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

Patients with obstructive sleep apnea (OSA) experience repetitive nocturnal oscillations of systemic arterial pressure that occur in association with changes in respiration and changes in sleep state. To investigate cardiac function during the cycle of obstruction (apnea) and resumption of ventilation (recovery), we continuously measured left ventricular stroke volume (LVSV) and mean arterial blood pressure (MAP) during non-rapid-eye-movement sleep in six males with severe OSA (apnea/hypopnea index > or = 30 events/h associated with oxygen saturation < 82%). LVSV was assessed continuously using an ambulatory ventricular function monitor (VEST; Capintec). The apnea-recovery cycle was divided into three phases: 1) early apnea (EA), 2) late apnea (LA), and 3) recovery (Rec). In all subjects recovery was associated with an abrupt decrease in LVSV [54.0 +/- 14.5 (SD) ml] compared with either EA (91.4 +/- 14.7 ml; P < 0.001) or LA (77.1 +/- 15.2 ml; P < 0.005). Although heart rate increased with recovery, the increase was not sufficient to compensate for the decrease in LVSV so that cardiac output (CO) fell (EA: 6,247 +/- 739 ml/min; LA: 5,741 +/- 1,094 ml/min; Rec: 4,601 +/- 1,249 ml/min; EA vs. Rec, P < 0.01; LA vs. Rec, P < 0.025). Recovery was also associated with a significant increase in MAP. We speculate that such abrupt decreases in LVSV and CO at apnea termination, occurring coincident with the nadir of oxygen saturation, may further compromise tissue oxygen delivery.
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PMID:Stroke volume and cardiac output decrease at termination of obstructive apneas. 147 46

Hypoxemia and decreased intrathoracic pressure have been postulated as contributing causes of cardiovascular morbidity in obstructive sleep apnea syndrome (OSAS). Because of the difficulty of manipulating experimental conditions in humans, we developed an anesthetized closed-chest dog model, simulating the periodic airway occlusions of OSAS by periodic occlusions of the endotracheal tube (PUO). Using a periodicity of 60 s occluded, followed by 60 s ventilation for five to seven cycles, we measured heart rate (HR), cardiac output (CO), arterial pressure (Pa); left ventricular (LV) end-diastolic and end-systolic transmural pressure; dp/dt of LV pressure; left anterior descending (LAD) coronary blood flow (CBF), and regional myocardial contractility and intramyocardial pH. Four experimental conditions were studied: room air (RA) breathing (PO2 = 40); 100% O2 breathing (O2), and RA and O2 breathing with critical LAD stenosis (CS). Under all conditions PUO produced decreases in CO (10 to 30%) and proportional decreases in Pa. HR decreased, and in all but RA conditions stroke volume was unchanged. During the obstructed phase, indices of LV preload decreased. Indices of LV afterload also decreased except for LAD-perfused myocardium under RACS conditions. This latter was shown to be associated with regional ischemia (decreased regional pH and shortening). Regional ischemia was also demonstrated in two of nine dogs even under O2CS conditions. Among our major conclusions: (1) decreased Pa during PUO is due to decreased CO; (2) LV afterload does not increase during PUO; (3) with limited coronary flow reserve (CS), PUO can lead to myocardial ischemia. This is mostly but not solely due to hypoxia.
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PMID:Cardiovascular effects of periodic occlusions of the upper airways in dogs. 148 19

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

Five men free of lung or cardiovascular diseases and with severe obstructive sleep apnea participated in a study on the impact of sleep states on cardiovascular variables during sleep apneas. A total of 128 obstructive apneas [72 from stage 2 non-rapid-eye-movement (NREM) sleep and 56 from rapid-eye-movement (REM) sleep] were analyzed. Each apnea was comprised of an obstructive period (OP) followed by a hyperventilation period, which was normally associated with an arousal. Heart rate (HR), stroke volume (SV), cardiac output (CO) (determined with an electrical impedance system), radial artery blood pressures (BP), esophageal pressure nadir, and arterial O2 saturation during each OP and hyperventilation period were calculated for NREM and REM sleep. During stage 2 NREM sleep, the lowest HR always occurred during the first third of the OP, and the highest was always seen during the last third. In contrast, during REM sleep the lowest HR was always noted during the last third of the OP. There was an inverse correlation when the percentage of change in HR over the percentage of change in SV during an OP was considered. The HR and SV changes during NREM sleep allowed maintenance of a near-stable CO during OPs. During REM sleep, absence of a compensatory change in SV led to a significant drop in CO. Systolic, diastolic, and mean BP always increased during the studied OPs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular changes associated with obstructive sleep apnea syndrome. 155 36

Increasing evidence suggests that snoring and sleep apnea are associated with cerebrovascular diseases. Several other factors may be involved in this association because many established or potential risk factors for stroke are related to snoring and sleep apnea. These include arterial hypertension, coronary heart disease, age, obesity, smoking, and alcohol consumption. Recent epidemiologic and clinical studies indicate, however, that snoring can increase the risk of stroke independently of these confounding factors. Accumulating epidemiologic evidence of long-term harmful effects of the obstructive sleep apnea syndrome appears to be related to increasing vascular morbidity and mortality. Potential mediators among snoring, obstructive sleep apneas, and stroke include cardiac arrhythmias and other hemodynamic disturbances, increased levels of catecholamines, and disturbances in cerebral blood flow caused by sleep apneas, as well as hypoxemic periods that may potentiate atherosclerosis.
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PMID:Snoring, sleep apnea syndrome, and stroke. 163 Jun 43

