Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although sleep apnea (SA) appears to be a cardiovascular risk factor, little is known about its frequency in patients with transient ischemic attack (TIA) and stroke. We prospectively studied 59 subjects (26 women and 33 men; mean age, 62 years) with stroke (n = 36) or TIA (n = 23) with the use of a standard protocol that included assessment of snoring and daytime sleepiness (Epworth Sleepiness Score [ESS]), a validated SA score (Sleep Disorders Questionnaire [SDQ-SA]), and a severity of stroke score (Scandinavian Stroke Scale [SSS]). SA was considered clinically probable (P-SA) when habitual snoring was associated with an ESS of > 10 or when SDQ-SA score was > or = 32 in women and > or = 36 in men. Polysomnography (PSG) was obtained in 36 subjects (group 1) a mean of 12 days after TIA or stroke. In 23 subjects (group 2), PSG was not available (n = 11), refused (n = 10), or inadequate (n = 2). Clinical and PSG data were compared with those obtained in 19 age- and gender-matched control subjects. Groups 1 and 2 were similar in mean age (61 versus 64 years), type of event (36% versus 44% TIA), reported habitual snoring (58% versus 52%), and P-SA (58% versus 50%). PSG showed SA (Apnea-Hypopnea Index [AHI], > or = 10) in 25 of 36 subjects (69%). The proportion of subjects with SA was similar in the TIA and stroke groups (69% versus 70%) and was well above the frequency found in our control group (15%). An AHI of > or = 20 and a minimal oxygen saturation of < 85% were each found in 20 of 36 subjects (55%). Gender and age did not correlate with severity of SA. Subjects with habitual snoring, P-SA, or severe stroke (SSS of < 30) had a significantly higher AHI (p < 0.05). The sensitivity of P-SA for SA was 64%, and the specificity was 67%. We conclude that SA has a high frequency in patients in the acute phase of TIA and stroke and SA cannot be predicted reliably on clinical grounds alone but is more likely in patients with habitual snoring, abnormal SDQ-SA, or severe stroke.
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PMID:Sleep apnea in patients with transient ischemic attack and stroke: a prospective study of 59 patients. 890 24

It is well established that nocturnal hypoxemia in sleep apnea causes an inversion of the circadian arterial pressure rhythm and triggers nocturnal hypertension. Since sleep apnea is very frequent in dialysis patients, we hypothesized that nocturnal hypoxemia may be a factor that contributes to alter the 24-hour arterial pressure profile in these patients. To test the hypothesis 32 dialysis patients underwent 24-hour blood pressure (BP) monitoring and continuous monitoring of arterial O2 saturation during the night-time. Hemodialysis patients were studied during the non-dialysis day. All patients underwent an echocardiographic study. Thirteen patients had no episode of nocturnal hypoxemia (group I), 7 had at least one episode overnight but less than 2 episodes/hr (group II) and 12 had > or = 2 episodes/hr (group III). The average daytime systolic pressure was similar in the three groups. However, the average nocturnal systolic pressure fell in the first group (-2.5 +/- 4.2%) and rose in the second (+2.0 +/- 3.6%) and in the third (+3.9 +/- 2.2%) group (one way ANOVA, P < 0.005). The relative wall thickness of the left ventricle (RWT) was significantly (P < 0.05) higher in group III than in group I, and in the aggregate (N = 32) there was an inverse relationship between average nocturnal SaO2 and RWT (r = -0.43, P = 0.015). The proportion of patients with concentric remodeling or concentric hypertrophy was higher (P = 0.05) in the group with a more severe degree of nocturnal hypoxemia (group III, 8 of 12) than in the other two groups (group I, 3 of 13; group II, 2 of 7). Nocturnal hypoxemia is associated with the "non-dipping" arterial pressure profile in dialysis patients. Disturbed respiratory control during the night may represent an important cardiovascular risk factor in dialysis patients.
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PMID:Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients. 955 20

