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Sleep, Stroke and Cardiovascular Disease
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Book description

The relationship between sleep disorders – in particular sleep apnea, a highly prevalent condition – and common vascular disturbances such as stroke and hypertension is an area of active research. Summarizing the clinical evidence to date between sleep disorders and vascular pathology, this is the first time a comprehensive overview of this relationship has been covered in a single volume. Bringing together some of the world's most renowned authors in the field, Sleep, Stroke and Cardiovascular Disease contains recommended treatment plans – allowing for rapid and accurate diagnosis and management of patients – enabling learning from real experience. Of interest, not only, to specialists who intervene in diagnosis and management of sleep and stroke disorders such as neurologists, cardiologists and pulmonologists, the book will also be of value to primary-care practitioners, allowing them to arrive at better diagnoses and management of sleep and vascular disorders.

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Contents

  • Chapter 7 - Patent foramen ovale, obstructive sleep apnea, and its association with ischemic stroke
    pp 85-96
  • View abstract

    Summary

    The sleep apnea syndrome occurs in 4% of adult men and 2% of adult women. Inflammation and hypoxia are intertwined at the molecular, cellular, and clinical levels. Sleep apnea influences heart rate variability, during sleep and during wakefulness. It is also an independent risk factor for stroke. Sleep apnea may also lead to cognitive dysfunction from the effects of chronic hypoxia and sympathetic stress associated with small-vessel disease in the brain, white matter ischemia, and lacunar strokes. This syndrome is a modifiable risk factor and therefore efforts to control this condition in patients at risk of vascular disease is a clinical endeavor that should be pursued vigorously, even though clinical research needs to persist in its quest to answer pressing pathophysiological questions. Emerging evidence suggests that restless legs syndrome (RLS) and periodic limb movements of sleep (PLMS) represent risk factors for cardio- and cerebrovascular disease, even leading to stroke.
  • Chapter 8 - Pathogenesis of cerebral small-vessel disease in obstructive sleep apnea
    pp 97-103
  • View abstract

    Summary

    This chapter highlights the significance of oxidative stress and vascular inflammation in promoting endothelial disease and atherosclerosis in sleep apnea patients, with an emphasis on the contribution of these mechanisms to the development of cardiovascular morbidity and stroke in these patients. Most studies investigating oxidative stress in patients with obstructive sleep apnea (OSA) present indirect findings by using various bodily fluid markers such as plasma, serum, or urine. The presence of IH is a key factor in initiating proatherogenic activity and a likely link for the close association between OSA and cardiovascular diseases. Increased oxidative stress, vascular inflammation, and endothelial dysfunction resulting from intermittent hypoxia (IH) can lead to high susceptibility of patients with OSA to stroke. The balance between proatherogenic and protective mechanisms may determine the predisposition of OSA patients to stroke or other cardiocerebrovascular diseases.
  • Chapter 9 - Sleep apnea and acute stroke deterioration
    pp 104-114
  • View abstract

    Summary

    This chapter discusses the interactions between obstructive sleep apnea syndrome (OSAS) and cardio- and cerebrovascular diseases, focusing on the mechanisms by which OSA may contribute to the onset and progression of cardiovascular diseases. The autonomic nervous system (ANS) is closely related to sleep from anatomical, physiological and neurochemical points of view, resulting in dynamic synchronous fluctuations in sleep phases and autonomic functions. Analysis of the circadian rhythm of heart rate variability shows that the mean high-frequency value from morning to noon is lower, whereas the mean low-frequency/high-frequency ratio is higher in OSAS patients than in controls. Measuring ANS function by means of spontaneous baroreflex cardiac modulation or other methods may not only help recognize the severity and prognostic relevance of the cardiovascular effect of OSA, but can shed light on the pathophysiological mechanisms that transform transient nocturnal alterations into sustained 24-hour derangements that require treatment.
  • Chapter 10 - Effect of continuous positive airway pressure on stroke risk factors and stroke
    pp 115-126
  • View abstract

    Summary

    Studies in hypertensive populations to date suggest that nondipping during the night, heightened blood pressure variability during the night, and nocturnal hypertension all predict future risk for cardiovascular morbidity and mortality, and are better prognostic factors than daytime hypertension. This chapter discusses the effects of sleep apnea treatment on hypertension. Although the prevalence of obstructive sleep apnea (OSA) increases with age, younger patients with OSA may be more prone to having cardiovascular consequences, including hypertension. Several studies suggest that the association between OSA and hypertension is more robust in the non-elderly. Different screening questionnaires have been developed and tested in attempts to identify patients at high risk for OSA. More studies are necessary to further elucidate pathogenetic mechanisms by which OSA causes hypertension and to determine the magnitude of the effect of OSA and its treatments on blood pressure.
  • Chapter 11 - Rehabilitation of stroke and sleep apnea
    pp 127-138
  • View abstract

    Summary

    Evidence suggests that untreated obstructive sleep apnea (OSA) is a significant health risk for the development of hypertension, cardiovascular disease, and stroke. OSA is independently associated with obesity, hypertension, and insulin resistance/diabetes mellitus, the three stroke risk factors of the metabolic syndrome. Studies in normal subjects and sleep apneic patients suggest that upper airway occlusion induces arousal from non-rapid eye movement (NREM) sleep once the level of inspiratory effort reaches a certain value, which varies among individuals. During apnea there are several stimuli that are well known to be able to induce arousal, including hypercapnia, hypoxia, and increased airway resistance. Cohort studies have shown OSA to be a risk factor for stroke. OSA is associated with a variety of stroke risk factors that may independently contribute to stroke risk. This suggests the potential for a cause-and-effect relationship between untreated OSA and stroke in some cases.
  • Chapter 12 - Restless legs syndrome, periodic limb movements in sleep, and vascular risk factors
    pp 139-150
  • View abstract

    Summary

    Anecdotal recognition of the relationship between sleep apnea and atrial fibrillation has recently given way to more rigorous observational data. The risk of recurrence after atrial fibrillation interventions has also been studied longitudinally. There are numerous pathophysiological mechanisms that may link sleep apnea to atrial fibrillation. One of the most important mechanisms may be the significant changes, both acute and chronic, in autonomic tone that occur with obstructive apneas. Most observational data suggest that the success rates of atrial fibrillation interventions, such as cardioversions and ablation, are significantly improved for patients whose sleep apnea is treated. Epidemiological studies suggest that sleep apnea is a risk factor for new-onset atrial fibrillation, and that its presence reflects a poorer prognosis after atrial fibrillation interventions. Randomized controlled trials are necessary to clarify the effects of sleep apnea therapy on atrial fibrillation outcomes in individuals and communities.
  • Chapter 13 - Physician as patient
    pp 151-154
  • View abstract

    Summary

    The mechanism by which patent foramen ovale (PFOs) are associated with ischemic stroke is believed to be paradoxical embolism. It has been observed that people with migraine with aura have a larger than expected concomitant prevalence of PFO compared to people without migraine. Transient global amnesia is considered to have a similar pathophysiology to migraine, and an association with PFO has also been observed. The mechanisms by which obstructive sleep apnea (OSA) increases the risk of ischemic stroke are multiple and all contribute to the ischemic event. As the risk seems associated with the multiple physiological abnormalities that accompany OSA and facilitated by a PFO, stroke prevention could potentially be achieved by improving OSA and reducing the right-to-left shunt treatment, antithrombotic therapy, PFO closure. Antithrombotic therapy should be given as well, in light of the greater overall cardiovascular risk.

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