2019
DOI: 10.3949/ccjm.86a.18033
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A sleeping beast: Obstructive sleep apnea and stroke

Abstract: Up to two-thirds of patients who have had a stroke have obstructive sleep apnea (OSA) afterward. These patients have worse outcomes than those without OSA in terms of short-term morbidity, functional and cognitive recovery, and mortality rates over the long term. Following a stroke, identifying OSA and treating it with positive airway pressure, if possible, are important clinical goals. KEY POINTS A low threshold for evaluating for OSA after a stroke is warranted: the prevalence is high in this population, and… Show more

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Cited by 18 publications
(8 citation statements)
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“…These individuals had poorer short-term sickness, cognitive and functional recovery, and long-term death rates than those without OSA. Detecting OSA and controlling it with positive airway pressure (PAP) are key therapeutic aims after a stroke [22]. People who have had a stroke often have trouble sleeping.…”
Section: Literature Reviewmentioning
confidence: 99%
“…These individuals had poorer short-term sickness, cognitive and functional recovery, and long-term death rates than those without OSA. Detecting OSA and controlling it with positive airway pressure (PAP) are key therapeutic aims after a stroke [22]. People who have had a stroke often have trouble sleeping.…”
Section: Literature Reviewmentioning
confidence: 99%
“…A AOS leva a piores desfechos clínicos após o AVC: maior tempo de hospitalização e de reabilitação, aumento na recorrência de AVC e elevada mortalidade. (61,63) A síndrome metabólica está fortemente associada à AOS, com consequente incremento no risco cardiovascular. (64) As características clínicas da síndrome metabólica são compartilhadas por pacientes com AOS: obesidade central, HAS, resistência à insulina, hiperglicemia e dislipidemia.…”
Section: Consequências Clínicasunclassified
“…The effects of apnoea/hypoxaemia cause stimulation of the sympathetic nervous system which releases catecholamines responsible for arterial hypertension which can be resistant, an increase in intra-thoracic pressure, cardiac rhythm disorders and altered cerebral haemodynamics [12][13].…”
Section: Pathophysiologymentioning
confidence: 99%
“…OSA may be the causative factor for silent brain infarcts [12][13] In OSA, platelet hyperaggregability is present and is thought to be due to high secretion of catecholamines. Increased haematocrit, fibrinogen and blood viscosity contribute to the development of thrombosis and early atherosclerosis, Another pathophysiological mechanism found in subjects with OSA that contributes to atherogenesis is increased levels of pro-inflammatory adipokines.…”
Section: Pathophysiologymentioning
confidence: 99%