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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea is a breathing disorder characterized by repeated collapse of the upper airway during sleep, with cessation of breathing. Four percent of middle-aged men and 2 percent of middle-aged women meet minimal criteria for the sleep apnea syndrome. Risk factors include loud, chronic snoring, obesity (especially nuchal), hypertension, excessive daytime sleepiness, and an increased tendency for automobile and work-related accidents. Cardiovascular comorbidity and complications include systemic hypertension, arrhythmias and possibly myocardial ischemia and myocardial infarction in patients with coronary artery disease. Diagnosis is confirmed by a sleep study; currently, polysomnography is the optimum test. Treatment options range from behavioral therapy alone for mild cases to a combination of behavioral approaches and continuous positive airway pressure and/or surgery for moderate and severe cases. Continuous positive airway pressure is the most effective noninvasive treatment. Primary care physicians play a key role in the identification, management and follow-up of patients with sleep apnea.
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PMID:Sleep apnea: is your patient at risk? National Heart, Lung, and Blood Institute Working Group on Sleep Apnea. 854 58

Obstructive sleep apnea syndrome (OSAS) is the most important form of sleep-related breathing disorders due to its high prevalence and its potential for developing cardiovascular diseases. The increased morbidity of these patients is explained by the coincidence with cardiovascular diseases, and the increased mortality of untreated patients is due to cardiovascular complications, which depend on the degree of the breathing disorder. Heavy snoring, as a partial obstruction of the upper airways, and OSAS are independent risk factors for the development of cardiovascular diseases and stroke. Causal associations exist between acute hemodynamic changes, pressure and volume load, changes in the humoral and the central nervous system, and blood gas alterations during the obstructive apnea and the long-term condition due to OSAS. Obstructive apnea can be divided into an early phase, a late phase, and a phase of the postapneic hyperventilation with respect to hemodynamic changes, blood gas alterations, and the autonomic nervous system. The most striking changes in these parameters are seen at the end of apnea and in the first resumption of breathing, with an increase in systemic and pulmonary blood pressure, decrease in stroke volume, and a distinct change in heart rate. Manifestation of systemic hypertension even in the awake state is promoted by changes in the volume system, with activation of neurohumoral changes and by a resetting of baro- and chemoreceptors. Similar mechanisms are discussed in the development of pulmonary hypertension. In this circumstance the role of hypoxemia as a causal factor for pulmonary hypertension or as a consequence due to structural changes of the pulmonary vessels is controversial. OSAS is frequent in patients with coronary heart disease and these patients must be classified as a particular risk group because of apnea-associated silent myocardial ischemia and electric instability of the myocardium. The occurrence of arrhythmia in patients with OSAS is closely related to the apnea and hyperventilation events and depends on the sympathovagal balance. Early diagnosis and suitable therapy of patients at risk not only abolishes the sleep-related breathing disorder but also improves long-term outcome.
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PMID:[Sleep apnea and cardiovascular risk]. 857 38

Although a high prevalence of hypertension has been observed in snorers, whether there is a direct link between hypertension and snoring remains controversial. It has recently been demonstrated that an abnormal amount of breathing effort during snoring is responsible for sleep fragmentation even in the absence of sleep apnea syndrome criteria. We hypothesized that sleep fragmentation during snoring may be a direct risk factor for the development of hypertension. On the basis of polysomnographic data, 105 nonapneic patients between 40 and 65 years of age referred for snoring with social impairment were selected and categorized as snorers with (n=55) or without sleep fragmentation (n=50) based on whether the arousals index was 10 or greater or less than 10/h of sleep, respectively. Sleep distribution did not differ between the two groups, except for a longer duration of wake after sleep onset (58 +/- 43 min vs 42 +/- 38 min) and a shorter duration of slow-wave sleep in the group with sleep fragmentation (72 +/- 34 min vs 97 +/- 34 min). Although there were no statistically significant differences between the snorers with and without sleep disruption in terms of age (51.3 +/- 7.7 vs 48.6 +/- 6.0 years), body mass index (26.9 +/- 4.0 vs 27.2 +/- 5.5 kg/m2), sex ratio, respiratory indexes during sleep, daytime sleepiness, and daytime tiredness, prevalence of systemic hypertension was significantly higher in the sleep-fragmented group (20/55 vs 7/50). This significant difference persisted (16/51 vs 6/49) when patients using antihypertensive drugs with possible effects on the CNS were excluded. Our data suggest that sleep fragmentation is common in patients who seek medical help for snoring with social impairment and may play a role in the development of hypertension.
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PMID:Sleep fragmentation as a risk factor for hypertension in middle-aged nonapneic snorers. 863 67

