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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During obstructive sleep apnea (OSA), systemic (Psa) and pulmonary (Ppa) arterial pressures acutely increase after apnea termination, whereas left and right ventricular stroke volumes (SV) reach a nadir. In a canine model (n = 6), we examined the effects of arousal, parasympathetic blockade (atropine 1 mg/kg iv), and sleep state on cardiovascular responses to OSA. In the absence of arousal, SV remained constant after apnea termination, compared with a 4.4 +/- 1.7% decrease after apnea with arousal (P < 0.025). The rise in transmural Ppa was independent of arousal (4.5 +/- 1.0 vs. 4.1 +/- 1.2 mmHg with and without arousal, respectively), whereas Psa increased more after apnea termination in apneas with arousal compared with apneas without arousal. Parasympathetic blockade abolished the arousal-induced increase in Psa, indicating that arousal is associated with a vagal withdrawal of the parasympathetic tone to the heart. Rapid-eye-movement (REM) sleep blunted the increase in Psa (pre- to end-apnea: 5.6 +/- 2.3 mmHg vs. 10.3 +/- 1.6 mmHg, REM vs. non-REM, respectively, P < 0.025), but not transmural Ppa, during an obstructive apnea. We conclude that arousal and sleep state both have differential effects on the systemic and pulmonary circulation in OSA, indicating that, in patients with underlying cardiovascular disease, the hemodynamic consequences of OSA may be different for the right or the left side of the circulation.
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PMID:Effects of arousal and sleep state on systemic and pulmonary hemodynamics in obstructive apnea. 1071 Apr 7

Obstructive sleep apnea (OSA) acutely increases systemic (Psa) and pulmonary (Ppa) arterial pressures and decreases ventricular stroke volume (SV). In this study, we used a canine model of OSA (n = 6) to examine the role of hypoxia and the autonomic nervous system (ANS) in mediating these cardiovascular responses. Hyperoxia (40% oxygen) completely blocked any increase in Ppa in response to obstructive apnea but only attenuated the increase in Psa. In contrast, after blockade of the ANS (20 mg/kg iv hexamethonium), obstructive apnea produced a decrease in Psa (-5.9 mmHg; P < 0.05) but no change in Ppa, and the fall in SV was abolished. Both the fall in Psa and the rise in Ppa that persisted after ANS blockade were abolished when apneas were induced during hyperoxia. We conclude that 1) hypoxia can account for all of the Ppa and the majority of the Psa response to obstructive apnea, 2) the ANS increases Psa but not Ppa in obstructive apnea, 3) the local effects of hypoxia associated with obstructive apnea cause vasodilation in the systemic vasculature and vasoconstriction in the pulmonary vasculature, and 4) a rise in Psa acts as an afterload to the heart and decreases SV over the course of the apnea.
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PMID:Neural and local effects of hypoxia on cardiovascular responses to obstructive apnea. 1071 Apr 8

Obstructive Sleep Apnea(OSA) is associated with an increased prevalence of cardiovascular complication such as systemic hypertension, ischemic heart disease and stroke, which may lead to unexpected or early death. Sleep in patients with OSA demonstrates a pattern of recurrent arousals, hemodynamic changes, and sympathetic neural activity that have been associated with adverse carviovascular events following awakening in the morning. Neurologic problems in patients with OSA include cognitive impairment, poor memory, and high risk for cerebral infarction. These central nervous system symptoms might be due to hypoxemia and sleep fragmentations. The vascular endothelial damage, platelet aggregation, and hemodynamic changes during sleep apnea are influenced by changes in oxygen and carbon dioxide tension inducing alterations of vascular tone. The cerebral hemodynamics in relation to apneas may not only influence daytime cerebral symptoms but may also have implications for the generation of cerebrovascular disease in OSA. These changes resulted from OSA might play an important role in pathophysiological aspects of the central nervous system. And these changes will be improved after CPAP application.
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PMID:[Abnormality of blood congulation]. 1094 24

