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PubMed2006

Circulating adrenomedullin in obstructive sleep apnoea.

Adrenomedullin (AM) is a potent endothelial-derived vasodilator secreted under the influence of various stimuli such as hypoxia, shear stress and cytokines. As all of these stimuli might be active under the conditions of obstructive sleep apnoea (OSA), we hypothesized that vascular AM production is increased in these patients. The study included 41 consecutive OSA patients and 28 control subjects without sleep-disordered breathing who were recruited from a pool of patients hospitalized for other reasons. Both groups were matched for anthropometric and comorbid factors. In all patients, i.e. OSA and controls, peripheral venous blood samples were taken at 07:00 hours after diagnostic polysomnography. In subsets of OSA patients, this was repeated after two nights of continuous positive airway pressure (CPAP) therapy (n = 28) and after several months of constant CPAP use (n = 11). The controls and the untreated OSA patients did not have serial blood sampling. In all blood samples, plasma AM levels were measured by an enzyme immunoassay kit. At baseline, the OSA patients had markedly elevated AM concentrations when compared to the controls. There were no differences between normo- and hypertensive OSA patients. After two nights of CPAP therapy, AM levels significantly decreased. Patients on long-term CPAP treatment showed complete normalization of plasma AM concentrations. In conclusion, this pilot study suggests that circulating AM is increased in untreated OSA irrespective of coexistent arterial hypertension and declines after CPAP therapy. AM upregulation might be considered as an adaptive mechanism to counteract the emergence of OSA-related cardiovascular disease.

Adrenomedullin↗

PubMed2006

Inflammatory measures in children with obstructive sleep apnoea.

AIM: To evaluate a range of inflammatory measures in children with obstructive sleep apnoea (OSA). METHODS: In total, 44 children with polysomnographically defined OSA (30 boys; mean age: 7.3 +/- 3.7 years) and 69 control subjects (44 boys; mean age: 7.6 +/- 4 years) were recruited. Controls were screened for symptoms of OSA by questionnaire at the time of elective surgery that was unrelated to the upper airway. Blood samples were analysed for C-reactive protein, and cytokines IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, GM-CSF, IFN-gamma and TNF-alpha. RESULTS: The majority of the children had mild OSA (32/44). Children with OSA (respiratory disturbance index 5.3 +/- 6.5 events/h) had significantly higher IFN-gamma and IL-8 levels than controls (P < 0.001 and 0.003, respectively), although correction for age, sex and body mass index reduced these differences (IFN-gammaP = 0.002, and IL-8 P = 0.051). There were no significant correlations between inflammatory measures and body mass index, respiratory disturbance index, or other sleep, desaturation, or arousal parameters including respiratory or spontaneous arousal indices, desaturation index or severity, sleep efficiency, or apnoea/hypopnoea duration in the OSA group. CONCLUSION: Children with OSA, even of mild severity, have significantly elevated IFN-gamma levels and a trend towards elevated IL-8 levels compared with asymptomatic controls, consistent with a pro-inflammatory effect of OSA. These changes seen in mild OSA may precede changes in other pro-inflammatory cytokines found in studies of adults with more severe and long-standing disease, implying a potential benefit from early disease identification and intervention.

Adolescent↗

PubMed1996

Craniofacial abnormalities in obstructive sleep apnoea: implications for treatment.

Obstructive sleep apnoea (OSA) is a common disorder, and is characterized by repetitive closure of the upper airway during sleep. Upper airway narrowing and sleep-induced loss of muscle tone are important factors in the development of OSA. Over the last decade there has been a growing recognition that craniofacial abnormalities occur commonly in OSA patients. The more commonly identified abnormalities include mandibular deficiency, an inferiorly placed hyoid bone relative to the mandibular plane, a narrowed posterior air space, a greater flexion of the cranial base, and elongation of the soft palate. It is thought that these abnormalities result in upper airway narrowing, thereby predisposing to OSA. When the well established role of obesity in the development of OSA is taken into account, a model of OSA emerges in which the degree of craniofacial abnormalities determines the extent of obesity required to produce OSA in a given individual. The recognition of the role of craniofacial abnormalities in the development of OSA has led to a number of treatment strategies aimed at correcting or improving craniofacial structure, thereby preventing upper airway collapse during sleep. These treatments include dental appliances, and various maxillofacial surgical procedures. An improved understanding of the evolution of OSA from childhood to adulthood, in relation to facial development, may lead to a preventative strategy for this disorder.

