension est à elle seule le plus important facteur évitable de risque d’AVC. Selon la recherche récente, une réduction du sel (sodium) dans les aliments éliminerait l’hypertension artérielle de près d’un Canadien sur trois. La majeure partie du sodium que consomme la population du pays (77 %) provient d’aliments transformés vendus à l’épicerie ou dans des établissements de restauration. Seuls 11 % du sodium consommé est ajouté pendant la préparation ou à table. Le pourcentage restant se trouve dans les aliments à l’état naturel. Les données disponibles portent à croire que la réduction de la consommation de sodium de façon à atteindre l’apport quotidien recommandé permettrait d’abaisser de 30 % ou moins l’incidence de l’AVC et des cardiopathies et contribuerait de manière importante à une réduction de la pression artérielle.

L’obésité au sein de la population canadienne, particulièrement chez les jeunes adultes, est une préoccupation de plus en importante. Il faut aborder cet enjeu avec tous les patients qui ont subi un AVC ou à risque d’en subir un. L’obésité peut être le résultat d’un environnement alimentaire obésogène qui inclut une exposition fréquente aux graisses, sucres, calories, etc. Les graisses saturées augmentent le taux de cholestérol LDL dans le sang. Un taux élevé de cholestérol LDL constitue un facteur de risque important de maladies du cœur et d’AVC. Quand les graisses saturées sont remplacées par des graisses mono- et polyinsaturées, le cholestérol LDL diminue. Selon les estimations, les graisses saturées représentent environ 10 % de l’apport total en calories de la population canadienne. Les aliments transformés sont une source importante de graisses saturées dans l’alimentation des Canadiens et des Canadiennes. Ces aliments hautement transformés contiennent beaucoup de calories, de sodium et de sucres libres, et peuvent être riches en graisses malsaines comme les acides gras trans.
L’exercice régulier diminue aussi le risque d’AVC et d’autres maladies vasculaires.5 La recherche a démontré un risque accru de thrombose en présence de thérapie hormonale basée sur des œstrogènes (autant les contraceptifs oraux que le traitement hormonal substitutif).

Même si les causes de l’AVC dans l’enfance sont généralement différentes, les questions relatives au mode de vie revêtent la même importance pour la population pédiatrique, particulièrement parce que le risque de récidive d’AVC s’étend sur une plus longue durée chez les enfants.

Le rapport de vérification sur la Qualité des soins de l’AVC au Canada a permis de constater que parmi tous les Canadiens victimes d’un AVC en 2008-2009, 41 % étaient des fumeurs actifs, principalement des jeunes adultes (moins de 49 ans). L’étude Interstroke a déterminé que les fumeurs actifs étaient à plus grand risque d’AVC, l’impact étant plus prononcé sur l’AVC ischémique comparé à l’AVC hémorragique, et que le risque allait de pair avec le nombre de cigarettes fumées par jour. Il y a lieu de noter que le tabagisme vient au deuxième rang après l’hypertension parmi les facteurs de risque d’AVC. Le groupe de travail de CAN-ADAPTT a signalé qu’environ 17 % des Canadiens sont des fumeurs actifs et qu’un grand pourcentage d’entre eux indiquent vouloir abandonner le tabac. Les professionnels de la santé jouent un rôle important dans l’aide qu’ils peuvent apporter à la renonciation au tabac. De surcroît, même de brèves interventions de leur part seraient efficaces pour augmenter les chances qu’un fumeur effectue une tentative d’abandon du tabac. Les lignes directrices pour la pratique clinique permettent de réduire efficacement l’écart entre les soins recommandés et les soins dispensés. Les données indiquent que l’abandon du tabac permet de réduire, voire d’annuler le risque d’AVC au fur et à mesure que se prolonge la période sans tabac. Les patientes avec AVC sont à risque accru de récidive si elles continuent de fumer et prennent des contraceptifs ou suivent un traitement hormonal substitutif.

