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

Obstructive sleep apnea syndrome (OSAS) has been associated with a higher than normal cardiovascular morbidity and mortality. Some OSAS patients lack the sleep-related, nocturnal decrease, or "dip," in blood pressure which is seen in normal individuals. These subjects, called "non-dippers," may be at greater risk for cardiovascular problems. We studied 40 OSAS patients (including 3 women) and 6 control subjects, all identified by polysomnography, for nocturnal blood pressure "dipping." We performed a second nocturnal polysomnogram to determine their apnea and hypopnea indices, (A + H)I, and oxygen saturation levels at the beginning of the study and then initiated 48 hours of ambulatory blood pressure monitoring, with data points collected every 30 minutes. Controls, which included one hypertensive subject, were all dippers. Nineteen OSAS subjects (48% of OSAS individuals) were systolic non-dippers and only 9 of them (22.5%) were diastolic non-dippers. We considered the following clinical variables as potential predictors of non-dipping: age, body mass index, respiratory disturbance index, years of reported loud snoring by bed partners, lowest oxygen saturation during nocturnal sleep, and percentage of sleep time spent with oxygen saturation below 90%. Multiple regression analyses indicated respiratory disturbance index as the only significant variable for systolic (p = 0.04) and diastolic (p = 0.03) blood pressure non-dipping. When we forced the following two nonsignificant variables into the model, they showed a very meager impact: number of years with reported loud snoring (p = 0.4 and p = 0.5, respectively for systolic and diastolic blood pressure non-dipping) and age (p = 0.5 and p = 0.6). The calculated model explained only a low percentage of the variance with an r2 of 0.25 and 0.26 for systolic and diastolic blood pressure non-dipping, respectively. Analysis of hypertension/normotension and dipping/non-dipping failed to show a significant relationship in the studied population. Fifty percent of the normotensive OSAS subjects were non-dippers and 43% of the hypertensive OSAS subjects were also non-dippers. We found a relationship between increasing respiratory disturbance index and increasing average 24-hour systolic blood pressure only when OSAS subjects were non-dippers and hypertensive.
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PMID:Blood pressure "dipping" and "non-dipping" in obstructive sleep apnea syndrome patients. 884 29

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

Obstructive sleep apnea (OSA) is a disorder in which there is repetitive collapse and closing of the pharynx during sleep. There is growing evidence to suggest that this disorder is a major cause of essential hypertension (EH) and that successful treatment of OSA can reduce the blood pressure (BP) significantly. In addition many other patients with EH have milder forms of sleep related breathing disorders (SRBD) like snoring, and upper airway resistance syndrome (UARS) which, while not as severe as OSA, may be severe enough to also cause systemic hypertension. We therefore propose a unifying hypothesis-that many patients with EH may have sleep related breathing disturbances (SRBD) and treatment of these disorders may improve the BP. SRBD could also explain many of the epidemiological, clinical, hereditary, biochemical, hematological and physiological characteristics seen in EH. In addition, many types of secondary hypertension (those caused by excessive alcohol intake, chronic renal failure, diabetes, hypothyroidism or acromegaly) have a higher than normal prevalence of OSA and OSA may contribute to the hypertension and organ damage found in these conditions as well. Thus SRBD may play an important role in the production of many cases of essential and secondary hypertension, and their early detection and treatment could reduce the hypertension and organ damage seen in these conditions.
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PMID:Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. 887 97

To determine the mean blood pressure relative to sleep stages, two nocturnal cardiorespiratory polysomnographs were recorded in 60 male patients with hypertension and obstructive sleep apnea (OSA). The mean age was 50.2 years, the BMI 32.0 kg/m2, the respiratory disturbance index (RDI) 44, and the blood pressure by the WHO protocol 158/98 mm Hg. A new evaluation program was used to determine the invasively measured mean arterial pressure (mean +/- SEM) and heart rate (mean +/- SEM) during sleep (mean total sleep time 361 +/- 48 min) referred to sleep stages 1 (99.5 +/- 1.5 mm Hg/67.6 +/- 1.1 bpm), 2 (98.7 +/- 1.6 mm Hg/66.6 +/- 1.1 bpm), 3 (97.6 +/- 1.8 mm Hg/67.4 +/- 1.3 bpm), and 4 (97.6 +/- 2.2 mm Hg/66.3 +/- 1.6 bpm) and to REM sleep (103.3 +/- 1.7 mm Hg/68 +/- 1.2 bpm) as 1 s mean values and to compare them with the waking state (98.3 +/- 1.6 mm Hg/83.6 +/- 1.1 bpm). There was no physiological fall in blood pressure in patients with pronounced OSA. Sleep-stage-specific analysis of invasive continuous blood pressure signals is the gold standard. The sleep structure is disturbed less than with other methods.
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PMID:Assessment of the nocturnal blood pressure relative to sleep stages in patients with obstructive sleep apnea. 889 11