Cephalometry↗

PubMed2006

The risk profile for obstructive sleep apnea does not affect the recurrence of atrial fibrillation.

BACKGROUND: Obstructive sleep apnea (OSA) has been linked to increased prevalence and recurrence of atrial fibrillation (AF). We hypothesized that OSA may aggravate AF in patients with pacemakers implanted for sinus bradycardia who had documented paroxysmal AF. METHODS: Seventy-two patients (36 M, aged 77 +/- 6 years) completed the study. All patients received a dual-chamber pacemaker equipped with diagnostic and preventive functions for AF. OSA was diagnosed with the Berlin Questionnaire, which is validated to identify patients with OSA. Four-month continuous pacemaker recordings were collected for all patients. RESULTS: OSA was diagnosed in 28% of patients. Patients at high risk for OSA (HR group) and patients at low risk for OSA (LR group) were equivalent for gender, age, and body mass index. The rate of hypertension was higher in HR than in LR group (90% vs 44%, P < 0.01). The prevalence of paroxysmal AF during the study period was similar in HR and LR group (53% vs 44%, P = NS). Overall number of AF episodes per month was not significantly different between HR and LR group (7 +/- 13 vs 36 +/- 122, P = NS). Similarly, AF burden (AF%) was not significantly different between HR and LR group (0.3 +/- 0.6 vs 2.0 +/- 4.8, P = NS). Circadian distribution of AF episodes was similar in both groups. CONCLUSION: Long-term pacemaker recording of AF recurrence, AF burden, and its circadian distribution is similar in patients with paroxysmal AF at high risk for OSA and those at low risk for OSA.

Aged↗

PubMed2006

Induced sputum inflammatory measures correlate with disease severity in children with obstructive sleep apnoea.

OBJECTIVE: To establish the association between airway inflammation and severity of obstructive sleep apnoea (OSA) in children. METHODS: Consecutive children presenting with symptoms suggestive of OSA were recruited. They completed a sleep apnoea symptom questionnaire, underwent physical examination, spirometry, sputum induction and an overnight polysomnography. Adequate sputum contained <50% squamous epithelial cells, and OSA was diagnosed if the obstructive apnoea index was >1. RESULTS: 73 children with a median (interquartile range (IQR)) age of 11.3 (10.0-13.2) years were recruited. There were 21 girls and the median body mass index of the group was 24.0 (18.0-27.0) kg/m2. The most common presenting symptoms were habitual snoring, mouth breathing and prone sleeping position. Sputum induction was successful in 43 (59%) children, of whom 14 were found to have OSA. Children with OSA had significantly greater percentage sputum neutrophil than those without OSA (18.5 (IQR 8.0-42.0) v 4 (IQR 3.0-11.3), p = 0.006). On multiple regression analysis, percentage sputum neutrophil was significantly associated with OSA (odds ratio = 1.1, p = 0.013). CONCLUSION: Children with OSA had airway inflammation characterised by a marked increase in neutrophils. Further studies are needed to confirm these findings and to better define the downstream cellular interactions and molecular pathogenesis in childhood OSA.

Adolescent↗

PubMed2006

Swallowing function and upper airway sensation in obstructive sleep apnea.