Exigences pour le système
  • Initiatives de promotion de la santé qui contribuent à la prévention de l’AVC dans toutes les collectivités (intégrées aux initiatives existantes en matière de maladies chroniques).
  • Services de prévention coordonnés et exhaustifs offerts par les dispensateurs de soins primaires et mécanismes visant à s’assurer que le thème du risque d’AVC est abordé à chaque consultation d’un professionnel de la santé dans le continuum des soins.
  • La santé publique et la santé de la population sont axées sur la santé cérébrovasculaire, la santé des patients pédiatriques est axée sur la diminution des risques grâce au régime alimentaire – notamment la limitation de la consommation de graisses, de sodium et de sucre, à l’activité physique, à l’absence de tabagisme et de consommation de drogues augmentant le risque d’AVC.
  • Efforts régionaux, nationaux et internationaux pour réduire la consommation de sodium en collaborant avec les gouvernements et en changeant l’approvisionnement alimentaire dans le commerce alimentaire et le secteur de la restauration.
  • Initiatives visant à sensibiliser le public aux risques engendrés par le sodium et ciblant l’ensemble de la population et des sous-groupes. Programmes scolaires qui enseignent des notions liées à l’alimentation, notamment la cuisine à partir d’ingrédients frais, naturels et complets.
  • Stratégies alimentaires locales, régionales et fédérales qui améliorent l’accès aux aliments complets non transformés dans toutes les communautés.
  • Dans toutes les collectivités, milieux de soins primaires et lieux de travail, un accès plus aisé aux programmes de prise en charge des facteurs de risque tels que l’hypertension et l’usage du tabac.
  • Accès facilité aux pratiques exemplaires de soutien dans l’arrêt du tabac grâce aux médicaments, au traitement de substitution de la nicotine et à la rééducation comportementale via des régimes publics et privés d’assurance-médicaments.
  • Interventions des différents ordres de gouvernement pour encourager l’abandon du tabac. Utilisation de la stratégie de contrôle du tabac MPOWER de l’OMS.
  • Concertation des intervenants tels que la fondation, les organismes de santé publique, les ministères de la Santé et les dispensateurs de soins dans le continuum des soins afin de fournir aux patients, aux familles et aux aidants du matériel éducatif livrant des messages cohérents sur la prise en charge des facteurs de risque.
  • Processus coordonné visant à assurer l’accès et la sensibilisation aux documents, programmes, activités et moyens de communication à contenu éducatif, destinés aux professionnels de la santé, aux patients, aux familles et aux aidants, et qui traitent de la prise en charge des facteurs de risque, notamment par une publicité sur leur disponibilité, des moyens efficaces de diffusion et le suivi qui s’impose.
  • Accès amélioré aux médicaments et aux consultations axées sur le comportement visant l’abandon du tabac par l’entremise des régimes publics et privés d’assurance-médicaments.
  • Interventions des différents ordres de gouvernement pour encourager l’abandon du tabac.
  • Réglementation en matière de cigarettes électroniques, notamment l’interdiction de la vente aux mineurs et de leur usage en milieu de travail et dans les lieux publics où l’usage du tabac ou la vente des produits de tabac sont interdits, et l’encadrement de la publicité et de la promotion des cigarettes électroniques.
  • Ressources éducatives adaptées à la culture et aux origines ethniques du public visé, disponibles dans de multiples langues, et ressources spéciales répondant également aux besoins des patients aphasiques.
  • Plus grande infrastructure active dans les communautés pour garantir un environnement qui soutient l’activité physique pour toutes les tranches d’âge.
  • Pour les personnes vivant dans les régions rurales et éloignées, plus grande accessibilité à des programmes de promotion du mode de vie sain, à du matériel didactique et à des professionnels de la santé, notamment par un usage novateur de la technologie.
Indicateurs de rendement
  1. Proportion des patients ayant d’importants facteurs de risque d’AVC, notamment l’hypertension, l’obésité, l’hyperlipidémie, le diabète, la fibrillation auriculaire, le tabagisme et le faible niveau d’activité physique (indicateur de qualité clé).
  2. Fréquence annuelle de la survenue de l’AVC dans chaque province et territoire par type d’AVC (indicateur de qualité clé).
  3. Proportion des patients victimes d’un AVC aigu ou d’une ICT qui reçoivent leur congé de l’urgence ou d’un séjour à l’hôpital, puis qui sont réadmis avec un nouveau diagnostic d’AVC ou d’ICT pour n’importe quelle raison moins de 7 jours après avoir obtenu leur congé des soins actifs pour l’AVC aigu de référence (indicateur de qualité clé).
  4. Taux de mortalité due à l’AVC à l’échelle des provinces et territoires, à l’hôpital ou à 30 jours et à un an (indicateur de qualité clé).
  5. Pourcentage de la population en mesure de nommer les principaux facteurs de risque d’AVC, notamment l’hypertension, l’apport sodé, le régime alimentaire, le poids, l’exercice, le tabagisme et la consommation d’alcool.
  6. Le taux annuel de réadmission pour AVC ou AIT récidivant des patients avec AVC ou accident ischémique transitoire antérieur.
  7. Proportion des patients dont les renseignements concernant l’usage du tabac sont consignés à leur dossier.
  8. Proportion des patients avec AVC ou AIT qui ont des antécédents de consommation de tabac et auxquels on a donné des conseils et une consultation en matière d’abandon du tabac durant le séjour à l’hôpital et en réadaptation à titre de patient hospitalisé ou ambulant ainsi qu’à l’occasion de visites en prévention secondaire.
  9. Proportion des patients avec AVC ou AIT qui ont participé à un programme d’abandon du tabac et qui n’ont pas recommencé à fumer après 6 mois, 1 an et 2 ans.

Notes sur la mesure des indicateurs

  • Indicateurs de rendement 1, 2 et 3 : Déclarations volontaires tirées des sondages provinciaux et nationaux sur la santé. Il faut normaliser ces données en fonction des plus récentes données de recensement national relatives à l’âge et au sexe.
  • Indicateurs de rendement 4 : Données administratives disponibles aux échelons local, provincial et national.
  • Les taux de mortalité doivent tenir compte, pour le calcul du risque, de l’âge, du sexe, de la gravité de l’AVC et des comorbidités.
Ressources pour la mise en œuvre et outils de transfert des connaissances

Renseignements destinés aux dispensateurs de soins de santé

Informations destinées au patient

Résumé des données probantes

Lifestyle Management Evidence Tables and Reference List

A healthy lifestyle, which includes a healthy balanced diet, exercise, weight control, reduction and avoidance of alcohol and tobacco, reduces the risk of an initial stroke and the risk of a subsequent stroke for patients with a prior history of stroke. Data from the Global Burden of Disease Study 2013 (Murray et al, 2013) were used to estimate the population-attributable fraction (PAF) of stroke-related disability-adjusted life-years (DALYs) associated with 17 potentially modifiable risk factors. While global estimates were provided, data from separate countries were also reported. Stroke burden among Canadians was attributed to a variety of modifiable risk factors, including 20% for diets low in fruits and vegetables, 13% for diets high in sodium, 11% for low levels of physical activity, 28% for a body mass index greater than 23.0, and 13% for tobacco use. These results are consistent with other reports. The recent INTERSTROKE 2 study (O'Donnell et al 2016) reported that among 10 risk factors, the odds of all stroke were 2.5 times higher among persons with a self-reported history of hypertension, 2 times higher among heavy alcohol consumers and over 1.5 times higher for tobacco smokers. The associated population attributable risk estimates were 34%, 5.8% and 12%, respectively.