Upper airway resistance syndrome (UARS) is a sleep-disordered breathing syndrome characterized by complaints of daytime fatigue and/or sleepiness, increased upper airway resistance during sleep, frequent transient arousals, and no significant hypoxemia. Of a population of 110 subjects (58 men) diagnosed as having UARS, we investigated acute systolic and diastolic BP changes seen during sleep in two different samples. First, six patients from the original subject pool were found to have untreated chronic borderline high BP, and were subjected to 48 h of continuous ambulatory BP monitoring before treatment and another 48 h of BP monitoring 1 month after the start of nasal-continuous positive airway pressure (N-CPAP) treatment. Five of six subjects used their equipment on a regular basis and had their chronic borderline high BP completely controlled. No change in BP values was seen in the last subject, who discontinued N-CPAP after 3 days. A second protocol investigated seven normotensive subjects drawn from the initial subject pool. Continuous radial artery BP recording was performed during nocturnal sleep with simultaneous polygraphic recording of sleep/wake variables and respiration. BP changes were studied during periods of increased respiratory efforts and at the time of alpha EEG arousals. Increases in systolic and diastolic BP were noted during the breaths with the greatest inspiratory efforts without significant hypoxemia. A further increase in BP was noted in association with arousals. Three of these subjects also underwent echocardiography during sleep, which demonstrated a leftward shift of the interventricular septum with pulsus paradoxus in association with peak end-inspiratory esophageal pressure more negative than -35 cm H2O. Our study indicates that, in the absence of classic apneas, hypopneas, and repetitive significant drops in oxygen saturation (below 90%), repetitive increases in BP can occur as a result of increased airway resistance during sleep. It also shows that, in some patients with both UARS and borderline high BP, high BP can be controlled with treatment of UARS. We conclude that abnormal upper airway resistance during sleep, often associated with snoring, can play a role in the development of hypertension.
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PMID:Upper airway resistance syndrome, nocturnal blood pressure monitoring, and borderline hypertension. 863 68

Obstructive sleep apnoea syndrome is due to pharyngeal obstruction of inspiratory airflow with preservation of thoraco-abdominal respiratory movements. This disease has been described for about thirty years, but is now the subject of growing interest. According to the increasingly abundant literature on this subject, OSAS is associated with essentially cardiovascular morbidity and mortality (systemic hypertension, pulmonary hypertension, heart failure, coronary heart disease, arrhythmias, cerebral vascular accidents and sudden death). The pathophysiology of its underlying mechanisms and its complications is complex and multifactorial. The diagnosis of this syndrome should be suspected on clinical interview (snoring, excessive daytime drowsiness, and apnoea during sleep) and is confirmed by polysomnography. Nasal continuous positive pressure with elimination of aggravating factors is the reference treatment in 1994. The diagnosis and management of this syndrome requires a multidisciplinary approach with collaboration between general practitioners, neurologists, maxillofacial/ENT surgeons, cardiologists and respiratory physicians.
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PMID:[Obstructive sleep apnea syndrome and cardiovascular diseases]. 874 61