The objective of this study was to determine whether impaired upper airway (UA) mucosal sensation contributes to altered swallowing function in obstructive sleep apnea (OSA). We determined UA two-point discrimination threshold (2PDT) and vibratory sensation threshold (VST) in 15 men with untreated OSA and 9 nonapneic controls (CL). We then assessed swallowing responses to oropharyngeal fluid boluses delivered via a catheter. The threshold volume required to provoke swallowing and the mean latency to swallowing were determined, as was the phase of the respiratory cycle in which swallowing occurred [expressed as percentage of control cycle duration (%CCD)] and the extent of prolongation of the respiratory cycle after swallowing [inspiratory suppression time (IST)]. 2PDT and VST were significantly impaired in OSA patients compared with CL subjects. 2PDT was positively correlated with swallowing latency and threshold volume in CL subjects, but not in OSA patients. Threshold volume did not differ between the groups [median value = 0.1 ml (95% confidence interval = 0.1-0.2) for OSA and 0.15 ml (95% confidence interval = 0.1-0.16) for CL], whereas swallowing latency was shorter for OSA patients [3.3 (SD 0.7) vs. 3.9 (SD 0.8) s, P = 0.04]. %CCD and IST were similar for OSA patients and CL subjects. However, among OSA patients there was a significant inverse relation between VST and IST. These findings suggest that oropharyngeal sensory impairment in OSA is associated with an attenuation of inhibitory modulating inputs to reflex and central control of UA swallowing function.

Adult↗

PubMed2001

Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics.

BACKGROUND: Limited information exists regarding the development of pulmonary hypertension in patients with obstructive sleep apnea (OSA) in the absence of lung and heart comorbidity. OBJECTIVES: The aims of this study were to investigate whether OSA patients without any other cardiac or lung disease develop pulmonary hypertension, and to assess the effect of continuous positive airway pressure (CPAP) treatment on pulmonary artery pressure (P(PA)). METHODS: Twenty-nine patients aged 51 +/- 10 years with OSA and 12 control subjects were studied with pulsed-wave Doppler echocardiography for estimation of P(PA) before and after 6-month effective treatment with CPAP. RESULTS: A significantly higher mean P(PA) was found in OSA patients as compared to control subjects (17.2 +/- 5.2 vs. 12.1 +/- 1.9 mm Hg, p < 0.001). Six out of the 29 OSA patients had mild pulmonary hypertension (P(PA) > or = 20 mm Hg). Significant differences were observed between pulmonary hypertensive and normotensive OSA patients with respect to age (62 +/- 4 vs. 48 +/- 15 years, respectively, p < 0.05), body mass index (41 +/- 7 vs. 32 +/- 4 kg/m(2), p < 0.02) and daytime P(a)O(2) (81 +/- 9 vs. 92 +/- 9 mm Hg, p < 0.05). CPAP treatment was effective in reducing mean P(PA) in both groups of pulmonary hypertensive and normotensive OSA patients (decreases in P(PA) from 25.6 +/- 4.0 to 19.5 +/- 1.5 mm Hg, p < 0.001; from 14.9 +/- 2.2 to 11.5 +/- 2.0 mm Hg, respectively, p < 0.001). CONCLUSIONS: A proportion (20.7%) of OSA patients without any other lung or heart disease and characterized by older age, greater obesity and lower daytime oxygenation develop mild pulmonary hypertension which has been partially or completely reversed after 6-month CPAP treatment. In conclusion, OSA alone constitutes an independent risk factor for the development of pulmonary hypertension.

Adult↗

PubMedDate not supplied

Sleep apnea syndrome and diastolic blood pressure elevation during exercise.