Diet
Examining the relationship between stroke risk and diet is challenging, in large part due to the limitations in methods for collecting long-term dietary intake and controlling for potential confounders. The results of studies evaluating individual dietary components (fruit/vegetable consumption, fats, dairy products and whole grains) and dietary patterns of eating have yielded ambiguous results.

There is evidence to suggest that regular consumption of fruits and vegetables reduces the risk of stroke. The results from the China Kadoorie Biobank Study (Du et al. 2016) included 512,891 adults, aged 35-74 years, without a history of cardiovascular disease or treatment for hypertension. During 3.2 million person-years of follow-up, the incidences of both ischemic and hemorrhagic stroke were significantly lower among those who consumed fruit at least monthly. The reduction was dose-dependent, such that daily consumption was associated with the lowest risk for both stroke types. The Hazard Ratios for daily consumption were 0.75 (ischemic stroke) and 0.64 (hemorrhagic stroke). Data from the Global Burden of Disease Study 2013 (Feigin et al. 2016) was used to estimate the population-attributable fraction (PAF) of stroke-related disability-adjusted life-years (DALYs) associated with 17 potentially modifiable risk factors, including diets low in fruits and vegetables. While data from 188 countries was reported, country-specific estimates were also provided. In Canada, 20.4% (95% uncertainty interval 9.7%-31.5%) of the stroke burden was attributed to diets low in fruits, while 19.5% (95% uncertainty interval 14.4%-25.5%) was attributed to diets low in vegetables. In a cohort study including 175,000 participants, Sharma et al. (2013) reported no protective effect of consuming fruit or vegetables in either men or women during 8 years of follow-up. The mean number of servings of fruit and vegetables between those who died of stroke was similar to all others, assessed by determining whether participants were compliant with the USDA’s food pyramid. In a case-control study, O’Donnell et al. (2010) reported that increased consumption of fruit was associated with a decreased risk of stroke (adj OR of tertile 1 vs. 3=0.61, 99% CI 0.66-0.91), while increased consumption of vegetables was not (adj OR of T3 vs. T1=0.91, 99% CI 0.75-1.00). A meta-analysis (He et al. 2006) that included 20 studies and 760,629 participants, with follow-up ranging from 4-37 years, reported the risk of stroke was significantly lower in the groups associated with the highest intake of fruits and vegetables (Total combined fruit and veg: RR=0.79, 95% CI 0.75-0.84; Fruit: RR=0.77, 95% CI 0.71-0.84; Vegetables: RR=0.86, 95% CI 0.79-0.93). For every increase of 200 g/day of vegetables, stroke risk was decreased by 11% (RR=0.89, 95% CI 0.81-0.98). The corresponding decrease in stroke risk for fruit was 32%.

The role of dietary fat as a risk factor for stroke remains unclear. Siri-Tarino et al. (2010) conducted a systematic review & meta-analysis that included the results of 21 prospective cohort studies, of which stroke was the outcome in 8 studies (n=179,436). The mean follow-up periods ranged from 8-23 years. There was no increased risk of stroke associated with the highest intakes of saturated fat compared with the lowest (adjusted RR=0.81, 95% CI 0.62-1.05, p=0.11). Results from the Prospective cohort study Multi-Ethnic Study of Atherosclerosis (MESA), suggest that the source of saturated fat is a greater indicator of cardiovascular risk (De Oliveira Otto et al. 2012). While stroke was not an outcome assessed in this study, saturated fat from dairy sources was found to be protective for incident cardiovascular disease, while the risk was increased for consumption of saturated fat from meat sources. He et al. (2003) did not find significant associations between amount of total fat, source of fat (animal or vegetable), type of fat (saturated, unsaturated, monounsaturated, polyunsaturated, trans fat or cholesterol) or selected high-fat foods, including red meat, high-fat dairy products, nuts and eggs, and incidence of ischemic or hemorrhagic stroke. This prospective cohort study included data from 43,732 men aged 40-75 years from the Health Professionals’ follow-up study who were free of cardiovascular disease and diabetes at baseline. The consumption of trans fat is generally thought to be associated with negative health outcomes. Using data from the REasons for Geographic And Racial Differences in Stroke (REGARDS) study, including 17,107 participants ≥45 years of age and without a history of stroke, Kiage et al. (2014) examined the relationship between incident stroke and trans-fat consumption. During a median of 7 years of follow-up, the risk of ischemic stroke was reported to be elevated significantly for men (HR=1.13, 95% CI 1.00-1.28), but not for women (HR=0.93, 95% CI 0.77-1.12).