To determine if a history of snoring is a risk factor for brain infarction, I conducted a case-control study of risk factors for ischemic stroke using 177 consecutive male patients aged 16-60 (mean 49) years with acute brain infarction. For each patient I chose an age-matched (+/- 6 years) male control. Arterial hypertension, coronary heart disease, snoring (habitually or often), and heavy drinking (greater than 300 g/wk) were risk factors in the stepwise multiple logistic regression analysis. The odds ratio of snoring for brain infarction was 2.13. By McNemar's test this association increased strongly if a history of sleep apnea, excessive daytime sleepiness, and obesity were all present with snoring (odds ratio 8.00). My study indicates that snoring may be a risk factor for ischemic stroke, possibly because of the higher prevalence of an obstructive sleep apnea syndrome among snorers than nonsnorers.
Stroke 1991 Aug
PMID:Snoring and the risk of ischemic brain infarction. 186 48

The OSA syndrome, described over 100 years ago, was rediscovered in 1966. It is a common disorder, especially among fat, middle-aged men. Stentorian snoring and diurnal somnolence are the cardinal manifestations and should always lead to an examination during sleep. That examination (polysomnography) can demonstrate the pathognomonic events--repetitive apneas occurring in sleep--which signal the failure of the sleeping brain to maintain the patency of the supraglottic airway. All evidence points to the problem being an abnormal pharyngeal airway, one which has a shape or size or compliance that allows inspiratory collapse as the normal loss of pharyngeal dilator muscle tone occurs with sleep. The apneas are asphyxic events terminated by arousals which fragment sleep continuity and lead to the daytime sleepiness. Because the snoring occurs during sleep, the arousals are unremembered, and the sleepiness can develop so gradually that the patient may forget what normal alertness is like. It is important to interview the patient's spouse or partner. Besides obesity and maleness, other risk factors for OSA are diseases that have an impact on the configuration or effective compliance of the pharyngeal passageway. Recent studies support the clinical intuition that sleep apnea is undesirable. Sleepiness leads to accidents. The hypoxemia occurring during apnea can lead to potentially fatal cardiac dysrhythmias. A number of reports suggest that snoring and sleep apnea are associated with an increased risk of stroke, myocardial ischemia, and infarction. Finally, there are now two papers showing a significantly decreased probability of 5-year survival in patients with symptomatic sleep apnea. The good news is that treatment with tracheostomy or NCPAP improves mortality rates to normal. Approximately 90 per cent of patients can tolerate a night's initial trial with CPAP. Long-term acceptance of CPAP has now been reviewed in a number of studies, and it appears to be about 65 to 70 per cent.
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PMID:Sleep disorders and upper airway obstruction in adults. 219 4

We describe a child with sickle cell anemia and multiple ischemic infarctions who was found to have severe obstructive sleep apnea and hypoxemia, secondary to adenotonsillar enlargement. The apnea-associated hypoxemia likely contributed to the development of the strokes in this child. Moreover, because stroke in patients with sickle cell anemia, and maximal tonsillar enlargement (the most common cause of obstructive apnea in children) both have peak incidence at the same age (6-7 years), obstructive sleep apnea may be an important factor in the development of stroke in other children with sickle cell anemia.
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PMID:Stroke associated with obstructive sleep apnea in a child with sickle cell anemia. 340 43

Sleep in normal individuals is associated with mild alveolar hypoventilation, which results in 2 to 8 mm Hg increases in PaCO2 and 3 to 11 mm Hg reductions in PaO2, which decreases mean arterial oxyhemoglobin saturation by less than 2 per cent. Arterial blood pressure and heart rate consistently decrease during sleep, and cardiac output either decreases or remains unchanged. Greater variability in these hemodynamic variables occurs during REM than during NREM sleep. Cyclical fluctuations in ventilation, blood pressure, and heart rate have been observed in normal subjects, and fewer than five apneas per hour sleep is considered to be normal. In patients with obstructive sleep apnea, reductions in SaO2 that occur with apneas and hypopneas are highly variable within and between individuals. Multiple variables interact to determine the severity of the episodes of oxyhemoglobin desaturation that are associated with cyclical changes in heart rate and systemic blood pressure. The magnitude of the increase in systemic pressure is related to the severity of the oxyhemoglobin desaturation, with mean elevations in systolic and diastolic pressures being on the order of 25 per cent. However, the magnitude of the systemic pressor response to oxygen desaturation varies widely between individuals. Pulmonary artery pressure often increases with sequential apneas to substantially elevated values, and this increase in combination with the large negative intrathoracic pressures generated during obstructive apneas increases ventricular afterload. Alterations in stroke volume and cardiac output in response to the dynamic events that occur with apneas have not been adequately investigated. Reductions in heart rate that occur during apneas are related to the severity of the oxyhemoglobin desaturation and the arterial chemoreceptor-mediated increase in vagal efferent activity. Marked sinus bradycardia, sinus pauses of 2 to 13 seconds' duration, second-degree heart block, and ventricular tachyarrhythmias have all been associated with severe arterial hypoxemia. Sudden death during sleep in obstructive sleep apnea presumably results from a lethal cardiac arrhythmia, but the relative contributions of severe bradyarrhythmias and ventricular tachyarrhythmias are unknown.
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PMID:Gas exchange and hemodynamics during sleep. 390 2

In the case reported here, a 34-year-old man with severe obstructive sleep apnea syndrome had arterial hypertension and had had a stroke that caused right hemiplegia. A review of the literature reveals a surprisingly high occurrence of arterial hypertension in subjects with obstructive sleep apnea syndrome, including children. The cause of hypertension in these patients is not clear. Surgical procedures and a new nonsurgical treatment have been successful in relieving the symptoms of obstructive sleep apnea. Our patient's symptoms resolved completely after uvulopalatopharyngoplasty and tonsillectomy. However, his arterial hypertension persisted.
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PMID:Hypertension and stroke in a young man with obstructive sleep apnea syndrome. 405 36


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