Although obstructive sleep apnea (OSA) appears to be a cardiovascular risk factor, its frequency in patients with transient ischemic attack (TIA) and stroke remains poorly known. We prospectively studied 128 patients (mean +/- SD age = 59 +/- 15 years) with stroke (n = 75) or TIA (n = 53). Assessment included body mass index (BMI); history of snoring and daytime sleepiness; cardiovascular risk factors and diseases; and severity of stroke (Scandinavian Stroke Scale = SSS). Polysomnography (PSG) was obtained in 80 subjects (group 1), a mean of 9 days (range, 1-71 days) after TIA or stroke. In 48 subjects (group 2), PSG was not available, refused, or inadequate. Groups 1 and 2 were similar with the exception of gender distribution. Clinical and PSG data were compared to those of 25 healthy controls matched for age, gender, and BMI. An apnea-hypopnea index (AHI) > 10 was found in 62.5% of subjects and 12.5% of controls. Between patients and controls there was a significant difference in AHI (mean [range]: 28 (0-140) vs 5 (0-24), p < 0.001), maximal apnea duration (mean + SD: 37 +/- 23 vs 23 +/- 13 seconds, p = 0.009), and minimal oxygen saturation (mean + SD: 82 +/- 10% vs 90 +/- 5%, p < 0.001). Conversely, frequency and severity of OSA were similar in stroke and TIA subjects. Multiple regression analysis identified age, BMI, diabetes, and SSS as independent predictors of AHI. Sleep apnea has a high frequency in patients with TIA and stroke, particularly in older patients with high BMI, diabetes, and severe stroke. These results may have implications for prevention, acute treatment, and rehabilitation of patients with acute cerebrovascular diseases.
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PMID:Sleep apnea in acute cerebrovascular diseases: final report on 128 patients. 1020 Oct 66

Myocardial infarction shows a circadian pattern with a maximum in the early morning hours. In patients with sleep-related breathing disorders (SRBD), it is assumed that apnea-associated changes of hemodynamics, blood gases, and rheology lead to a higher frequency of myocardial infarction during sleep. This investigation analyzes the circadian pattern of myocardial infarction in patients with and without SRBD. Within a time period of 20 months, 89 male patients with acute myocardial infarction were consecutively admitted to the intensive care unit. A nocturnal long-term registration of oxygen saturation, heart rate, breathing sounds, and body position by means of a 4-channel recording system (MESAM IV) was carried out in 59 of the 89 patients 6 to 10 days (evaluation I) and in 43 of 59 patients 22 to 28 days after infarction (evaluation II). Sleep apnea with a respiratory-disturbance-index (RDI > or = 10/h was found in 44.1/39.5% of the patients (evaluation I/II). In 22% of the patients, time of infarction was during a sleeping period. Patients with myocardial infarction during sleep had a clearly higher RDI in comparison to patients with a myocardial infarction during wakefulness (evaluation I: 22.7 versus 9.4/h; p = 0.08; evaluation II: 20.3 versus 7.3; p < 0.05). 53.6% of all myocardial infarctions occurred during the time period 5:00-11:00 a.m. Investigations in a larger number of patients are necessary to confirm these results as well as the relevance of sleep apnea as a cardiovascular risk factor.
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PMID:[Does sleep apnea increase the risk of myocardial infarct during sleep?]. 1044 11

Nocturnal hypoxemia secondary to sleep apnea has long been implicated as a cardiovascular risk factor in renal failure, but to date there is no study that links nocturnal hypoxemia to cardiovascular outcomes in end-stage renal disease. Fifty uremic patients on regular dialysis treatment without primary sleep apnea, pulmonary diseases, or other illnesses that may cause sleep apnea underwent pulse oximetry studies during night and were followed up for 32 mo. Average nocturnal SaO(2), minimal SaO(2), and the number of episodes of hypoxemia were similar in patients who died during the follow-up and in patients who survived, and none of these parameters predicted all-cause mortality. Average nocturnal SaO(2) was significantly lower (P = 0.006) in patients who had cardiovascular events during the follow-up (94.7 +/- 2.9%) than in event-free patients (97.1 +/- 1.3%). In a Cox model, average nocturnal SaO(2) was the second factor in rank explaining these outcomes. In this model a 1% decrease in average nocturnal SaO(2) was associated with a 33% increase in the incident risk of fatal and nonfatal cardiovascular events. Furthermore the risk of cardiovascular events was 5.05 times higher in patients with average nocturnal SaO(2) <95% (95% CI 1.61 to 15.86) than in those above this threshold (P = 0.005). This study adds weight to the hypothesis that nocturnal hypoxemia in dialysis patients represents an important cardiovascular risk factor.
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PMID:Nocturnal hypoxemia predicts incident cardiovascular complications in dialysis patients. 1185 78