The results from two recent systematic reviews (Hu et al. 2014, Qin et al. 2015), including the results from 15 and 22 cohort studies, respectively, suggest that dairy consumption may be protective for stroke (RR=0.80, 95% CI 0.76-0.84 and RR=0.87, 95% CI 0.77-0.99). While increased consumption of dairy products in general was associated with a lower risk of stroke, in sub group analyses the effect was most pronounced for low-fat dairy, cheese and fermented milk products. Hu et al. (2014) reported a non-linear dose-response relationship between milk consumption and stroke risk whereby 200 mL/day was most protective (RR=0.82, 95% CI 0.79-0.86). Larsson et al. (2012) also reported that consumption of low-fat dairy products was associated with a decreased risk of all stroke (RR=0.88, 95% CI 0.80-0.97) and ischemic stroke (RR=0.87, 95% CI 0.78-0.98) in a cohort study including 74,961 Swedish men and women, aged 45-83 years without a history of stroke.

In terms of reductions in stroke risk associated with different dietary patterns, Agnoli et al. (2011) compared adherence to four commonly-recognized diet regimes and their impact on stroke risk, including the Healthy Eating Index 2005 (HEI-2005), Dietary Approaches to Stop Hypertension (DASH), Greek Mediterranean Index, and the Italian Mediterranean Index. There was an inverse relationship between adherence to each of the regimens and stroke occurrence. Overall, the Italian Mediterranean Index was the most protective (HR = 0.37, 95% CI = 0.19–0.70). A systematic review & meta-analysis was conducted by Psaltopoulou et al. (2013) to examine the protective effects associated with adherence to the Mediterranean diet. Of the 11 studies that were included that assessed stroke as an outcome, high adherence to a Mediterranean diet was associated with reduced risk of total stroke and ischemic stroke (total stroke: RR=0.71, 95% CI 0.57-0.89; ischemic stroke: RR=0.52, 95% CI 0.28-0.96). One of the key components of the Mediterranean diet is olive oil, which has been shown to decrease the risk of cardiovascular diseases. The Prevención con Dieta Mediterránea Trial (PREDIMED) evaluated the benefits of 2 types of Mediterranean diet, increased consumption of extra-virgin olive oil or mixed nuts, as compared to a control group in which participants were advised to follow a low-fat diet (Estruch et al. 2013). After a median follow-up of 4.8 years, the two Mediterranean diets were associated with 30% reductions in the primary outcome, a composite of myocardial infarction, stroke, or death from cardiovascular causes. The majority of this protective effect was driven by a reduction in stroke events. The results of the PREDIMED study were included in a systematic review (Martınez-Gonzalez et al. 2014) specifically examining the protective effect of olive oil. For each 25 g/day increase in olive oil consumption there was a significant reduction in the risk of stroke (RR=0.76, 95% CI 0.67-0.86, p<0.001). A systematic review and meta-analysis authored by Soedamah-Muthu et al. (2013) provides evidence of the reduced risk of stroke associated with a dietary approach similar to the Mediterranean-style diet, the DASH style diet, which is characterised by fruits, vegetables, and low-fat or non-fat dairy, as well as less-refined grains. High adherence was protective for the development of cardiovascular disease (RR=0.80, 95% CI 0.74-0.86). Larsson et al. (2016) also reported that high adherence to a modified DASH diet was associated with a reduced risk of ischemic stroke, particularly among women. The study included a population-based sample of almost 75,000 individuals without history of stroke, heart disease or cancer, who were followed for an average of 11.9 years.

Vitamin B supplementation to Reduce the Risk of Recurrent Stroke
Hyperhomocysteinemia has been associated with premature atherosclerosis and an increased risk of cardiovascular events, including stroke. Since low serum levels of B vitamins, including B6, B12 and folic acid are associated with elevated homocysteine levels, supplementation has been examined as a potential means to reduce stroke risk. Two large trials have been published which included persons exclusively with recent stroke. In the VITAmins TO Prevent Stroke (VITATOPS) trial (Hankey et al. 2010) participants were randomized to receive B vitamins (2 mg folic acid, 25 mg vitamin B6, and 0.5 mg vitamin B12) or placebo for the duration of the trial. After a median duration of follow-up of 3.4 years, there was a borderline significant reduction in the risk of the composite outcome, which included stroke, MI and vascular death in the vitamin B group (15% vs. 17%, RR=0.91, 95% CI 0.82-1.00, p=0.05, absolute risk reduction of 1.56%, 95% CI -0.01-3.16). The risk of fatal or nonfatal stroke was not reduced significantly with vitamin supplementation (9% vs. 10%, RR=0.92, 95% CI 0.81-1.06, p=0.25). Toole et al. (2004) randomized 3,680 patients with a total homocysteine level ≥25th percentile to receive high-dose B vitamins (25 mg B6, 0.4 mg B12, and 2.5 mg folic acid) or low-dose B vitamins (200 µg B6, 6 µg B12, and 20 µg folic acid) in the Vitamin Intervention for Stroke Prevention (VISP) trial. The mean duration of follow-up was 20.3 months. There was no significant difference between groups in the relative 2-year risk of recurrent cerebral infarction (8.1% vs. 8.4%, RR=1.0, 95% CI 0.8-1.3).