BACKGROUND: Several studies assessing the role of obstructive sleep apnea syndrome (OSAS) as an independent risk factor for hypertension have produced conflicting results. Although the sleep apnea syndrome is associated with hypertension, there are no references regarding the blood pressure response of normotensive OSAS patients during exercise. STUDY OBJECTIVES: The aim of this study was to investigate the relationship between diastolic blood pressure (DBP) response during exercise and the severity of OSAS. METHODS: We performed exercise testing a day after polysomnography in 17 normotensive males who were admitted for the first time because of OSAS and in 10 normal subjects who were members of the same families. During maximal incremental exercise test (bicycle ergometry) oxygen consumption (VO(2)) and the DBP were estimated at rest and at peak exercise. VO(2) was also measured when DBP were 100 and 110 mm Hg. RESULTS: At peak exercise DBP was significantly higher in OSAS patients (115.3 +/- 9.2 mm Hg) than in normal subjects (101 +/- 8.4 mm Hg, p < 0.01). OSAS patients reached a DBP of 110 mm Hg with a significantly lower VO(2) than normal subjects (1,881.5 +/- 703.4 vs. 1,972.3 +/- 108.6 ml/min, p = 0.045). VO(2) was not different between the two groups at a DBP of 100 mm Hg (1,211.2 +/- 371.7 vs. 1,536.6 +/- 267.2 ml/min, p = 0.089) but OSAS patients had a significantly lower heart rate than normals (111.2 +/- 13 vs. 118.6 +/- 27.6, p = 0.009). None of the aspects of quality of life, according to the Nottingham Health Profile Questionnaire, Part 1, were significantly different between patients and normal subjects. CONCLUSIONS: Normotensive OSAS patients develop DBP elevation at an earlier stage during exercise compared to normal subjects. This hypertensive response was not correlated with the severity (apnea-hypopnea index, oxygen desaturation parameters) of OSAS. DBP elevation could be a limiting factor of physical performance in this group of patients.

Adult↗

PubMedDate not supplied

Decreased plasma levels of orexin-A in sleep apnea.

BACKGROUND: Orexin-A, also known as hypocretin, is a neuropeptide implicated in appetite and sleep regulation. Because the obstructive sleep apnea syndrome (OSAS) is characterized by obesity and excessive daytime sleepiness, we hypothesized that orexin-A levels may be abnormal in patients with OSAS. Further, since treatment with continuous positive airway pressure (CPAP) in patients with OSAS is very effective in normalizing daytime sleepiness, we also hypothesized that the chronic use of CPAP may influence plasma levels of orexin-A in these patients. OBJECTIVE: To evaluate plasma levels of orexin-A in patients with OSAS and the effect of CPAP treatment. PATIENTS AND METHODS: We compared the plasma levels of orexin-A in 13 healthy controls, 27 untreated patients with OSAS and 14 patients treated with CPAP during at least 1 year (4.5 +/- 0.5 h/night; mean +/- SEM). All patients had severe OSAS (apnea-hypopnea index, 57 +/- 4 h(-1)). RESULTS: Orexin-A plasma levels were significantly lower in untreated (9.4 +/- 1.9 pg.ml(-1), p < 0.01) and treated patients with OSAS (4.2 +/- 1.5 pg.ml(-1), p < 0.001) than in healthy subjects (20.6 +/- 4.5 pg.ml(-1)). In untreated patients, orexin-A levels were not significantly related to daytime somnolence assessed by Epworth scale (r = -0.18, p = 0.37) or the body mass index (r = -0.13, p = 0.52). CONCLUSIONS: Orexin-A plasma levels are abnormally low in patients with OSAS, independently of the level of somnolence and/or presence of obesity. These results suggest that these low orexin-A levels may be related to the pathogenesis of OSAS.

Adult↗

PubMed2005

Altered blood rheology in obstructive sleep apnea as a mediator of cardiovascular risk.

