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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because sleep apnoea syndrome is often associated with arterial hypertension, it has been suggested that sleep apnoea might be responsible for hypertension. This hypothesis is mainly based on epidemiological studies showing a statistically significant association between snoring and arterial hypertension; this association remains true even after data correction to take into account the increased frequency of snoring with age and overweight. However, this statistical link is no evidence of a cause-effect relationship, and the mechanism through which sleep apnoea syndrome could produce arterial hypertension remains unknown. Yet treatment of sleep apnoea syndrome seems to improve arterial hypertension, and this alone would justify a search for sleep apnoea syndrome in all patients presenting with arterial hypertension.
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PMID:[Role of sleep apnea in essential arterial hypertension]. 214 5

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

To evaluate cardiac structure and function as well as blood pressure in the obstructive sleep apnoea syndrome (OSAS), we investigated 61 male patients and 61 male controls with M-mode and two-dimensional echocardiography. All patients had a history of habitual snoring and a diagnosed light to severe OSAS by previous investigations of nocturnal oxygen saturation status. No subject in the control group had a history of OSAS or hypertension. Body weight was higher in the OSAS patients than in the controls (P less than 0.001). Fifty per cent (31 out of 61) of the OSAS patients had systemic hypertension; 17 of these 31 were on pharmacological antihypertensive treatment. Neither the systolic nor the diastolic blood pressures were found to correlate to the severity of the OSAS (desaturation index). The heart rate was higher at rest in the OSAS patients with or without systemic hypertension compared to the controls with or without a blood pressure level above 165/95 mmHg (P less than 0.05 and P less than 0.01, respectively). Left ventricular (LV) internal dimensions as assessed by echocardiography did not differ between the two groups, while the interventricular septum and the LV posterior wall were thicker in the OSAS group. Thus, the LV mass and the LV mass index were significantly higher among the OSAS patients (P less than 0.001 and P less than 0.001). The LV mass index was approximately 15% higher among the 30 normotensive OSAS patients with no history of cardiac disease compared with the normotensive controls (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular hypertrophy independent of hypertension in patients with obstructive sleep apnoea. 217 47

Patients with sleep apnoea syndrome suffer considerable morbidity and an increased mortality. We reviewed the characteristics of 14 patients with sleep apnoea syndrome (11 males and 3 females) who were studied since 1986. All were less than or equal to 60 years of age with the majority in their 4th and 5th decade. Obesity was present in 8 patients (57%) and hypertension in 6 (43%). Overnight sleep studies showed that 11 patients had obstructive sleep apnoea, 2 had central and one had predominantly mixed sleep apnoea. Ten patients (71%) had some form of nose and/or throat pathology. Tonsillectomy seemed an effective therapeutic procedure in those with upper airway obstruction due to enlarged tonsils. Four out of 5 patients had significant symptomatic improvement post-tonsillectomy. Nasal continuous positive airway pressure was also effective in alleviating apnoeas and relieving symptoms in 4 other patients who had no obvious upper airway obstruction. A high proportion of our patients had obstructive sleep apnoea due to enlarged tonsils. Tonsillectomy offered a simple and effective therapy for such patients. Nasal continuous positive airway pressure was also effective in the treatment of obstructive sleep apnoea.
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PMID:Sleep apnoea syndrome--a report of 14 cases. 225 33

A 39-year old Chinese man presented with an acute onset of severe headache, accelerated hypertension and subsequently an unexpected extensive right occipital haemorrhage. These were found to be related to a sleep apnoea syndrome which had been unrecognized for many years despite its typical symptoms of loud snoring and excessive daytime sleepiness. Weight reduction led to significant clinical but not polysomnographic improvement of the sleep apnoea syndrome.
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PMID:Sleep apnoea presenting as severe hypertension and silent occipital haemorrhage. 225 42

Arterial hypertension was found in 78 of 224 consecutive patients operated for nasal polyposis. An exacerbated degree of hypertension was significant in groups aged above 50 years. In total, 46% of patients whose nasal polyposis was of a duration of more than 10 years suffered from hypertension. Fifty of 78 patients developed hypertension after nasal polyposis was established and the mean duration time from polyposis to hypertension was 11.1 years. Hypertension was established in 50% of patients suffering from the triad asthma, intolerance to acetylsalicylic acid and nasal polyposis. In analogy with knowledge that sleep apnoea and snoring are aetiological factors for arterial hypertension, we propose that long-standing nasal obstruction by nasal polyposis be a risk factor for arterial hypertension.
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PMID:Nasal polyposis as a risk factor for hypertension. 227 22