Sodium
It is well documented that a consistently high dietary sodium intake is associated with elevated blood pressure, while modest decreases may lower blood pressure and reduce stroke risk. Mozaffarian et al. (2014) used various data sources and national-level surveys to estimate that, in 2010, 99% of all adults in the world exceeded the WHO recommendations of 2.0 g/day. Worldwide, the mean global level of sodium intake was 3.95 g/day. An estimated 1.65 million deaths were attributed to sodium intake above the recommended level, of which 685K (42%) were caused by stroke. Feigin et al. (2016) estimated that 22.6% of the global stroke burden was attributed to diets high in sodium (12.6% in Canada). In a Cochrane review, He et al. (2013) examined 34 RCTs (n=3,230) comparing the effect of moderately restricted sodium intake (2.3-7.0 g/day or 40-120 mmol/day urinary sodium excretion) for a minimum of 4 weeks with usual intake over the same duration. The mean difference in sodium intake between groups was 1,955 mg per day, which was associated with a significant decrease in SBP (-4.18 mmHg, 95% CI -5.18 to -3.18; p<0.001) and DBP (-2.06 mmHg, 95% CI -2.67 to -1.45; p<0.001). Results were similar in a subgroup analysis of 22 trials that included 990 patients with hypertension. Reduced intake was associated with a significant reduction in both SBP (-5.39 mmHg, 95% CI -4.15 to -6.62; p<0.001) and DBP (-2.82 mmHg, 95% CI -2.11 to -3.54; p<0.001). Abuerto et al. (2013) identified 36 RCTs (n=5,508; n with hypertension=1,478) also comparing the effects of decreased sodium vs. higher sodium intake. The mean between group difference in sodium intake was ≥40 mmol/day. Reduced sodium intake was associated with a mean SBP reduction of 3.39 mm Hg (95% CI 2.46 to 4.31) in all participants and a mean SBP reduction of 4.06 mm Hg (95% CI 2.96 to 5.15) in participants with hypertension. In trials where the relative sodium reduction of subjects in the intervention group was <1/3 of the control group, there was a significant reduction in both SBP (MD= -1.45, 95% CI -2.29 to -0.60) and DBP (MD= -0.74, 95% CI -1.28 to -0.19). In trials where the relative sodium reduction of subjects in the intervention group was ≥1/3 of the control group, the reductions in both SPB and DBP were even greater (SBP: MD= -3.79, 95% CI -4.82 to -2.75 and DBP: MD= -1.68, 95% CI -2.34 to -1.02). There is evidence of a U-shaped pattern associated with sodium intake and stroke risk/mortality. Graudal et al. (2014) included the results of 23 cohort studies (n=274,683) and reported that usual daily sodium intake (115 -215 mmol) was associated with a significantly lower risk of all-cause mortality compared with low-sodium intake (<115 mmol), with no effect on stroke risk. High sodium intake (>215 mmol) was associated with an increased risk of both stroke and all-cause mortality, compared with usual sodium intake. O’Donnell et al. 2014 reported that sodium intake between 3 g (130 mmol) and 6 g (260 mmol) per day was associated with a lower risk of death and cardiovascular events than either a higher or lower level of sodium intake.

Exercise
Physical activity is an important modifiable lifestyle factor that can play a protective role in both primary and secondary prevention of stroke. Using data from 188 countries, obtained from the Global Burden of Disease Study, Feigin et al. (2016) reported that 7.7% of the global stroke burden was attributed to low physical activity. In Canada, the estimate was 10.9%. The results from several large cohort studies provide some estimates of the magnitude of the protective effect of physical activity. Armstrong et al. (2015) included 1.1 million women who were participants of the Million Women Study, which investigated how various reproductive and lifestyle factors affect women’s health. Women who engaged in strenuous physical activity 1-3x/week had a lower risk of both intracerebral hemorrhage and ischemic stroke compared with women who rarely or never engaged in such activity. The effect was U-shaped such that the risk of stroke was not reduced significantly for women who engaged in strenuous activity more than three times per week. In the REGARDS study,a large prospective cohort study including 30,239 US residents aged ≥45 years, McDonnell et al. (2013) reported that the risk of stroke was increased in persons who engaged in no physical activity, compared to persons who exercised ≥4x/week (HR= 1.20, 95% CI, 1.02–1.42). In phase 1 of the INTERSTROKE case-control study, O’Donnell et al. (2010) reported that regular physical activity was associated with a reduced risk of total and ischemic stroke (total stroke: OR=0.69, 99% CI 0.53-0.90, ischemic stroke: OR=0.68, 99% CI 0.51-0.91). In phase 2 of the INTERSTROKE study (O’Donnell et al. 2016, the pattern of results was similar. There was a decreased risk of total, ischemic and hemorrhagic stroke associated with regular physical activity. While Sattelmair et al. (2010) reported that increasing amount of time spent engaged in physical activity was not associated with decreased total stroke risk in 39,315 healthy women who had been participants of the Women’s Health Study (1992-1995), those who walked ≥2 hours per week had a 30% lower risk of any stroke than women who did not walk (RR=0.70 95% CI, 0.52 to 0.94). Additionally, women who reported walking at a brisk pace (4.8 km/hour) had a 37% lower risk (RR=0.63, 95% CI, 0.44 to 0.91) compared with women who did not walk. Lee et al. (2003) published a meta-analysis of 23 studies published between 1983 and 2002 examining the association between physical activity and stroke incidence or mortality and reported a dose-response relationship. Highly active individuals had a 27% lower risk of stroke than individuals who were designated as “low active.” Individuals who were designated as moderately active also had a significantly reduced risk of ischemic and hemorrhagic strokes when compared with low active individuals (RR = 0.80, 95% CI 0.69-0.91< 0.001).

