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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report documents how respiratory sleep disorders can adversely effect ischaemic heart disease. Three male patients (aged 60-67 years) with proven ischaemic heart disease are described. They illustrate a spectrum of nocturnal cardiac dysfunction, two with nocturnal angina and one with nocturnal arrhythmias. Full sleep studies were performed in a dedicated sleep laboratory on all patients, and one patient had 48 hours of continuous Holter monitoring. Two patients were found to have obstructive sleep apnoea with apnoea/hypopnoea indices of 57 and 36 per hour, respectively, the former with nocturnal arrhythmias and the latter with nocturnal angina. In both cases, nasal continuous positive airways pressure successfully treated the sleep apnoea, with an associated improvement in nocturnal arrhythmias and angina. The third patient who presented with nocturnal angina, did not demonstrate obstructive sleep apnoea (apnoea/hypopnoea index = 7.2) but had significant oxygen desaturation during rapid eye movement (REM) sleep. This patient responded to a combination of nocturnal oxygen and protriptyline, an agent known to suppress REM sleep, and had no further nocturnal angina. All patients were considered to be an optimum cardiac medication and successful symptom resolution only occurred with the addition of specific therapy aimed at their sleep-related respiratory problem. We conclude that all patients with nocturnal angina or arrhythmias should have respiratory sleep abnormalities considered in their assessment.
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PMID:Role of respiratory sleep disorders in the pathogenesis of nocturnal angina and arrhythmias. 818 72

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

Sleep apnea and snoring are widely discussed as risk factors for internal and neurological diseases. The prevalence of snoring in an Austrian population survey is about 27.2% (males 36.5%, females 18.9%), and that of apnea (respectively irregularity and/or cessation of breathing) about 8.5% (31% of all snorers). Clinical symptoms like naps, daytime sleepiness, unquiet sleep, hypertonia, headache in the morning and psychological symptoms may be characteristics of sleep apnea. They should lead to further diagnosis and removal of this risk factor for ischemic heart disease and stroke.
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PMID:[Sleep apnea as a risk factor]. 883 23

Obstructive and central sleep apnea are common in patients with congestive heart failure (CHF). These sleep-related breathing disorders are characterized by two pathophysiologic features that could have important implications for disease progression in CHF: sympathetic nervous system activation, and adverse changes in cardiac loading conditions. In patients with obstructive sleep apnea, blood pressure is frequently elevated as a result of excessive sympathetic nervous system activity elicited by the combination of apnea, hypoxia, and arousals from sleep. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular afterload, reduces cardiac output, and may promote the progression of pump failure. Increased afterload and hypoxia can also predispose such patients to myocardial ischemia and arrhythmias. In patients with CHF, abolition of coexisting obstructive sleep apnea by nasal continuous positive airway pressure improves left ventricular function. Central sleep apnea (i.e., Cheyne-Stokes respiration) is also characterized by apnea, hypoxia, and increased sympathetic nervous system activity and, when present in CHF, is associated with increased risk of death. Recent medium-term trials involving small numbers of patients have demonstrated that nocturnally applied continuous positive airway pressure in patients with CHF and central sleep apnea alleviates central sleep apnea, improves left ventricular function, reduces sympathetic nervous system activity and improves symptoms of CHF. These studies emphasize the importance of considering obstructive and central sleep apnea in the differential diagnosis of conditions that could contribute to the development or progression of CHF. They also suggest that continuous positive airway pressure is a promising nonpharmacologic adjunctive therapy for patients with CHF and coexisting sleep-related breathing disturbances that warrants further investigation.
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PMID:Pathophysiologic and therapeutic implications of sleep apnea in congestive heart failure. 889 61

In normal subjects, the level and variability of blood pressure decrease during non-rapid eye movement (non-REM) sleep. In contrast, sleep apnea is associated with large swings in nocturnal pressure. In this study, we evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. We also examined this index in snorers receiving medical treatment for coexistent ischemic heart disease. Beat-to-beat blood pressure was recorded with a photoplethysmographic device (Finapres) throughout polysomnography. Subjects were categorized into four groups: those without cardiovascular disease without or with sleep apnea (> or = 15 apnea plus hypopnea per hour of sleep), and those with ischemic heart disease without or with sleep apnea. A frequency distribution histogram of all increases and decreases of blood pressure according to their amplitudes was drawn and the SD of the distribution used as an estimation of variability. Mean systolic and diastolic pressures during the total sleep time were not different among the four groups. In contrast, the SD of the distribution of systolic and diastolic pressure variations that were higher in the apneic than in the nonapneic groups (P < .05) correlated with apnea plus hypopnea (P < .0001) and transient electroencephalographic arousal number per hour of sleep (P < .0001). In both apneic and nonapneic subjects, blood pressure variability as assessed by SD decreased during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep (P < .001). Blood pressure variability was similarly increased in apneic subjects with or without ischemic heart disease. We speculate that in apneic individuals with coexistent ischemic heart disease, pressure variability that is increased despite treatment with beta-blockers or calcium antagonists may be a risk factor for acute coronary events.
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PMID:Short-term variability of blood pressure during sleep in snorers with or without apnea. 895 80

