Article

Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components.

Brooklyn Center for Health Disparities, SUNY Downstate Medical Center Brooklyn, NY 11203-2098, USA.
Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine (Impact Factor: 2.83). 07/2008; 4(3):261-72.
Source: PubMed

ABSTRACT Although obstructive sleep apnea and cardiovascular disease have common risk factors, epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension). Individuals with severe sleep apnea are at increased risk for coronary artery disease, congestive heart failure, and stroke. The underlying mechanisms explaining associations between obstructive sleep apnea and cardiovascular disease are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of cardiovascular disease. Linkage between obstructive sleep apnea and cardiovascular disease is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and cardiovascular disease, which may be compounded by the involvement of diseases comprising the metabolic syndrome (i.e., central obesity, hypertension, diabetes, and dyslipidemia). Large-scale, population-based studies testing causal models linking among sleep apnea, cardiovascular morbidity, and metabolic syndrome are needed.

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    ABSTRACT: Sleep disorders are the " orphans " of medical practice , despite the fact that up to 40% of all primary care attendees have sleep symptoms and in psychiatry and neurology practice this percentage rises (1). The disturbances of sleep include: difficulty falling asleep or staying asleep, abnormal daytime sleep, and special phenomena occurring during sleep. The first description of periodic breathing in a patient with cardiac disease and " apoplexy " appeared in 1818 in Cheyne'a paper (2), and. Jackson later recognized that this breathing pattern frequently accompanies bilateral hemispheric stroke (3). In 1877, Broad-bent reported features consistent with obstructive sleep apnea in a patient with intracerebral hemorrhage (4). At the beginning of the 20th century thalamic and mesencephalic strokes were recognized as more commonly associated with severe, post-stroke hyper-somnia (5). Neurogenic insomnia (agrypnia) related to thalamo-mesencephalic stroke was first described by Lhermitte in 1922 and van Bogaert in 1926, respectively (6). More recently, the link between sleep-disordered breathing and vascular disorders including stroke has been recognized and discussed in detail. Sleep-disordered breathing (SDB, e.g., Cheyne-Stokes breathing) and sleep-wake disturbances (SWD) are frequent in stroke patients, and SDB may increase the risk of stroke recurrence. They deserve attention, because they may significantly influence rehabilitation process and functional outcome. However, SDB and SWD are often neglected in stroke patients. Recent studies suggest that they are frequent and have an impact on stroke outcome. More than 50% (50-70%) of stroke patients have SDB, mostly obstructive sleep apnea (OSA)(6,7,8). Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. In recent paer Fava et al (9) underly that even increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease-related mortality , but it still largely unclear whether this association is causative or simply speculative and epidemiological. Basically, reliable clinical evidence supports the hypothesis that OSAS might be associated with essential and resistant hypertension, as well as with an incremental risk of developing stroke, cardiac rhythm perturbations (e.g., atrial fibrillation, bradyarrhyth-mias, supraventricular and ventricular arrhythmias), coronary artery disease, acute myocardial infarction, and heart failure. Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes , and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intratho-racic pressure, micro-arousal, sympathetic hyperactiv-ity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulabil-ity, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders (9). So, the epidemiologic studies show that sleep ap-nea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking,
    Acta Clinica Croatica, Supplement 01/2011; 50(Suppl 3):33-34.
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    ABSTRACT: This study aimed to explore the impact of an 8-year therapy with autoadjusting positive airway pressure (APAP) on fasting lipid level in a sample of Portuguese moderate/severe obstructive sleep apnea (OSA) patients. Besides contributing to the comprehension of the complex relationship between dyslipidemia and OSA, it provided new data regarding the effectiveness of a long term APAP treatment. Thirty-nine male patients with moderate to severe OSA were included in the study. APAP was prescribed to all patients. Fifteen patients were under lipid-lowering medication throughout the study, and another 15 patients never used lipid-lowering medication at any time during the study. Fasting morning venous blood samples were collected at three time points (baseline 6 months and 8 years) and lipids were estimated. Statistical analysis was performed using Statistical Package for the Social Sciences (SPSS) 21.0 software. After 8 years of APAP treatment, patients presented a similar body mass index but a significantly less severe daytime sleepiness. Patients on lipid-lowering medication exhibited a higher reduction in total cholesterol than those naïf from that medication, but the reduction was not statistically significant after adjusting for medication and APAP adherence. Long-term APAP treatment improves OSA but does not seem to contribute to changes in fasting lipids.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sleep disorders are the " orphans " of medical practice , despite the fact that up to 40% of all primary care attendees have sleep symptoms and in psychiatry and neurology practice this percentage rises (1). The disturbances of sleep include: difficulty falling asleep or staying asleep, abnormal daytime sleep, and special phenomena occurring during sleep. The first description of periodic breathing in a patient with cardiac disease and " apoplexy " appeared in 1818 in Cheyne'a paper (2), and. Jackson later recognized that this breathing pattern frequently accompanies bilateral hemispheric stroke (3). In 1877, Broad-bent reported features consistent with obstructive sleep apnea in a patient with intracerebral hemorrhage (4). At the beginning of the 20th century thalamic and mesencephalic strokes were recognized as more commonly associated with severe, post-stroke hyper-somnia (5). Neurogenic insomnia (agrypnia) related to thalamo-mesencephalic stroke was first described by Lhermitte in 1922 and van Bogaert in 1926, respectively (6). More recently, the link between sleep-disordered breathing and vascular disorders including stroke has been recognized and discussed in detail. Sleep-disordered breathing (SDB, e.g., Cheyne-Stokes breathing) and sleep-wake disturbances (SWD) are frequent in stroke patients, and SDB may increase the risk of stroke recurrence. They deserve attention, because they may significantly influence rehabilitation process and functional outcome. However, SDB and SWD are often neglected in stroke patients. Recent studies suggest that they are frequent and have an impact on stroke outcome. More than 50% (50-70%) of stroke patients have SDB, mostly obstructive sleep apnea (OSA)(6,7,8). Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. In recent paer Fava et al (9) underly that even increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease-related mortality , but it still largely unclear whether this association is causative or simply speculative and epidemiological. Basically, reliable clinical evidence supports the hypothesis that OSAS might be associated with essential and resistant hypertension, as well as with an incremental risk of developing stroke, cardiac rhythm perturbations (e.g., atrial fibrillation, bradyarrhyth-mias, supraventricular and ventricular arrhythmias), coronary artery disease, acute myocardial infarction, and heart failure. Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes , and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intratho-racic pressure, micro-arousal, sympathetic hyperactiv-ity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulabil-ity, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders (9). So, the epidemiologic studies show that sleep ap-nea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking,
    Acta Clin Croat 2011; 50 (Supl 3): 33-34.; 01/2011

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