Weight
Evidence suggests there is an increased risk of stroke associated with being overweight or obese. Feigin et al. (2016) reported that 23.5% of the global stroke burden was attributed to high BMI (>23.0), while in Canada the estimate was 28.4%. Twig et al. (2016) included 2.3 million adolescents who were followed over time to examine the association between BMI and cardiovascular death. During 42,297,007 person-years of follow-up, there were 32,127 deaths, including 528 from stroke. Compared with the reference category (BMI percentile 5th-24th), the risk of death from stroke was significantly increased in the 3 highest BMI categories, in which the median BMI (men and women combined) were 24.4, 26.6 and 31.0, respectively (75th-85th: HR=1.42, 85th-94th: HR=1.81, ≥95th: HR=2.64). Saito et al. (2011) compared stroke risk in 32,847 men and 38,875 Japanese women, aged 45–74 years with no history of cardiovascular disease, who were of normal weight (BMI 23.0-24.9 kg/m2) with persons who had high BMIs (27.0 to 29.9 and ≥ 30.0). The risk of stroke significantly increased with increasing BMI (HR= 1.09 and 1.25 for men, and HR=1.29 and 2.16 for women, respectively, relative to healthy weight). In women, a weight increase of greater than 10% over the previous five years was also associated with increased stroke risk. Bazzano et al. (2010) reported similar findings in a study of 154,736 Chinese men and women ≥ 40 years. The risk for stroke increased significantly for persons considered overweight (BMI 25.0 to 29.9, HR=1.43, 95% CI 1.36-1.52) and for those who were obese (BMI≥ of 30, HR=1.72, 95% CI 1.55-1.91). In phases 1 and 2 of the INTERSTROKE case-control study, O’Donnell et al. (2010, 2016) reported that increasing weight-to-hip ratio was associated with increased risk of total stroke, ischemic stroke and hemorrhagic stroke. Hu et al. (2007) studied 49,996 men and women aged 25-74 years with no history of stroke or coronary heart disease. BMI, waist circumference and waist-hip measures were obtained at baseline and stroke risk was assessed after an average follow up of 9.5 years. The risk of all stroke and ischemic stroke were increased in both men and women with increasing BMI, while increased waist circumference and waist-to-hip ratio were risk factors for total and ischemic stroke in men, but not women.

Alcohol Consumption
Evidence from several studies suggest that light to moderate alcohol consumption may reduce the risk of stroke, while excessive consumption may increase risk. Zhang et al. (2014) used the results of 27 prospective studies including 1,425,513 adult participants to estimate this dose-response relationship. The relationship between ETOH dose and stroke risk was found to be j-shaped, with alcohol intake of 0-20 g/day associated with a significant reduction and intake above 40 g/day associated with increased risk. The association between alcohol consumption and risk of stroke may be different for men compared with women. Zheng et al. (2015) pooled the results from 23 cohort studies and found that, compared with the lowest or no alcohol groups, the risk of stroke was not significantly increased in men or women as alcohol consumption increased; rather, the risk of ischemic stroke was lower in men who were light drinkers and for women who were light or moderate consumers. In contrast, using the results from 26 studies, Patra et al. (2010) reported a dose-response relationship that was linear for hemorrhagic stroke, with increasing risk associated with increasing consumption, whereas there was a curvilinear relationship for ischemic stroke, with a protective effect of alcohol for low to moderate consumption and increased risk for higher exposure. Women who consumed 3 or more drinks on average/day had higher risk than men. O’Donnell et al. (2010) reported that moderate alcohol consumption (1-30 drinks/month) was associated with reduced risk of ischemic stroke (OR=0.79, 95% CI 0.63-1.00), but with an increased risk of hemorrhagic stroke (OR=1.52, 95% CI 1.07-2.16) compared with never/former drinkers. Binge drinking, or >30 drinks/month, was associated with an increased risk of ischemic and hemorrhagic stroke compared with never/former drinkers. In phase 2 of INTERSTROKE (O’Donnell et al. 2016) low or moderate ETOH intake was associated with significantly higher odds of total and hemorrhagic stroke compared with former/never drinkers, with no risk in the increase of ischemic stroke. A meta-analysis including 35 observational studies examining the effects of alcohol consumption on stroke risk over a follow-up period of 4-30 years revealed a J-shaped relationship between the amounts of alcohol consumed per day and the risk of ischemic stroke (Reynolds et al. 2003). Individuals who consumed <12 grams of alcohol per day had the lowest risk for ischemic stroke (RR = 0.80, 95% CI 0.67-0.96), while those having more than 60 grams/day had the highest risk (RR = 1.69, 95% CI 1.34-2.15) when compared with a group of abstainers.

Birth Control/Hormone Replacement Therapy
Women taking oral contraceptive or hormone replacement therapy (HRT) may be at an increased risk of stroke. Bath & Gray (2005) conducted a meta-analysis including the results from 28 RCTs and found that HRT was associated with significant increases in the risk of total stroke (OR =1.29, 95% CI 1.13 to 1.47), non-fatal stroke (OR=1.23, 1.06 to 1.44), stroke leading to death or disability (OR=1.56, 1.11 to 2.20), and ischaemic stroke (OR=1.29, 1.06 to 1.56). They also reported that hormone replacement therapy was not associated with hemorrhagic stroke (OR=1.07, 0.65 to 1.75) or transient ischaemic attack (OR=1.02, 0.78 to 1.34). Similarly, Renoux et al. (2010) reported that, compared to non-users, women using oral hormone replacement therapy within the previous year had a higher risk of stroke (RR= 1.28, 1.15-1.42). Use of oral HRT for >1 year was associated with increased risk of stroke (RR=1.35, 95% CI 1.20-1.52), but not for a duration of ≤1 year. High dose transdermal patch use was associated with an increased risk of stroke (RR=1.89, 95% CI 1.15-3.11), although low- dose patches were not (RR=0.95, 0.75-1.20).