We studied 176 patients with habitual snoring (HS) and obstructive sleep apnea (OSA) to find out whether Japanese patients with OSA differ from those in western countries. The prevalence and pathophysiology of hypertension may substantially differ between OSA patients in Japan and in western countries: body mass index may be more closely associated with hypertension in western patients. No statistical relationship was found between obesity and hypertension in Japanese patients. Although the reason is unknown, thinner body builds in Japanese patients could account for this difference. However, if Japanese patients complain of severe obesity or excessive daytime sleepiness, or both, and have a saw-tooth sign in the flow-volume curve or hypertension, or both, a polysomuography should be indicated.
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PMID:[Sign and symptoms in Japanese patients with obstructive sleep apnea: present status and problems]. 875 81

1. The aim of the study was to assess the effect of ambulatory monitoring of blood pressure on sleep and on blood pressure in middle-aged patients. 2. Nine consecutive patients (seven men, two women; mean age 57 years) complaining of snoring and various degrees of excessive daytime somnolence were studied. Five patients were normotensive and four were being treated for hypertension. During one night standard laboratory polysomnography was performed with monitoring of blood pressure by a silent ambulatory monitor and continuous infrared blood pressure by photoplethysmography. 3. Ambulatory blood pressure significantly disturbs sleep architecture, causing EEG arousals in 64% of measurements, and induces a significant rise in blood pressure during systolic pressure measurement by the ambulatory monitor (rise in systolic pressure, 13.7 +/- 15.9 mmHg, P < 0.001; rise in diastolic pressure, 3.7 +/- 8.2 mmHg, P < 0.01). At the time of diastolic measurement, blood pressure had returned to the preinflation value. The rise in systolic blood pressure was higher when an arousal was associated with cuff inflation (P < 0.001). This rise in blood pressure is probably the consequence of sympathetic nervous system activation. 4. We conclude that ambulatory blood pressure recordings of systolic blood pressure during sleep should be interpreted with caution as systolic blood pressure may be significantly increased in patients suspected of suffering from sleep-disordered breathing.
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PMID:Ambulatory monitoring of blood pressure disturbs sleep and raises systolic pressure at night in patients suspected of suffering from sleep-disordered breathing. 877 59

Sleep apnea is associated with many adverse cardiovascular sequelae, including hypertension, nocturnal angina, decreased cardiac output, and bradyarrhythmias. The purpose of this study was to determine if patients referred for pacemaker therapy with asymptomatic bradyarrhythmias have underlying sleep apnea as the etiology of their bradyarrhythmias. This study included eight patients (7 males, 1 female) referred to a cardiac electrophysiology practice for pacemaker therapy. Patients included had asymptomatic bradyarrhythmias that consisted of severe sinus bradycardia, second-degree atrioventricular block, and complete heart block. In 7 of 8 patients, the bradyarrhythmias occurred at night or during the day while asleep. No patients were conditioned athletes. Symptoms often associated with bradyarrhythmias, such as lightheadedness and syncope, were not present. However, seven patients had at least one symptom suggestive of sleep apnea, such as excessive daytime fatigue, snoring, cessation of breathing during sleep (apnea), or frequent night-time awakenings. Overnight polysomnography studies were obtained on patients who had one or more symptoms suggestive of sleep apnea. In this study 7 of 8 patients (88%) referred for pacemaker therapy with asymptomatic bradyarrhythmias were documented by polysomnography to have sleep apnea. When treated with either sleep position modification, nasal continuous positive airway pressure (nasal CPAP), or tracheostomy, all seven patients had improvement in sleep apnea symptoms and remained asymptomatic from their bradyarrhythmias without pacemaker therapy over an average follow-up period of 22 months. One patient without symptoms suggestive of sleep apnea declined pacemaker therapy and remained asymptomatic. From these results, we concluded that asymptomatic transient bradyarrhythmias may suggest a diagnosis of sleep apnea. The evaluation of a patient referred for pacemaker therapy with asymptomatic bradyarrhythmias should include questions related to sleep apnea symptoms. Establishing the diagnosis of sleep apnea may reduce the need for pacemaker therapy and permit appropriate treatment of the underlying cause of these bradyarrhythmias.
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PMID:Asymptomatic bradyarrhythmias as a marker for sleep apnea: appropriate recognition and treatment may reduce the need for pacemaker therapy. 877 19