The diagnosis of obstructive sleep apnea is frequently made by taking a meticulous history coupled with a high index of suspicion. Snoring and hypersomnolence are clinical features common to individuals with sleep apnea. Since snoring is said to be a "disease of listeners," it is not uncommon that bed partners reported an increased incidence of depression and marital displeasure. It is for this reason that the spouse or bed partner should be interviewed, since the patient may not be aware of any sleeping problems. Physicians should also be alert to complaints of excessive daytime somnolence, because studies have shown that patients with obstructive sleep apnea are at increased risk for automobile crashes. It has been estimated that approx 58,000 motor vehicle accidents involving people with sleep apnea will occur in the US each yr. By proper diagnosis and treatment, the physician is in a unique position to prevent at least some of the automobile accidents that result from falling asleep while driving. Polysomnography is the only definitive way to obtain a diagnosis of sleep apnea. This allows the physician not only to diagnosis the disorder, but also helps in the evaluation of the severity of the syndrome and selection of therapy. An ENT evaluation is also important in ruling out anatomic disorders that can cause upper airway obstruction. Certain factors, such as alcohol and sedative ingestion, may aggravate the condition in a person predisposed to sleep apnea, and subtle changes, such as unexplained hypertension, polycythemia, and cor pulmonale, should lead one to investigate the possibility of sleep apnea as the etiology.
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PMID:Diagnosis of obstructive sleep apnea. 229 95

To evaluate the morbidity associated with obstructve sleep apnea syndrome (OSAS), we undertook a seven-year follow-up study of 198 OSAS patients seen between 1972 and 1980. The patients had been submitted to tracheostomy (71 patients) or had received a weight-loss recommendation (127 patients). Despite a lower mean apnea index (AI) (43 vs 69) and a lower mean body mass index (BMI) (31 vs 34 kg/m2) at entry, excessive daytime sleepiness (EDS) and vascular morbidity were significantly higher in the conservatively treated group. The relative risk (odds ratio) of finding EDS in the conservatively treated group, after adjustment for BMI at seven-year follow-up, was 3.7 (95 percent confidence interval [CI] = 2.6-5.3). The relative risk of developing new vascular problems in the same population, estimated by Cox models, was 2.3 (95 percent CI = 1.5-3.6). The effect of tracheostomy, independent of age, BMI, and AI at entry, was highly significant. At entry, 56 percent of the population already had a vascular problem, particularly hypertension, thus emphasizing the need for earlier treatment of the sleep-related abnormal breathing.
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PMID:Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. 229 60

Snoring was investigated in a survey of respiratory disease in Hispanic-Americans of a New Mexico community. A population-based sample of 1222 adults was studied with questionnaires and measurements of height, weight, and blood pressure. The age-adjusted prevalence of regular loud snoring was 27.8% in men and 15.3% in women. Snoring prevalence increased with age and obesity in both men and women. Cigarette smoking was also associated with snoring, but chronic obstructive lung disease and alcohol consumption were not. Snorers more frequently had hypertension, ischemic heart disease, and excessive daytime sleepiness. In contrast to other studies, after adjustment for confounding factors, there was no effect of snoring on hypertension (odds ratio, 1.0; 95% confidence interval, 0.7 to 1.5), but an effect on myocardial infarction was still demonstrable (odds ratio, 1.8; 95% confidence interval, 0.9 to 3.6). The association of snoring with sleepiness suggests that respiratory disturbance of sleep related to upper airway obstruction, such as sleep apnea, occurs more frequently in snorers in this population.
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PMID:Snoring in a Hispanic-American population. Risk factors and association with hypertension and other morbidity. 231 Feb 78

Two groups of patients with nocturnal arterial oxygen desaturation were compared. The degree of nocturnal oxygen desaturation, as reflected by the percentage of total sleep time spent with an oxygen saturation less than 90 and 80%, was similar in patients with the obstructive sleep apnoea syndrome (OSAS) and in those with nocturnal hypoventilation (NH) secondary to restrictive chest wall disease. Systemic hypertension was present in 16 of the 24 OSAS patients but in only 6 of the 24 with NH (p less than 0.005). Multiple regression analysis demonstrated that this difference remained significant even after adjustment for age, sex, weight and history of smoking. It is likely that factors other than nocturnal hypoxaemia are important in the aetiology of systemic hypertension in patients with sleep-related breathing disorders.
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PMID:Role of nocturnal hypoxaemia in the genesis of systemic hypertension. 235 75


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