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

In view of the limited capacity of hospital sleep labs, and the high prevalence of the sleep apnea syndrome, there is a requirement for a preliminary ambulatory diagnostic work-up. Nocturnal polygraphy has proved to be a useful screening method. The continuous measurement of respiratory flow, oxygen saturation, heart rate and body position enables the severity and frequency of respiratory events to be monitored. With consideration being given to the patient's symptoms, examination findings, cardiovascular disease and the risks resulting from disturbed vigilance, a decision can be made on the need for an inpatient diagnostic work-up, and its urgency. Ambulatory apnea screening is not suitable for the differential diagnosis of nocturnal respiratory disorders, since it does not permit the correlation of symptoms to sleep stages and respiratory movements.
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PMID:[Apnea diagnosis in general practice. Indications, possibilities and limits]. 1134 Sep 4

Sleep apnea (intermittent periods of hypoxia with or without hypercapnia) is associated with systemic hypertension and increased mortality from cardiovascular disease, but the relationship to pulmonary hypertension is uncertain. Previous studies on intermittent hypoxia (IH) in rats that demonstrated pulmonary hypertension utilized relatively long periods of hypoxia. Recent studies that utilized brief periods of hypoxia have conflicting reports of right ventricular (RV) hypertrophy. In addition, many studies have not measured pulmonary hemodynamics to asses the severity of pulmonary hypertension in vivo. Given the increasing availability of genetically engineered mice and the need to establish a rodent model of IH-induced pulmonary hypertension, we studied the effect of IH (2-min cycles of 10% and 21% O2, 8 h/day, 4 wk) on wild-type mice, correlating in vivo measurements of pulmonary hypertension with RV mass and pulmonary vascular remodeling. RV systolic pressure was increased after IH (36 +/- 0.9 mmHg) compared with normoxia (29.5 +/- 0.6) but was lower than continuous hypoxia (44.2 +/- 3.4). RV mass [RV-to-(left ventricle plus septum) ratio] correlated with pressure measurements (IH = 0.27 +/- 0.02, normoxia = 0.22 +/- 0.01, and continuous hypoxia = 0.34 +/- 0.01). Hematocrits were also elevated after IH and continuous hypoxia (56 +/- 1.6 and 54 +/- 1.1 vs. 44.3 +/- 0.5%). Evidence of neomuscularization of the distal pulmonary circulation was found after IH and continuous hypoxia. We conclude that mice develop pulmonary hypertension following IH, representing a possible animal model of pulmonary hypertension in response to the repetitive hypoxia-reoxygenation of sleep apnea.
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PMID:Selected Contribution: Pulmonary hypertension in mice following intermittent hypoxia. 1135 19

The prevalence of several cardiovascular diseases is increased with obstructive sleep apnoea syndrome (OSAS), due to, as yet, unclear reasons. Angiotensin converting enzyme (ACE) abnormalities have been implicated in the pathogenesis of various cardiovascular diseases. In this study, plasma ACE activity and the distribution of an insertion (I)/deletion (D) polymorphism of the ACE gene were determined in OSAS patients and in healthy controls. A total of 63 patients with OSAS (mean+/-SEM 54.5+/-2.5 apnoea/hypopnoeas.h(-1)) and 32 healthy subjects were studied. To avoid potential confounding factors, patients treated with ACE inhibitors or continuous positive airway pressure were excluded, as well as controls in whom a blood sample was not obtained early in the morning. ACE activity was determined spectrophotometrically in 46 OSAS patients and 25 controls. The I/D ACE polymorphism was determined by polymerase chain reaction in 44 patients and 32 controls. ACE activity was higher in OSAS patients (53.9+/-2.5 IU.L(-1)) than in healthy controls (42.4+/-3.1 IU.L(-1), p<0.01). This was independent of the presence of arterial hypertension. The frequency distribution of the DD, II and ID genotypes in OSAS patients (30%, 16%, 54%, respectively) was not significantly different from that seen in healthy subjects (31%, 28%, 41%, respectively, p=0.356). These results indicate that ACE plasma activity is increased in untreated OSAS patients. This increased activity may contribute to the pathogenesis of the cardiovascular disease in these patients.
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PMID:Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms. 1140 Oct 71