Obstructive sleep apnea syndrome (OSAS) has been associated with a higher than normal cardiovascular morbidity and mortality. Some OSAS patients lack the sleep-related, nocturnal decrease, or "dip," in blood pressure which is seen in normal individuals. These subjects, called "non-dippers," may be at greater risk for cardiovascular problems. We studied 40 OSAS patients (including 3 women) and 6 control subjects, all identified by polysomnography, for nocturnal blood pressure "dipping." We performed a second nocturnal polysomnogram to determine their apnea and hypopnea indices, (A + H)I, and oxygen saturation levels at the beginning of the study and then initiated 48 hours of ambulatory blood pressure monitoring, with data points collected every 30 minutes. Controls, which included one hypertensive subject, were all dippers. Nineteen OSAS subjects (48% of OSAS individuals) were systolic non-dippers and only 9 of them (22.5%) were diastolic non-dippers. We considered the following clinical variables as potential predictors of non-dipping: age, body mass index, respiratory disturbance index, years of reported loud snoring by bed partners, lowest oxygen saturation during nocturnal sleep, and percentage of sleep time spent with oxygen saturation below 90%. Multiple regression analyses indicated respiratory disturbance index as the only significant variable for systolic (p = 0.04) and diastolic (p = 0.03) blood pressure non-dipping. When we forced the following two nonsignificant variables into the model, they showed a very meager impact: number of years with reported loud snoring (p = 0.4 and p = 0.5, respectively for systolic and diastolic blood pressure non-dipping) and age (p = 0.5 and p = 0.6). The calculated model explained only a low percentage of the variance with an r2 of 0.25 and 0.26 for systolic and diastolic blood pressure non-dipping, respectively. Analysis of hypertension/normotension and dipping/non-dipping failed to show a significant relationship in the studied population. Fifty percent of the normotensive OSAS subjects were non-dippers and 43% of the hypertensive OSAS subjects were also non-dippers. We found a relationship between increasing respiratory disturbance index and increasing average 24-hour systolic blood pressure only when OSAS subjects were non-dippers and hypertensive.
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PMID:Blood pressure "dipping" and "non-dipping" in obstructive sleep apnea syndrome patients. 884 29

The purpose of this commentary is to review the evidence linking simple snoring with hypertension and cardiovascular and cerebrovascular disease. This has been a topic of numerous investigations with seemingly divergent results, mainly because of the differences in methodology employed in various studies, such as inclusion of confounding factors, type of population examined, methods of measurements and analysis, etc. Nevertheless, despite these limitations, a review of 19 studies examining the association between snoring and hypertension clearly shows that in the majority of them (14 studies) snoring was not found to be an independent risk factor. An association between snoring and cardiovascular and cerebrovascular disease is somewhat more difficult to assess. Analysis of 15 recent studies dealing with this issue shows that 9 of them concluded that snoring is a risk factor for vascular disease, whereas 6 studies reached the opposite conclusion. However, a detailed review of the studies showing positive association between snoring and vascular disease indicates that in some of them unsuspected sleep apnea may have accounted for this increased risk. In addition, these studies exhibit a number of inconsistencies that raise doubts as to the true validity of association between snoring and vascular disease. Finally, it does not seem biologically plausible that snoring should be a risk factor for cardiovascular and cerebrovascular disease without also being a risk factor for hypertension. Consequently, based on the available information, one cannot conclude that snoring is an independent risk factor for such adverse vascular complications as hypertension and cardiovascular and cerebrovascular disease.
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PMID:Is snoring dangerous to your health? 886 10


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