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

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

A review of the literature shows that more than 50% of examined patients suffering from coronary heart disease were also suffering from sleep-related apnea. We were able to diagnose a pathological sleep apnea in 9 out of 25 patients (36%) suffering from an angiographically confirmed coronary 2-vessel and 3-vessel disorder. Patients with this combination--this is the hypothesis derived from our study--are at risk due to nocturnal apnea-induced myocardial ischaemia and rhythmic disorders. In 15 patients with sleep apnea and coronary heart disease or small vessel disease, nocturnal polysomnography was conducted, in parallel a 6-channel ECG was recorded. The apnea index (second night) was on the average 33 phases/h, the maximal duration of an apnea phases being 120 seconds. The minimal blood gas saturation recorded during sleep was between 46 and 89% (median 76.0%). In 4 of the 15 patients it was possible to confirm myocardial ischaemia (correlated via REM and also via NREM) with a maximum duration of 60 seconds, mainly during the phases of maximal apnea activity and blood gas desaturation. On comparing the ventricular arrhythmias waking/sleep, the Lown class did not change in 12 patients; there was deterioration in 2 patients and in one patient a qualitative improvement during the sleep phase. Patients suffering from sleep-related respiratory disorders and coronary heart disease are at cardiac risk, the more so since long-lasting apneas can lead to conditions of hypoxia at the heart in pre-existing changes in the coronary arteries, restricted coronary reserves and reduced tolerance to hypoxia. Such hypoxia can in turn induce enhanced electrical instability and a disturbance of the contractile function.
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PMID:[Sleep-related respiratory disorders and coronary heart disease]. 186 2

It is assumed, that patients with coronary heart disease (CHD) more often suffer from sleep related disorders of breathing than healthy subjects. A relation to an impaired left ventricular performance is discussed. In 40 CHD-patients and 30 cardio-respiratory healthy controls we therefore measured arterial oxygenation during sleep by means of pulse-oximetry. Our results show a marked increase in the frequency of nocturnal oxygen-desaturations along with the degree of impaired left ventricular function independent of a special sleep apnea risk. In case of cardiac insufficiency at rest cyclical oxygen-desaturations were observed ten times as often as in the healthy controls. A central disturbance of the respiratory control, which leads to periodic breathing (type Cheyne-Stokes) has to be discussed. Because of the general high risk of CHD-patients concerning the development of nocturnal complications of their disease, sleep-related disturbances of ventilation have to be detected early by means of routinely applied screening-methods.
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PMID:[Nocturnal oxygen saturation in patients with coronary heart disease--dependent on degree of left ventricular functional impairment]. 186 4

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.
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PMID:Snoring and the risk of ischemic brain infarction. 186 48

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.
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PMID:Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease. 192 Dec 30

Sleep apnea (SA) is associated with increased morbidity of the cardiovascular system, the interaction between the disordering of respiratory coordination and cardiovascular regulation being largely unknown. In 64 patients (age: mean = 54.1; range: 35-67 years) with an increased apnea index (AI greater than 10), a cardiac catheterisation investigation was performed to exclude coronary heart disease (CHD) or cardiomyopathy. CHD was excluded in 39 patients, 6 patients had coronary single-vessel disease, 9 patients coronary two-vessel, and 10 three vessel disease. In 10 patients, cardiomyopathy was detected, while high-grade impairment of the left ventricular ejection fraction (greater than 30%) was observed in five patients. With the exception of a single patient, CHD was observed only in patients in the over-fifty age group. Arterial hypertension was seen in 84% of the patients with, and in 69% of the patients without, CHD. The patient groups with and without coronary heart disease did not differ with respect to apnea index, ten minute index, or the average duration of the 30 longest apneic episodes. Anginal complaints, observed in a total of 72% of the patients, were one of the major indications for coronary angiography. These results do not support the assumption that SA is primarily a consequence of underlying cardiac disease, but do indicate that SA must be considered a cardiac risk factor, especially in view of the fact that pronounced nocturnal changes in blood gases and haemodynamics, together with malignant arrhythmias, are found in conjunction with this disturbance of breathing.
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PMID:[Results of left heart catheterization study in 64 patients with nocturnal disorders of respiratory control (sleep apnea)]. 260 54

Sleep apnea syndrome is a relatively common disease, with an overwhelmingly male predominance. The female:male ratio is about 1:15-20, depending on the specific age group. In light of findings linking sleep apnea syndrome to essential hypertension, it is hypothesized that the syndrome may contribute to the sex differential in mortality. In most of the developed countries women have longer life expectancy than men even after adjustment for various lifestyles and biologica variables Mortality from heart disease accounts for 40% of the total sex differential. The fact that the 2-5 fold sex differential for heart disease mortality is reduced to much lesser extent by multivariate adjustment than the sex differential for mortality from all causes, and that it is minimally affected by the exclusion of all persons with a history of chronic diseases, indicates that other risk factors should be sought. I propose the hypothesis that Sleep Apnea Syndrome (SAS), which almost exclusively affects males, contributes to the sex differential in mortality from coronary heart disease. Sleep Apnea Syndrome is a relatively common disease. It is the most preponderant finding among patients referred to diagnostic sleep laboratories, particularly among patients complaining of excessive daytime sleepiness. Its incidence among the adult male population (age greater than 21 years) was estimated to be at least 1-1.5%. It is considerably higher than that, at least 5 to 7 fold, in the 40 to 60 years age group, and in specific high-risk populations such as the morbidly obese. The female:male ratio is about 1:15-20, depending on the specific age group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnea syndrome: is it a contributing factor to the sex differential in mortality? 364 99

Patients with obstructive sleep apnoea demonstrate an increased rate of ventricular arrhythmias. The present study was designed in order to investigate whether these arrhythmias may be related to myocardial injury, since myocardial injury of various aetiologies has been observed to change the signal averaged electrocardiogram (ECG). Signal averaged ECG was registered in 23 patients with obstructive sleep apnoea diagnosed by polysomnography (apnoea index 43 +/- 20 events.h-1, age 55 +/- 10 yrs). QRS duration, root mean square voltage of the last 40 ms of QRS, and low amplitude (< 40 mV) signal duration were determined from the vector magnitude of the QRS, high-pass filtered at 40 Hz. Patients with coronary heart disease or bundle branch block were excluded. No patient showed an abnormal signal averaged ECG. Mean duration of the filtered QRS complex was 96 +/- 9 ms, root mean square voltage 38 +/- 18 microV and low amplitude signal duration 26 +/- 8 ms. These results were not significantly different from 14 snoring subjects with an apnoea/hypopnoea index < 10. Four patients showed no ventricular arrhythmias and six patients had Lown III or IVa in the Holter ECG. Echocardiography revealed increased left atrial (43.7 +/- 4.1 mm) and interventricular septal diameters (11.3 +/- 1.4 mm). In conclusion, obstructive sleep apnoea does not generate a substrate for late potentials in the signal averaged ECG.
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PMID:Obstructive sleep apnoea and signal averaged electrocardiogram. 766 52

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.
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PMID:Obesity and the heart. 836 92

The medical hazards of obesity are discussed. Risks include insulin resistance, diabetes mellitus, hypertriglyceridemia, decreased levels of high-density lipoprotein cholesterol, and increased levels of low-density lipoprotein cholesterol. Obesity is also associated with gallbladder disease and some forms of cancer as well as sleep apnea, chronic hypoxia and hypercapnia, and degenerative joint disease. Obesity is an independent risk factor for death from coronary heart disease. A central distribution of body fat enhances the risk for most of these conditions.
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PMID:Medical hazards of obesity. 836 92


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