In terms of elevated risk of stroke associated with hormonal forms of birth control, the evidence is equivocal. In a large cohort study including the results of over 1.6 million women between the ages of 15 and 49 years, Lidegaard et al. (2012) reported that current use of ethinyl estradiol at doses of 20 to 50 μg was associated with an increased risk of thrombotic stroke, compared with nonusers, while current use of progestin only was not. In a large cohort study of 49, 259 Swedish women aged 30-49, Yang et al. (2009) reported that the risk of fatal or nonfatal ischemic or hemorrhagic stroke was not significantly increased. The associations were not influenced by age at menarche nor with parity status.

Recreational Drug Use
The most commonly-used illicit drugs associated with increased stroke risk are cocaine, amphetamines, Ecstasy, heroin/opiates, phencyclidine (PCP), lysergic acid diethylamide (LSD), and cannabis/marijuana. These drugs may increase the risk for stroke through a variety of mechanisms, including hypertensive surges, vasospasm, enhanced platelet aggregation, vasculitis, accelerated atherosclerosis and cardioembolism. Kaku & Lowenstein (1990) reported that the risk of stroke associated with (any) drug abuse was significantly higher compared with non-drug users (RR=06.5, 95% CI 3.1-13.6). There was a strong temporal relationship whereby the risk was highest during the first 6 hours after use and decreased over time. Cheng et al. (2016) examined whether recent cocaine use increased the risk of stroke. Cocaine use within 24 hours of the reference date was associated with a significantly increased risk of ischemic stroke (OR=6.4, 95% CI 2.2-18.6, p<0.001), as was frequent use (≥1/week; OR=2.6, 95% CI 1.6-4.3, p<0.001). An increased risk of stroke associated with cocaine use was also reported by Westover et al. (2007) in a cohort of patients recently discharged from hospital. Previous cocaine use was associated with an increase in the risk of both hemorrhagic and ischemic stroke (OR=2.33, 95% CI 1.74-3.11and OR=2.03, 95% CI 1.48-2.79, respectively). In the same study, amphetamine use was also associated with an increase in the risk of hemorrhagic stroke (OR=4.95, 95% CI 3.24-7.55) and an increased risk of hemorrhagic stroke resulting in death (OR=2.63, 95% CI 1.07-6.50). The association between cannabis use and stroke does not appear to be as strong. While Barber et al. (2013) found no association between stroke and cannabis use (OR=1.59, 95% CI 0.71-3.70), Westover et al. (2007) reported that cannabis use was associated with an increased risk of ischemic stroke (OR=1.76, 95% CI 1.15-2.71) but not hemorrhagic stroke (OR=1.36, 95% CI 0.90-2.06), after adjusting for age, sex, ethnicity and current tobacco use.

Smoking
Smoking is a major risk factor for cardiovascular disease, including stroke and heart attacks. Smokers are significantly more likely to have a stroke compared with non-smokers.   It has been estimated that globally, 20.7% of the stroke burden is attributable to tobacco use (Feigin et al. 2016). There appears to be a dose-response relationship between increased cigarette smoking and stroke risk. In The Physician’s Health Study (Robbins et al. 1994), the risk of non-fatal stroke was significantly higher among those currently smoking ≥20 cigarettes/day compared with those who never smoked. (RR=2.52, 95% CI 1.75 to 3.61). For those currently smoking <20 cigarettes/ day, the stroke risk remained elevated (RR=2.02, 95% CI 1.23 to 3.31). A recent systematic review & meta-analysis (Peters et al. 2013) that reported sex-specific risk of current smokers vs. non-smokers included the results from 81 prospective cohort studies, which represented 3,980,359 persons. The prevalence of current smoking ranged from 8% to 59% in men and from 1% to 51% in women. Most studies reported higher smoking rates among men. Over the duration of follow up, which ranged from 6-40 years, there were 42,401 strokes. The risk of stroke was higher in current smokers compared with non-smokers in both women: (RR=1.83, 95% CI 1.58-2.12) and men (RR=1.67, 95% CI 1.49-1.88). The risk of stroke was also higher in former smokers compared with never smokers (women: RR=1.17, 95% CI 1.12-1.22; men: RR=1.08, 95% CI 1.03-1.13). The risk of hemorrhagic, but not ischemic stroke, was significantly increased in women who smoked compared with men who smoked (RR=1.17, 95% CI 1.02-1.34, p=0.02). An increased risk of all stroke (OR=2.09, 99% CI 1.75-2.51), ischemic stroke (OR=2.32, 99% CI 1.91-2.81) and hemorrhagic stroke (OR=1.45, 99% CI 1.07-1.96) was also associated with current smoking in Phase 1 of the case-control INTERSTROKE Study (O’Donnell et al. 2010). In phase 2 of the study (O’Donnell et al. 2016), which included a larger sample size (26,919), the risk of ischemic stroke was higher among current smokers compared with the risk of hemorrhagic stroke (OR=1.93, 99% CI 1.69-2.21 vs. OR=1.14, 99% CI 0.95-1.36). The risk of both stroke types increased with the number of cigarettes smoked daily. Results from the Cardiovascular Health Study (Kaplan et al. 2005) including persons over the age of 65 years, indicated that smoking was associated with a significantly increased risk for stroke recurrence (HR= 2.06; 95% CI, 1.39–3.56).