A number of novel and important observations have recently arisen that emphasize the interaction between sleep apnea and cardiovascular function. New evidence of a role for obstructive sleep apnea as an independent factor in the genesis of hypertension and nocturnal myocardial ischemia has been described. Advances have been made in the understanding of the acute impact of sleep-disordered breathing on hemodynamic function, and a better understanding of the interaction between sleep-disordered breathing and congestive heart failure is now emerging. There is now strong evidence that reversal of sleep-related breathing disorders by nasal continuous positive airway pressure leads to improvements in markers of cardiovascular outcome in selected patients with congestive heart failure. These findings augur well for the development of new diagnostic approaches and treatment strategies for patients with sleep apnea and coexisting cardiovascular disease.
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PMID:Cardiovascular disease and sleep apnea. 936 91

Death from heart disease is sometimes observed at night. Life threatening arrhythmias or ischemic heart disease are suspected to be the cause of sudden death during night. Cheyne-Stokes respiration (CSR) is frequently observed in patients with chronic cardiac failure. CSR augments sympathetic nervous activity and reduces the quality of sleep. Sleep apnea or snoring is another stressful condition during sleep. During hyperventilatory phase of sleep apnea, the blood pressure, heart rate, end-systolic ventricular volume and vosomotor tone increases, and the periodic EEG arousal patterns are observed. Sleep apnea is suspected to be one of the risk factors of hypertension. The detection and early treatment of sleep apnea or Cheyne-Stokes respiration are required to reduce the mortality due to cardiac events during sleep.
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PMID:[Cardiovascular diseases]. 950 52

We investigated the prevalence of ischemic heart disease (IHD) in sleep apnea syndrome (SAS) and the presence of coronary risk factors involved in the onset of IHD in 386 subjects with suspected SAS due to heavy snoring. The prevalence of IHD among patients with untreated SAS was found to be 23.8%, and the percentage of patients having SAS complicated with IHD was high among those with moderate or severe SAS. Sleep apnea syndrome patients with IHD also showed high prevalences of hypertension and hyperlipidemia. It appears that sleep apnea aggravates the factors that cause coronary vascular disorders, and is involved in the onset of IHD.
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PMID:Prevalence of ischemic heart disease among patients with sleep apnea syndrome. 962 61

Obstructive sleep apnoea (OSA) is described by some authors as a potentially lethal disease and by others as an almost harmless condition. Excessive daytime sleepiness, neuropsychological dysfunction, altered quality of life, cardiovascular disease (systemic and pulmonary hypertension, cardiac arrhythmias, stroke and ischaemic heart disease) and increased mortality have been described as OSA complications. There is little argument that OSA may determine sleepiness, alter cognitive functions, and worsen quality of life, although with great interindividual variability: this should induce OSA to be considered an important illness per se, since sleepiness in OSA was shown to lead to important consequences, like road traffic accidents. Besides, OSA may interact with coexisting cardiac and respiratory disease and favour the appearance of heart and respiratory failure. Therefore, OSA is certainly also worth careful consideration as an important aggravating factor of other diseases. The evidence that obstructive sleep apnoea is an independent risk factor for cardiovascular complications other than owing to the recurrent transient blood pressure surges associated with apnoeas during sleep, and for an increased mortality is more conflicting. More studies are necessary to identify which characteristics of obstructive sleep apnoea may be considered important markers of its severity and as risk factors for different possible complications.
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PMID:What is the evidence that obstructive sleep apnoea is an important illness? 1006 35

Nocturnal oxygen desaturation and sleep apnea may provoke myocardial ischemia and arrhythmias in patients with coronary artery disease (CAD). Additionally, these factors may accelerate coronary atherosclerosis in the long term and they may play a role in the progression of the disease process. On the other hand, studies related to this subject are limited. This study was conducted to investigate the nocturnal oxygen desaturation and apneas during sleep in patients with CAD and to assess the possible association of these factors with CAD. We studied 22 male patients with CAD confirmed by coronary angiography who did not have symptomatic pulmonary disease and fourteen male healthy controls without known heart disease. Patients were randomly selected from men undergoing coronary angiography. Controls were age and sex matched and selected from the population registry. The normal controls were of similar body mass index to the patients. None of them were obese. The patients and controls underwent standard polysomnography. Men with CAD and controls had a similar apnea-hypopnea index (2.3 +/- 3.8 vs. 1.2 +/- 1.7). Mean oxygen desaturation index was higher among patients than controls (2.1 vs. 0.5, p < 0.05). Patients with CAD spent 3.1% (9.7 +/- 13.6) of total sleep time desaturated, while the same proportion in controls were 0.5% (1.9 +/- 4.1)(p < 0.05). Although both groups of patients were of similar heart rates at initial, the development of bradycardia during sleep was significantly higher in patients compared with controls (43.3% vs. 25.3%, p < 0.05). The results demonstrate that sleep disordered breathing, in particular nocturnal oxygen desaturation, occurs more common in patients with CAD compared to controls. Additionally, patients are at higher risk of developing bradycardia during sleep. This findings suggest that oxygen desaturation during sleep might contribute to the progression of CAD.
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PMID:Nocturnal oxygen desaturation in coronary artery disease. 1037 Mar 94


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