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

The frequent association of sleep apnea syndrome and essential hypertension led to think of sleep apnea as an etiology of hypertension, especially as a good correlation has been found between the severity of both diseases. Moreover, treating the apnea syndrome results in a decrease of blood pressure. The aim of our study is to depict the outlines of a severe hypertensive individual with sleep apnea by comparing 9 men primarily referred to the hypertension clinic with refractory hypertension and finally found to have sleep apnea (study group) to 23 men whose diagnosis of sleep apnea was made in the pulmonary unit (controls). Fifteen of these were hypertensives. Mean age of the study group was 47 +/- 7 years vs 60 +/- 11. Controls were less overweighted: BMI = 33 +/- 6 kg/m3 vs 39 +/- 5. Mean blood pressure was 171 +/- 16/107 +/- 4 mmHg in the study group vs 157 +/- 19/92 +/- 12 mmHg in controls. Prevalence of glucose metabolism disorders was significantly greater in the study group: 6 patients with maturity onset diabetes and 3 with proven glucose intolerance, vs respectively 4 and 6 controls. Triglycerides were elevated in both groups whereas mean cholesterol was slightly above normal values. Six patients of the study group could have an echocardiogram which showed left ventricular hypertrophy (mean left ventricular mass index = 206 +/- 31 g/m2 after the Penn convention).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Should arterial hypertension in sleep apnea syndrome be stressed?]. 183 55

The present study reports on polysomnographic findings of sleep apnea syndrome in a representative sample of otherwise healthy middle-aged blue collar workers (age 45.7 +/- 8.5) with normal to borderline blood pressure (systolic 135.5 +/- 16.1; diastolic: 88.3 +/- 10.2), mild overweight (Broca 114.9 +/- 14.7) and with reported nocturnal sleep disturbances. The prevalence of sleep apnea in this sample (N = 20 out of a total of 78 workers with reported sleep disturbances) is 40%. Mean frequency of apnoeic episodes during night was 97.6 +/- 42.7 in the apnea-positive group as compared to 27.1 +/- 19.9 in the apnea-negative group (T = 5.0; p less than 0.0001), with an apnea index of 13.3 +/- 6.2 as compared to 3.5 +/- 2.3 (T = 7.2, p less than 0.0001). Left ventricular hypertrophy (mean diameter of end diastolic left ventricle: 64.0 +/- 9.5 mm) was found in individuals with apnea although manifest hypertension was absent in most individuals.
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PMID:Prevalence of sleep apnea in healthy industrial workers. 293 98

Hypoxia is the major cause of pulmonary hypertension and right ventricular hypertrophy in chronic obstructive pulmonary disease, cystic fibrosis, kyphoscoliosis, chronic mountain sickness, and the obesity-hypoventilation and sleep apnea syndromes. Pulmonary hypertension develops in these patients because the long-standing vasoconstriction produced by hypoxia causes muscular hypertrophy of the pulmonary arteries and arterioles. These pathologic changes may regress if alveolar hypoxia is corrected and hypoxic pulmonary vasoconstriction is continuously inhibited. Intermittent inhibition of hypoxic pulmonary vasoconstriction does not reverse these pathologic changes. Since patient noncompliance with oxygen therapy makes it difficult to achieve continual relief of alveolar hypoxia, a drug that inhibits hypoxic vasoconstriction may be useful. Experimental findings indicate that hypoxic pulmonary vasoconstriction requires calcium influx and can be inhibited by certain slow-channel calcium blockers. Studies also demonstrate that slow-channel calcium antagonists can attenuate the pulmonary hypertension and right ventricular hypertrophy produced in rats by chronic hypoxia. Recently, two studies have shown that nifedipine inhibits hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease. If further studies demonstrate that these short-term effects are sustained, certain slow-channel calcium blockers may become a useful adjuvant to low-flow oxygen therapy in the treatment of hypoxic pulmonary hypertension.
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PMID:Calcium channel blockers in hypoxic pulmonary hypertension. 397 91