Several epidemiological studies have suggested that sleep-disordered breathing is a risk factor for cardiovascular disease, particularly hypertension, stroke and IHD. The relative risk for IHD among obstructive SAS(OSAS) patients is 1.2 to 6.9 higher compared with the general population. The prevalence of SAS with an apnea-hypopnea index(AHI) of 10 and over was 35 to 40% in IHD, while 23.8% of SAS patients had IHD. These evidence suggests that IHD is an important prognostic factor in SAS patients. Characteristic pathophysiological conditions such as sleep apnea-induced hypoxemia and sympathetic activation may play an important role in the genesis of nocturnal angina pectoris. Most patients with OSAS are obese, and the complication of non-insulin dependent diabetes mellitus is quite a few. Insulin resistance is also attracting great attention as a cause of the cardiovascular complication of SAS.
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PMID:[Sleep apnea syndrome (SAS) and ischemic heart disease (IHD)]. 1094 39

In the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of repetitive episodes of hypoxia, hypercapnea, arousals, and a striking surge in sympathetic excitation, and altered baroreflex control during sleep. Obstructive sleep apnea (OSA) may lead to the cardiac arrhythmias and myocardial ischemia and it is a possible risk factor for stroke. We confirmed that nasal CPAP has been shown to lower blood pressure in some hypertensive OSA patients. Early recognition and treatment of sleep-apnea may improve cardiovascular function.
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PMID:[Hypertension and altered cardiovascular variability associated with obstructive sleep apnea]. 1094 41

Cerebrovascular accident is one of the most serious complications of sickle cell anemia. The specific factors that predispose patients with sickle cell anemia to stroke are increased disease severity, higher baseline white blood cell count and lower baseline hematocrits. Likewise the presence of a co-existent alpha thalassemia trait and/or high fetal hemoglobin (HbF%) may reduce the risk. We report a child with sickle cell anemia and marked adenotonsillar hypertrophy resulting in obstructive sleep apnea syndrome. There was no other known risk factor for developing cerebrovascular accident in this child during her hospitalization for adenotonsillectomy.
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PMID:Adenotonsillar hypertrophy: a precipitating factor of cerebrovascular accident in a child with sickle cell anemia. 1099 92

Obstructive sleep apnea (OSA) has many consequences. There is an independent association between OSA and hypertension. The Sleep Heart Health Study reported that hypertension prevalence increased as sleep disordered breathing severity increased. The Nurses' Health Study noted an age-adjusted relative risk of cardiovascular events of 1.46 for occasional snorers and 2.02 for regular snorers, and a risk of stroke of 1.60 for occasional snorers and 1.88 for regular snorers. Sleep apnea is also associated with pulmonary hypertension, neurocognitive effects, depressed quality of life, motor vehicle accidents, awakening headache, childhood growth interruption, pregnancy-induced hypertension, fetal growth retardation, and disruption of the patients' bed-partners' sleep quality. Further research will examine the possibility of causality, pathophysiologic mechanisms, and outcomes of therapeutic interventions for OSA on the many consequences of OSA.
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PMID:Complications and consequences of obstructive sleep apnea. 1110 Sep 57

The plasma level of fibrinogen is felt to be an independent risk factor for vascular events. Obstructive sleep apnea (OSA) has a high prevalence in patients with stroke and may also be an independent risk factor. The aim of our study was to determine the association between OSA and plasma levels of fibrinogen in patients with stroke. Polysomnography was performed during neurological rehabilitation in 113 patients (82 men, 31 women, age 58 +/- 11.1 yr, mean +/- SD) with ischemic stroke. OSA was absent (RDI < 5) in 44 patients, 42 had mild OSA (5 < or = RDI < 20), and 27 had moderate to severe OSA (RDI > or = 20). Parameters of OSA (respiratory disturbance index [RDI], oxygen indices) were correlated to plasma levels of fibrinogen, measured in the morning after admission to rehabilitation. Fibrinogen was positively correlated with RDI (r = 0.24, p = 0.007), duration of the longest apnea (r = 0.18, p = 0.049), and negatively correlated with several oxygen indices including average minimal oxygen saturation (r = -0.41, p < 0.001). Correlation coefficients were slightly higher when excluding patients with stroke of presumed cardiac origin. Multiple linear regression identified minimal mean oxygen saturation and sex as independent predictors of fibrinogen level. The correlation between severity of coexisting OSA and fibrinogen level in patients with stroke suggests a possible pathophysiological mechanism for an increased risk of stroke in patients with OSA.
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PMID:Fibrinogen levels and obstructive sleep apnea in ischemic stroke. 1111