We studied 24-h blood pressure (BP) in 17 hypertensive patients with polysomnographic verified moderate to severe obstructive sleep apnea (OSA) before, after 1-3 days and after 4-6 months of treatment with nasal continuous positive airway pressure (nCPAP). BP was recorded using an ambulatory blood pressure monitoring (ABPM) device with oscillometric measurement method (SpaceLabs 90207) over a period of 24 h with intervals of 15 min in daytime and nighttime. Hypertension was defined as mean BP in the daytime period > 135/85 mm Hg; OSA was diagnosed when a full night polysomnography indicated an apnea hypopnea index (AHI) > 10/h. Hypertensive systolic/diastolic daytime BP values decreased significantly from 144.8/94.4 mm Hg at baseline to 138.9/89.4 mm Hg after short-term, and to 136.4/86.9 mm Hg after long-term nCPAP-therapy. Nighttime BP values, too, were reduced significantly from 137.6/87.1 mm Hg at baseline to 129.9/82.3 mm Hg after short-term, and to 128.6/ 79.8 mm Hg after long-term therapy. In addition to these data the heart rate fell significantly from 82.5 b/min to 74.8 b/min after 4-6 months in daytime, and from 70.9 b/min to 63.6 b/min in nighttime. The beneficial effect on diurnal and nocturnal hypertension in patients with nCPAP-therapy of OSA suggests a causal relationship between systemic hypertension and obstructive sleep apnea.
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PMID:Hypertension and obstructive sleep apnea. Ambulatory blood pressure monitoring before and with nCPAP-therapy. 889 21

Obstructive sleep apnoea (OSA) has been implicated through epidemiologic studies as a co-morbid factor in cardiovascular disease. There is a greater incidence of hypertension and atherosclerosis related diseases such as stroke, angina, and acute myocardial infarction in patients with OSA. However, obesity is a common problem in OSA as well as cardiovascular disease and is argued by some to be the etiologic factor for both OSA and cardiovascular morbidity. Clearly, there is shortened longevity in patients with untreated or inadequately treated OSA. Other factors which could account for this early mortality in OSA are sudden death during sleep (arrhythmia) or even fatalities from sleep related automobile accidents. The reason that the association between OSA and cardiovascular disease remains unclear is that the relationship thus far is demonstrated only by epidemiological association, not by mechanisms showing a cause-effect relationship. Some of these possible mechanisms are discussed below. Regardless of the mechanisms, the evidence is that OSA needs to be treated aggressively if patient morbidity and mortality from cardiovascular disease is to be reduced.
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PMID:Obstructive sleep apnoea and cardiovascular morbidity. 890 28

Several health hazards and social disabilities are associated with obesity. Increased mortality is associated with increased body weight. A high rate of mortality results from heart disease, diabetes mellitus, gallbladder disease, high blood pressure, and cancer. Physiologic cardiovascular changes occur, leading to left ventricular hypertrophy and lipid abnormalities. Hypertension, stroke, and venous stasis are increased. Pulmonary abnormalities include obstructive sleep apnea, which can be associated with secondary polycythemia and right ventricular hypertrophy. Gallstones, gallbladder disease, and accumulation of fat on the liver are significantly increased. Gout and reproductive abnormalities in women are common. Osteoarthritis of the knees and spine occur, although osteoporosis is rare. Risk for endometrial and breast cancer is increased, particularly in the presence of increased central fat. Changes in the skin include stretch marks, acanthosis negricans, hirsutism, intertrigo, and multiple papillomas. Impaired psychosocial function is manifested as social isolation, loss of job mobility, increased employee absenteeism, and economic and social discrimination.
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PMID:Health hazards of obesity. 897 52