The cardio-respiratory complications of sleep apnea syndrome have been prospectively assessed in 60 patients with massive obesity and free of chronic obstructive lung disease while the associated cardiovascular diseases and the alterations of pulmonary function were taken into account. These cardio-respiratory complications were observed only in patients with a number of apneas per hour of sleep greater than 20. The sleep apneas induced nocturnal hypoxemia that is frequently severe and independently correlated to the apnea index, diurnal hypoxemia and hypercapnia that are usually moderate, and presumably left ventricular hypertrophy that is not related to the development of daytime hypertension. However the nocturnal apneas were not associated with the development of an impairment of right or left ventricular function, or with the occurrence of cardiac arrhythmias or conduction disturbances. The absence of severe cardiac complications in this study may be related to the fact that the patients were relatively young and that the sleep apnea syndrome was diagnosed at an early stage of evolution. The findings of this study could help to define a more rationale approach in several therapeutic indications of sleep apnea syndrome.
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PMID:[Cardio-respiratory complications of sleep apnea in obese patients]. 822 Nov 69

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.
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PMID:Hemodynamic consequences of obstructive sleep apnea. 884 30

We reviewed clinical data, autopsy reports, and microscopic slides on 10 patients with sleep apnea/obesity hypoventilation syndrome (SA/OHS) to define the cardiopulmonary pathological features and establish clinicopathologic correlations. Ten obese (>136 kg) patients without SA/OHS were studied as controls. Patients with SA/OHS exhibited biventricular cardiac failure and pulmonary hypertension with a higher prevalence of moderate/severe pulmonary hemosiderosis (8 v 0 patients), alveolar hemorrhage (7 v 4 patients), capillary proliferation (4 v 0 patients), iron encrustation of elastica (1 v 0 patients) and medial hypertrophy of muscular pulmonary arteries (11.9 +/- 2.4 v 9.7 +/- 1.6%) (P < .05). In two patients capillary proliferation resembled capillary hemangiomatosis. Mean right ventricular thickness was higher in the SA/OHS group (0.71 +/- 0.17 v 0.42 +/- 0.1 cm) (P < .01). Four patients with SA/OHS and three controls had moderate/severe myocardial fibrosis. Biventricular cardiac failure caused death in seven patients with SA/OHS. Hypoxia is probably the most important cause of pulmonary hypertension, arterial muscularization, and right ventricular hypertrophy in SA/ OHS. Left ventricular failure in some SA/OHS patients may be the result of hypertensive cardiac disease. In others, the etiology of left ventricular failure was not determined morphologically, suggesting functional abnormalities related to obesity and/or apneic episodes.
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PMID:Cardiopulmonary pathology in patients with sleep apnea/obesity hypoventilation syndrome. 938 47

Obstructive sleep apnoea (OSA) produces immediate effects on pulmonary haemodynamics during sleep in all subjects. In addition, in some subjects, OSA is accompanied by chronic abnormalities of the pulmonary circulation. During sleep, pressure in the main pulmonary artery oscillates within each apnoea, in synchrony with intrathoracic pressure changes; in addition, it may increase progressively as a consequence of prolonged severe hypoxaemia. Pulmonary capillary wedge pressure may increase during inspiratory efforts, possibly reflecting a mechanical limitation of left ventricular function. Cardiac output decreases at apnoea resolution as an effect of a decreased right ventricular stroke volume, despite increased cardiac frequency. During wakefulness, postcapillary pulmonary hypertension occurs on exercise in many OSA patients, whilst pulmonary hypertension at rest is precapillary and occurs in patients with an altered daytime respiratory function. Development of right ventricular hypertrophy and a decrease in right ventricular ejection fraction appear to be related to the severity of respiratory alterations during sleep, whilst an overt right heart failure requires an altered daytime respiratory function. Long-term treatment of the obstructive sleep apnoea syndrome is more effective in increasing right ventricular ejection fraction than in decreasing pulmonary artery pressure during wakefulness.
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PMID:Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation. 927 Feb 54