Sleep disordered breathing (SDB), i.e., obstructive, central or mixed sleep apneas, has been recognized as a common occurrence in the elderly. Aging is per se associated with a decrease in the quality of sleep; SDB may further disrupt the sleep architecture in older subjects. The prevalence of obstructive sleep apnea (OSA) increases with aging; available studies report prevalence rates of 11-62%. Furthermore, OSA has been associated with increased mortality in older adults. Central apneas and periodic breathing occur with increased frequency either in subjects with neurological disorders such as infarction, tumor, sequelae of infection, diffuse encephalopathies, or in chronic heart failure. Patients with cerebrovascular disease (stroke, or transient ischemic attacks) have a markedly high prevalence of SDB, mainly OSA. In these patients, SDB is associated with a poorer functional prognosis at 3 and 12 months after the acute event, and a higher mortality. The clinical impact of SDB on cognitive function appears to be modest in patients without dementia, although there is a moderate increase in daytime sleepiness. In Alzheimer's disease (AD) however, SDB occurs more frequently than in non-demented older subjects, and its severity is correlated with the degree of cognitive impairment. The hypothesis of a causal relationship between AD and SDB remains a subject of controversy. The possibility of SDB should be considered in the elderly in the differential diagnosis of "reversible dementias", increased daytime sleepiness, or unexplained right-sided heart failure.
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PMID:Sleep disordered breathing in the elderly. 1121 51

We tested the hypothesis that intermittent apneas performed by awake subjects simulate obstructive sleep apnea (OSA) and change dynamic complexity of the cardiovascular control system by repetitive short time stimulation of arterial chemoreceptors. Correlation dimension (CD) and reccurent plot quantification calculated as ratio % determinism versus % recurrence (RDR) were used.as indices of chaotic dynamics. Thirty three normotensive subjects of mean age 21,58 +/- 4,1 performed 10 voluntary apneas 1 min. each separated by 1 min free breathing period. Systolic (SYS), diastolic (DIAS) arterial blood pressure was continuously recorded by finger volume clamp. Stroke volume (SV) was estimated by pulse pressure analysis. Cardiac output (CO) and total peripheral resistance (TPR) were calculated by Portapress system. Cardiac inter-beat interval (IBI) was measured from R-R intervals of ECG. Standard deviation (SD), an index of linear variability, was calculated in 1 min epoch. Dynamics of cardiovascular variables was computed in each subject during 20 min. rest (C), 20 min. of 10 apneas, 1 min each, separated by 1 min free breathing (A), and in 20 min. recovery free breathing (R). In A period CD of all circulatory variables was significantly reduced and RDR augmented. In 23 out of 33 subjects decreased nonlinear dynamics of TPR was carried over from A to R. In contrast, SD increased significantly in A. In conclusion, intermittent brief chemoreflex stimulations by repetitive apneas increase blood pressure and TPR and decrease chaotic behaviour and complexity of the cardiovascular autonomic control system, presumably by inhibition of some regulatory loops such as baroreflex, less vital for survival at oxygen deprivation. Reduced complexity could be implicated in the mechanism of arterial hypertension linked with OSA.
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PMID:Repetitive apneas reduce nonlinear dynamical complexity of the human cardiovascular control system. 1132 11


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