BACKGROUND: Cardiovascular complications are common in patients with obstructive sleep apnea (OSA). Blood rheology is a major determent of coagulation and an established risk factor for cardiovascular events. Since nocturnal hypoxemia could influence parameters of blood rheology, we hypothesized that OSA alters blood rheology independent of other cardiovascular risk factors. METHODS: One hundred and ten consecutive patients admitted to the sleep laboratory were included. The association of plasma fibrinogen and viscosity (as parameters of blood rheology) with OSA was evaluated. RESULTS: One hundred and ten patients aged 61.4+/-10.1 years (body mass index 28.4+/-4.1 kg/m2) were included. OSA was confirmed in 63 patients (57.2%) with an apnea-hypopnea index (AHI) of 28.7+/-14.9 events/hour. Patients with OSA showed higher levels of plasma viscosity (1.36+/-0.09 vs. 1.31+/-0.08 mPas, p=0.005). Nevertheless, hypertensive apneics have even higher levels of plasma viscosity than nonapneics (1.38+/-0.091 vs. 1.32+/-0.028 mPas, p=0.018). Similar results were found in patients with coronary artery disease, where OSA was associated with elevated plasma viscosity (1.36+/-0.076 vs. 1.31+/-0.081 mPas, p=0.007). Plasma fibrinogen was correlated with nocturnal minimal oxygen saturation (r=-0275, p=0.0036) and AHI (r=0.297, p=0.001). OSA was associated with higher plasma fibrinogen (353+/-83 vs. 317+/-62 mg/dl, p=0.015). These differences persist with control for cardiovascular risk factors. CONCLUSIONS: Patients with OSA have elevated morning fibrinogen levels and a higher plasma viscosity, which correlate positively with indices of sleep apnea severity. These changes in blood rheology are independent of cardiovascular risk factors, and therefore, might be specific mechanisms of OSA. This supports the pathophysiological concept that sleep apnea is a cardiovascular risk factor.

Adult↗

PubMed2005

Prevalence of moderate or severe left ventricular diastolic dysfunction in obese persons with obstructive sleep apnea.

We investigated prior to gastric bypass surgery the prevalence of left ventricular diastolic dysfunction (LVDD) by Doppler and tissue Doppler echocardiography in 14 obese women and in 6 obese men, mean age 45 years, with a mean body mass index of 49+/-5 kg/m2 who had nocturnal polysomnography for obstructive sleep apnea (OSA). The Doppler and tissue Doppler echocardiographic data were analyzed blindly without knowledge of the clinical characteristics or whether OSA was present or absent. Of 20 patients, 8 (40%) had no OSA, 4 (20%) had mild OSA, and 8 (40%) had moderate or severe OSA. Moderate or severe LVDD was present in 4 of 8 patients (50%) with moderate or severe OSA and in none of 12 patients (0%) with no or mild OSA (p<0.01). Obese patients with moderate or severe OSA have a higher prevalence of moderate or severe LVDD than obese patients with no or mild OSA.

Adult↗

PubMed2006

Clinical, anthropometric and upper airway anatomic characteristics of obese patients with obstructive sleep apnea syndrome.

BACKGROUND: Obese subjects are at increased risk of developing obstructive sleep apnea syndrome (OSAS). However, the individual role of local (i.e., upper airway-related) and general (clinical and whole-body anthropometric) characteristics in determining OSAS in obese patients is still controversial. OBJECTIVES: To contrast the clinical, anthropometric and upper airway anatomical features of obese subjects presenting or not presenting with OSAS. METHODS: Thirty-seven obese (BMI > or =30 kg/m(2)) males with OSAS and 14 age- and gender-matched obese controls underwent clinical and anthropometric (BMI, waist-to-hip ratio and neck circumference) evaluation. In a subgroup of subjects (18 and 11 subjects, respectively), magnetic resonance imaging (MRI) during wakefulness was used to study the upper airway anatomy. RESULTS: OSAS patients showed significantly higher BMI, waist-to-hip ratio and neck circumference as compared to controls (p < 0.05). They also referred to nonrepairing sleep, impaired attention, and previous car accidents more frequently (p < 0.05). The transversal diameter of the airways (TDAW) at the retroglossal level by MRI was found to be an independent predictor of the presence and severity of OSAS (p < 0.05). Parapharyngeal fat increase, however, was not related to OSAS. A TDAW >12 mm was especially useful to rule out severe OSAS (apnea-hypopnea index >30, negative predictive value = 88.9%, likelihood ratio for a negative test result = 0.19). CONCLUSIONS: MRI of the upper airway can be used in association with clinical and anthropometric data to identify obese males at increased risk of OSAS.