Patients with obstructive sleep apnea (OSA) are at increased risk for cardiovascular disease. Altered cardiovascular variability is a prognostic indicator for cardiovascular events. This review examines the evidence that OSA is accompanied by alterations in cardiovascular variability. This alteration is evident even in the absence of hypertension, heart failure or other disease states, and may be linked to the severity of OSA. The presence of clear-cut abnormalities in time and frequency-domain measures of blood-pressure and heart-rate variability in normotensive OSA patients provides intriguing evidence for the concept of an etiologic interaction between sleep apnea and cardiovascular disease. Mechanisms that could contribute to altered cardiovascular variability in patients with sleep apnea include abnormalities in chemoreflex, baroreflex and endothelial function.
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PMID:Cardiovascular variability characteristics in obstructive sleep apnea. 1148 97

The sleep apnea syndrome is a common disease, recognised as a public health problem. Cardiovascular disease is the most frequent cause of morbidity and mortality in these patients, however the underlying mechanisms of this association have not been clearly established. In sleep apnea syndrome different phenomena can be produced which may explain the appearance of cardiovascular problems, such a progressive hypoxia in relationship with the apnea, the increases of intrathoracic pressure cause by the efforts of ventilation system against close upper airway and the modifications of the autonomic nervous system associated with the arousals. In addition, the hypoxia episodes and reoxygenation, which appear in the sleep apnea syndrome, may play a important role in the alteration of the balance between vasoconstriction and vasodilatation substances affecting the vascular homeostasis and conditioning endothelial dysfunction. On the other hand, the increasing of platelets aggregation and the decreased of fibrinolisis in this group of patients may cause vascular diseases.
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PMID:[Sleep apnea syndrome and cardiovascular diseases]. 1149 65

Snoring and excessive daytime somnolence (EDS) are very common in middle-age adults. The goal of the investigation was to assess links between those symptoms and risk for cardiovascular diseases (CVD). The population studied included 1186 inhabitants of Warsaw (mean age 52 years), participants of the international multicentre study of cardiovascular disease MONICA II, who completed the sleep disordered breathing (SDB) questionnaire. Snoring was reported by 78% of males (48% habitual and 30% occasional) and 59% of females (27% habitual and 32% occasional). Every fourth (26.8%) subject declared observed apnoeas, in 9.2% apnoeas were observed every night. EDS was declared by 28.7% of studied sample. The results of the questionnaire were compared to the results of MONICA study. Snorers had significantly higher systolic and diastolic blood pressure (133.2 +/- 23/84.6 +/- 13 mm Hg) compared to non-snorers (126.4 +/- 22/80.4 +/- +/- 12 mm Hg) (p < 0.0001). The high total serum cholesterol (> or = 200 mg%) and triglycerides (> or = 200 mg%) concentration, and also obesity (BMI > or = 30 kg/m2) were more prevalent in snorers. Subjects reporting apnoeas more often had coronary artery disease (p < 0.001) or history of stroke (p = 0.002) compared to non-apnoeics. There was no relationship between EDS and risk of cardiovascular disorders, and also between diabetes and SDB. In conclusion, snoring was strongly associated with hyperlipidaemia, obesity or hypertension, well known risk factors for development of cardiovascular disorders. Reported apnoeas were related to risk of coronary artery disease.
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PMID:[Snoring and excessive daytime somnolence and risk of cardiovascular diseases]. 1150 94