Hypertension is a cardiovascular risk factor which needs a good evaluation before treatment. When this latter is decided, the target is to normalize high blood pressure. This requires a complete information of the patient; the latter will also receive individualized non pharmacological advices and, also, possibly different antihypertensive drugs. When blood pressure does not normalize, one must check the blood pressure measurement technique, the compliance to treatment and potential pharmacologic interferences. Secondary hypertension is only considered if resistance to therapy cannot be found. It should be remembered that obesity and sleep apnea disorders are responsible of many instances of refractory hypertension.
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PMID:[How I investigate...a refractory hypertension]. 1223 25

Sleep apnea syndrome (SAS) is an important cardiovascular risk factor in patients with hypertension or myocardial infarction (MI). We evaluated the influence of SAS on autonomic nervous activity and QT dispersion in patients with hypertension or coronary artery disease with old MI. A portable sleep polygraph was attached to 30 healthy volunteers (N group), 30 patients with essential hypertension (HT group), and 30 patients with old myocardial infarction (MI group) to serially record oronasal respiration, tracheal sound, thoracic respiratory movement, and percutaneous arterial oxygen saturation. In addition, a digital Holter ECG was used to examine heart rate variability during nighttime sleep. Heart rate variability was analyzed by obtaining low-frequency (LF) power, high-frequency (HF) power, the LF/HF ratio, and very low-frequency (VLF) power. Dispersion of QT intervals was obtained by CM5 and CM1 leads. VLF and LF powers were significantly higher in the HT-SAS group (hypertensive patients with SAS) than the N and HT-NSAS groups (hypertensive patients without SAS). The HF power was significantly lower in the HT-NSAS group than the N group, but the decrease in HF power in hypertension was not observed in the HT-SAS group. The LF/HF ratio was significantly higher in the HT-NSAS group than the N group, and this value was further increased in the HT-NSAS group. Percutaneous arterial oxygen saturation was decreased, and QT dispersion was significantly increased in the MI group during sleep apnea episodes. More severe autonomic nervous dysfunction and increased QTc dispersion were observed in hypertensive patients with SAS during episodes of apneas and hypopneas compared to those without SAS. These findings suggest that SAS may be associated with the future development of cardiac events.
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PMID:Influence of sleep apnea on autonomic nervous activity and QT dispersion in patients with essential hypertension and old myocardial infarction. 1513 67

Obesity is a multifactorial, chronic disorder that has reached epidemic proportions in most industrialized countries and is threatening to become a global epidemic. Obese patients are at higher risk from coronary artery disease, hypertension, hyperlipidemia, diabetes mellitus, cancers, cerebrovascular accidents, osteoarthritis, restrictive pulmonary disease, and sleep apnoea. In particular, visceral fat accumulation is usually accompanied by insulin resistance or type 2 diabetes mellitus, hypertension, hypertriglyceridemia, high uremic acid levels, low high density lipoprotein (HDL) cholesterol to define a variously named syndrome or metabolic syndrome. Metabolic syndrome is now considered a major cardiovascular risk factor in a large percentage of population in worldwide. Both obesity and metabolic syndrome are particularly challenging clinical conditions to treat because of their complex pathophysiological basis. Indeed, body weight represents the integration of many biological and environmental components and relationships among fat and glucose tolerance or blood pressure are not completely understood. Efforts to develop innovative anti-obesity drugs, with benefits for metabolic syndrome, have been recently intensified. In general two distinct strategies can be adopted: first, to reduce energy intake; second, to increase energy expenditure. Here we review some among the most promising avenues in these two fields of drug therapy of obesity and, consequently, of metabolic syndrome.
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PMID:Emerging aspects of pharmacotherapy for obesity and metabolic syndrome. 1545 65

Hypertension is a cardiovascular risk factor which needs a good evaluation before treatment. When this latter is decided, the target is to normalize high blood pressure. This requires a complete information of the patient; the latter will also receive individualized non pharmacological advices and also possibly different antihypertensive drugs. When blood pressure does not normalize, one must check the pressure measurement technique, the compliance to treatment and potential pharmacological interferences. Secondary hypertension is only considered if resistance to therapy cannot be found. It should be remembered that obesity and sleep apnea disorders are responsible of many instances of resistant hypertension.
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PMID:[Resistant hypertension]. 1581 36

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.
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PMID:Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP. 1638 45


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