We studied pulmonary haemodynamics in 19 male patients, mean age 45 +/- 5 years, suffering from severe OSA, mean apnea/hypopnea index (AHI) 68 +/- 17. Pulmonary haemodynamisc were studied using Swan-Ganz thermodilution catheter in the supine position at rest, and at the end of the 7th minute of steady-state exercise (40 W). Investigations were repeated after one year of treatment with nasal CPAP. At rest mean pulmonary artery pressure (PPA), pulmonary wedge pressure (PW) and cardiac output (CO) were normal, PPA = 16.6 +/- 5.7 mmHg, PW = 5.2 +/- 1.8 l/min. Pulmonary vascular resistance (PVR) was slightly elevated = 155 +/- 65 d.sec.cm-5. On exercise only PVR remained unchanged. After a year of treatment PPA changed to 15.8 +/- 4.0 mmHg (NS), Pw-7.5 +/- 3.1 mmHg (NS), CO-4.9 +/- 1.6 L/min (NS), PVR - 145 +/- 35 d.sec.cm-5 (NS). In two patients with resting hypertension PPA dropped from 33 mmHg to 25 mmHg and 28 mmHg to 18 mmHg respectively. Statistical analysis showed no significant change in any of the studied variables after one year of the CPAP therapy.
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PMID:[Pulmonary circulation at rest and during exercise in patients with obstructive sleep apnea before and after one year of treatment with CPAP]. 899 59

Seven normotensive untreated patients with obstructive sleep apnea (OSA) and five control subjects without OSA were compared. Patients with cardiac dilation, chronic airflow limitation, liver and kidney disease, or diabetes mellitus were excluded. Change in pressure-heart rate relation to alpha-adrenergic stimulation (P-HRR), extracellular volume (ECV), and plasma volume (Vp) were measured during daytime. Plasma atrial natriuretic peptide (ANP), plasma renin and aldosterone concentrations were obtained at 1 hour intervals during the night. A mean apnea/hypopnea index (AHI) of 52.2 +/- 23.9/h and a mean lowest arterial oxygen saturation (SaO2) of 61.2 +/- 19.3% (mean +/- SD) were determined from polysomnographic monitoring in the patient group. Release of ANP was significantly higher during sleep in OSA patients than in control subjects (P < .01), with a maximum concentration between 4 and 6 AM in the former. Daytime ECV was significantly higher (P < .05) and Vp significantly lower (P < .05) in OSA patients. Night maximum concentration of ANP (max ANP) was negatively related to AHI (P < .05). P-HRR was negatively related to AHI (P < .05) and positively related to max ANP (P < .05). In conclusion, OSA syndrome alters hormonal system control of body fluid compartment regulation. The decreased response in night max ANP secretion in the most severe OSA patients could be explained by the smaller Vp observed in these patients, decreasing atrial and ventricular pressure loading. Furthermore, alteration of P-HRR, correlated to AHI and max ANP, strengthens the hypothesis that patients who develop hypertension are those in whom the protective mechanism of ANP release failed.
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PMID:Pressure-heart rate responses to alpha-adrenergic stimulation and hormonal regulation in normotensive patients with obstructive sleep apnea. 900 45

Several epidemiological studies have identified obstructive sleep apnea (OSA) as a risk factor for systemic hypertension, but a direct etiologic link between the two disorders has not been established definitively. Furthermore, the specific physiological mechanisms underlying the association between OSA and systemic hypertension have not been identified. The purpose of this study was to systematically examine the effects of OSA on daytime and nighttime blood pressure (BP). We induced OSA in four dogs by intermittent airway occlusion during nocturnal sleep. Daytime and nighttime BP were measured before, during, and after a 1-3-mo long period of OSA. OSA resulted in acute transient increases in nighttime BP to a maximum of 13.0+/-2.0 mmHg (mean+/-SEM), and eventually produced sustained daytime hypertension to a maximum of 15.7+/-4.3 mmHg. In a subsequent protocol, recurrent arousal from sleep without airway occlusion did not result in daytime hypertension. The demonstration that OSA can lead to the development of sustained hypertension has considerable importance, given the high prevalence of both disorders in the population.
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PMID:Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model. 901 62


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