Cardiovascular disease is the leading cause of morbidity and mortality in end-stage renal disease. Causes include those usually found in the general population, those related to the uremic status, and those related to dialytic treatment. Hypertension, hypotension, anemia, hypoalbuminemia, malnutrition, dyslipidemia, reactive C protein, calcium-phosphate product, dialysis modalities, and hyperhomocysteinemia are discussed extensively. Special emphasis is put on hyperparathyroidism as a traditional toxin. The emergent role of sleep apnea has been confirmed in animal models as well as in humans studied using polysomnography. There are difficulties in diagnosing coronary disease, because angiography is not risk-free, is expensive, and should be reserved for patients having symptoms of heart failure and/or patients having diabetes mellitus, and/or patients entering a transplantation list. This allows patients with coronary disease to undergo coronary artery bypass (preferably) or percutaneous transluminal angioplasty. Patients for whom surgery is not appropriate should be treated using more traditional medical procedures.
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PMID:The heart in uremia: role of hypertension, hypotension, and sleep apnea. 1157 20

Obstructive sleep apnoea is a complex multifactorial condition produced by a combination of anatomical and physiological factors. There is a significant associated mortality and morbidity to obstructive sleep apnoea. There is an at least 25 per cent increased mortality from cardiovascular disease when obstructive sleep apnoea patients are compared to age and gender matched healthy people. Obstructive sleep apnoea sufferers also have a much higher industrial and motor vehicle accident rate. Management of the condition should be undertaken by a multidisciplinary team including respiratory physicians, sleep laboratory technicians, otorhinolaryngologists, oral and maxillofacial surgeons and dental specialists. The diagnostic and therapeutic interactions of team members are the key to successful treatment. The treatment regime utilises nasal continuous positive airway pressure devices, mandibular advancement splints and soft and hard tissue surgery. This review provides the dental practitioner with an introduction to obstructive sleep apnoea with particular emphasis on the orofacial aspects.
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PMID:Obstructive sleep apnoea: a review of the orofacial implications. 1169 53

Patients with sleep apnea may be at increased risk for cardiovascular disease. Recently, the link between hypertension and sleep apnea has been strengthened by findings of two large epidemiologic studies. Neurohumoral and hemodynamic responses to repetitive episodes of hypoxemia and apnea may offer a pathophysiologic basis for patients with sleep apnea having an increased risk for hypertension. Sympathetic, humoral, and cellular responses to sleep apnea over the long term may cause vascular dysfunction and consequent hypertension. These responses may be exacerbated by sleep deprivation, which occurs commonly in patients with sleep apnea because of poor sleep architecture. Patients with sleep apnea are often obese and may be predisposed to weight gain. Hence, obesity may further contribute to cardiovascular risk in this patient population. Alleviation of sleep disordered breathing may be accompanied by lower blood pressure in hypertensive patients with sleep apnea.
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PMID:Sleep disordered breathing and hypertension. 1170 13

Cardiovascular diseases are frequent among patients with the obstructive sleep apnoea syndrome (OSAS), The aetiopathogenesis of this association is unclear. Type 1 plasminogen activator inhibitor (PAI-1) is one of the primary regulators of the fibrinolytic system. A reported association between PAI-1 activity and an insertion/deletion polymorphism (4G/5G) in the promoter region of the PAI-1 gene suggests a critical role for this genomic region in the pathogenesis of several cardiovascular diseases. In this study, we determined the prevalence of this polymorphism in patients with OSAS and in healthy control subjects. The 4G/5G polymorphism in the promoter region of the PAI-1 gene was determined in 78 male patients with severe OSAS (56 +/- 2 apnoeas per hour) and in 70 healthy male, non-smoker volunteers of similar age, without personal or familial history of cardiovascular disease. The frequency ofthe 4G/4G, 4G/5G and 5G/5G genotypes in patients with OSAS (18%, 62%, 19%, respectively) was not significantly different from that seen in healthy subjects (16%, 60%, 24% P=NS). These results show that the distribution of the 4G/5G polymorphism in the promoter region ofthe PAI-1 gene in patients with OSAS is similar to that observed in healthy subjects. This observation suggests that the PAI-1 polymorphism has no relationship with the increased risk of cardiovascular diseases seen in patients with OSAS.
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PMID:Plasminogen activator inhibitor-I (PAI-I) polymorphisms in patients with obstructive sleep apnoea. 1190 12


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