Assessment of cardiorespiratory consequences of sleep apnoea syndrome (SAS) is difficult owing to confounding factors, especially obesity, that are strongly associated with SAS. This study was designed to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with massive obesity. In a retrospective chart-review study, we studied 60 patients with massive obesity defined by a body mass index (BMI) >40 kg.m(-2), presenting no chronic respiratory disease, who underwent an extensive assessment of cardiorespiratory consequences of obesity, including overnight polysomnography, lung function tests, arterial blood gas analysis, evaluation of vascular risk factors, myocardial scintigraphy with dipyridamole stress-test, isotopic ventriculography, Doppler echocardiography and Holter electrocardiogram recording. SAS defined by an apnoea + hypopnoea index (AHI) > or = 10 was diagnosed in 42% of patients (25 out of 60). Mean+/-SD AHI of SAS-positive (SAS+) patients was 38+/-24. Age, BMI, ventilatory function parameters, prevalence of smoking history and diabetes mellitus did not differ significantly in SAS+ versus SAS-negative (SAS-) groups. The following complications were observed more frequently in SAS+ than in SAS- patients: daytime hypoxaemia (35 vs 9%, p<0.02), pulmonary arterial hypertension (36 vs 7%, p<0.05) and increased interventricular septal thickness (50 vs 15%, p<0.03). No association was found between SAS on the one hand and systemic arterial hypertension, coronary artery disease, left ventricular dysfunction and nocturnal cardiac arrhythmias on the other. Nocturnal apnoeas in massive obesity may thus be associated with moderate daytime hypoxaemia, mild pulmonary arterial hypertension and moderate left ventricular hypertrophy, but not with severe cardiorespiratory complications.
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PMID:Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity. 954 65

Chronic continuous hypoxia increases haematocrit and causes right ventricular hypertrophy and pulmonary hypertension. In obstructive sleep apnoea, the exposure to hypoxia is intermittent rather than continuous but the effects of chronic intermittent hypoxia on haematocrit and right ventricular mass are unclear. Wistar rats were exposed to alternating periods of hypoxia and normoxia twice per min for 8 h per day for 5 weeks in order to mimic the intermittent hypoxia of obstructive sleep apnoea in humans. Haematocrit was significantly raised at day 7, 14, 21, 28 and 35 of the treatment period. At the end of the treatment, there was a significant increase in right ventricular mass. Therefore, chronic intermittent hypoxia increases haematocrit and right heart mass. These results suggest that the raised haematocrit and pulmonary arterial pressure observed in some cases of obstructive sleep apnoea in humans may be caused by intermittent nocturnal hypoxaemia.
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PMID:Chronic intermittent hypoxia increases haematocrit and causes right ventricular hypertrophy in the rat. 1050 79

Ventricular hypertrophy is associated with an increased risk of cardiovascular death and cardiac events. In response to a haemodynamic load, ventricular hypertrophy may either be eccentric (dilation in response to volume overload) or concentric (increase in wall thickness in response to pressure overload). Ventricular hypertrophy increases with age, weight, blood pressure, and the presence of cardiovascular disease. It is greater in men than in women when adjusting for other variables. Echocardiography is the best method for accurate quantification of left ventricular mass and for detecting right ventricular hypertrophy. In obstructive sleep apnoea there are reports of both eccentric and concentric hypertrophy of the left ventricle. However, many of these reports have failed to control for patient weight or age. More recent reports indicate that much of the hypertrophy of the left ventricle reported in obstructive sleep apnoea can be related to patients' age, blood pressure, or size. However, right ventricular hypertrophy appears to be distinctly associated with the presence and severity of obstructive sleep apnoea. Right ventricular hypertrophy secondary to obstructive sleep apnoea may be the substrate for the eventual development of cor pulmonale and right heart failure. Its pathophysiological significance and potential use as a marker of severe OSA requires further investigation. Further investigation into left ventricular hypertrophy and sleep apnoea must control for the potentially confounding variables listed above and will require population-based and/or carefully matched case control studies.
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PMID:Ventricular hypertrophy in sleep apnoea. 1060 97


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