Both pharmacological agents and behavioural intervention strategies have proved effective as smoking cessation interventions. A Cochrane review of reviews that examined the effectiveness of pharmacological treatments to promote smoking cessation in adults was included the results of 12 Cochrane reviews, aggregating the results from 267 RCTs, 101,804 participants (Cahill et al. 2013). Treatments evaluated included nicotine replacement products, such as gums, transdermal patches, nasal sprays or inhalers, the non-tricyclic antidepressant, bupropion and varenicline, a nicotinic receptor partial agonists. Compared with placebo, all forms of therapies significantly increased the odds of sustained smoking cessation (odds ratios ranged from 1.82-2.88). Varenicline was superior to single forms of nicotine replacement therapy (OR= 1.57, 95% Credible interval [Cred I] 1.29 to 1.91) and was also superior to bupropion (OR= 1.59, 95% CredI 1.29 to 1.96). The odds of serious adverse events (chest pains and heart palpitations) associated with nicotine replacement therapy were significantly increased (OR= 1.88, 95% CI 1.37- 2.57). The most common side effects associated with bupropion were insomnia, occurring in 30% to 40% of patients, dry mouth (10%) and nausea. The main serious adverse event was seizures. The main adverse event for varenicline was mild-moderate nausea, which subsided over time and was rarely reported. Typical drop-out rates due to adverse events ranged from 7% to 12%.

Non-pharmacological and combination therapy have been shown to be effective in achieving sustained smoking cessation. A recent Cochrane Review authored by Stead & Lancaster (2012a) evaluated behavioral support with the addition of the availability of pharmacotherapy compared with a control condition receiving usual care or brief advice or less intensive behavioural support. The results from 41 RCTs including participants from both community and healthcare settings, most of whom smoked >20 cigarettes/day, were included. Most studies supplied nicotine replacement therapy (provided as patch or gum) while behavioural support was typically provided by specialists in cessation counselling, but was also provided by peer counsellors, trained nurses and usual care providers and took the forms of telephone, mail, individual and group sessions. Combination therapy was associated with the greatest chance of cessation of smoking at 6 months (RR=1.82, 95% CI 1.66-2.00, p< 0.0001). In studies that recruited participants from healthcare settings, the probability of success was greater (RR=2.06 vs. 1.53). There was no association between number of sessions provided and success of quitting (1-3 vs. 4-8 vs. >8) or the planned duration of contact (total minutes) (up to 30 vs. 31-90 vs. 91-300 vs. >300).

Mullen et al. (2016) examined the use of the Ottawa Model’ for Smoking Cessation (OMSC), a systematic approach to tobacco dependence treatment delivered within healthcare settings, which included in-hospital counselling, and pharmacotherapy follow-up support post hospitalization. At one and two years, the cumulative incidences of death and all-cause re-hospitalizations, and smoking-related readmissions were significantly lower in the OMSC group. All-cause emergency department visits were also significantly reduced in the intervention group. In this trial patients in the control group were randomized to usual care, which generally consisted of a self-help pamphlet.

Motivational interviewing, by itself has also shown to be an effective strategy to achieve sustained smoking cessation. Using the results from 14 RCTs, Lai et al (2010) examined the use of 1-4 sessions (15-45 minutes/session) of motivational interviewing (MI) compared with control groups who received brief advice, or routine care. Motivational interviewing was associated with a significantly increased probability of achieving long-term smoking cessation (RR 1.27, 95% CI 1.14- 1.42). Chances of success were greater when delivered by a general practitioner, compared with a nurse or counsellor. While both single compared and multiple sessions were both effective, sessions of >20 minutes duration were more effective compared with shorter sessions (RR= 1.31, 95% CI 1.16 to 1.49 vs. 1.14, 95% CI 0.80 to 1.16).

The use of electronic cigarettes (e-cigarettes) has increased in recent years, and remains controversial. They may be used as an alternative to conventional cigarettes or as an aid in smoking cessation programs. The current practice recommendations make no statements regarding their use. Although the use of e-cigarettes has been shown to significantly reduce the use of conventional cigarettes, in persons who wish to quit smoking (and in those with no desire to quit), data regarding their safety are limited.

Compliance with Secondary Prevention Measures
Since rates of recurrent stroke, and other vascular disorders are known to be significantly elevated during the first four years after hospitalization for first stroke (Feng et al. 2010), and potentially modifiable risk factors represent approximately 90% of the population-attributable risk for stroke (O’Donnell et al. 2016), secondary prevention measures represent an important opportunity to reduce the risk. While the effectiveness of many of the interventions designed to prevent recurrent stroke, including medications associated with hypertension, diabetes, dyslipidemia and cardiac conditions (described in other sections of the guidelines) are well-established, their protective effects are diminished by poor compliance. Poor- or non-compliance to recommended medications may be due to several factors including inadequate or marginal health literacy, number of co-morbid conditions, adverse effects of treatment and cost (MacLaughlin et al. 2012). Non-compliance with diet regimens and other lifestyle factors is often a result of the interplay between patients’ age, emotions, the reason they were given to control diet as well as their ability or desire to return for follow-up education (Travis 1997). Additional stroke-related factors, such as a lack of motivation, musculoskeletal issues, fatigue, and increasing age, may pose barriers to compliance with exercise programs or reduced leisure activities (Jurkiewicz et al. 2011). Therefore, early initiation of effective post stroke prevention strategies, maintained indefinitely with continuous monitoring by way of follow-up appointments, home visits or telephone check-in is essential. Bushnell et al. (2014) suggest a comprehensive model of stroke prevention, including the recognition of non-adherence, and understanding the factors associated with non-adherence. Moreover, clinician need to consider their patient demographic how they deliver secondary prevention treatment, with an emphasis on communication and education (Travis 1997, Hedegaard et al. 2015).