Adult↗

PubMed1993

Nocturnal pollakiuria is a symptom of obstructive sleep apnea.

An increased urine excretion has been reported in obstructive sleep apnea (OSA) patients, but it is not clear whether it results in an increased number of nocturnal micturitions. The present study was aimed at investigating the frequency of nocturnal micturitions in OSA patients using a standardized questionnaire prospectively given to 102 OSA patients and 86 healthy male subjects. The frequency of nocturnal micturitions was significantly greater in the OSA patients than in the healthy subjects (more than 70% of the OSA patients with an apnea+hypopnea index > 50 reported nocturnal micturitions more than twice a week versus less than 25% of the healthy subjects, p < 0.0001). The number of nocturnal micturitions was also greater in the OSA patients than in the healthy subjects. There was an effect of age on the frequency of nocturnal micturitions; however, when age-matched subsamples were considered, there was still a significant difference between OSA patients and healthy subjects. In a subgroup of 25 OSA patients reevaluated after at least 1 year of home treatment with nasal continuous positive airway pressure the reported frequency of nocturnal micturitions had significantly decreased (p < 0.001). These results suggest that investigations aimed at establishing a diagnosis of OSA should be part of the work-up of patients complaining of nocturnal pollakiuria.

Adult↗

PubMed2003

Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure.

BACKGROUND: C-reactive protein (CRP) and interleukin (IL)-6 are important risk factors for atherosclerosis and coronary heart disease. In the present study, we examined serum levels of CRP and IL-6, IL-6 production by monocytes, and the effect of nasal continuous positive airway pressure (nCPAP) in patients with obstructive sleep apnea syndrome (OSAS). METHODS AND RESULTS: After polysomnography, venous blood was collected at 5 AM from 30 patients with OSAS and 14 obese control subjects. Serum levels of CRP and IL-6 and spontaneous production of IL-6 by monocytes were investigated. In addition, the effects of 1 month of nCPAP were studied in patients with moderate to severe OSAS. Levels of CRP and IL-6 were significantly higher in patients with OSAS than in obese control subjects (CRP P<0.001, IL-6 P<0.05). IL-6 production by monocytes was also higher in patients with OSAS than in obese control subjects (P<0.01). In patients with OSAS, the primary factors influencing levels of CRP were severity of OSAS and body mass index and those influencing levels of IL-6 were body mass index and nocturnal hypoxia. nCPAP significantly decreased levels of both CRP (P<0.0001) and IL-6 (P<0.001) and spontaneous IL-6 production by monocytes (P<0.01). CONCLUSIONS: Levels of CRP and IL-6 and spontaneous production of IL-6 by monocytes are elevated in patients with OSAS but are decreased by nCPAP. Therefore, OSAS is associated with increased risks for cardiovascular morbidity and mortality, and nCPAP may be useful for decreasing these risks.

C-Reactive Protein↗

PubMed2004

Association of atrial fibrillation and obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with recurrent atrial fibrillation (AF) after electrocardioversion. OSA is highly prevalent in patients who are male, obese, and/or hypertensive, but its prevalence in patients with AF is unknown. METHODS AND RESULTS: We prospectively studied consecutive patients undergoing electrocardioversion for AF (n=151) and consecutive patients without past or current AF referred to a general cardiology practice (n=312). OSA was diagnosed with the Berlin questionnaire, which is validated to identify patients with OSA. We also assessed its accuracy compared with polysomnography in a sample of the study population. Groups were compared with the 2-tailed t, Wilcoxon, and chi2 tests. Logistic regression modeled the association of AF and OSA after adjustment for relevant covariates. Patients in each group had similar age, gender, body mass index, and rates of diabetes, hypertension, and congestive heart failure. The questionnaire performed with 0.86 sensitivity, 0.89 specificity, and 0.97 positive predictive value in our sample. The proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, P=0.0004). The adjusted odds ratio for the association between AF and OSA was 2.19 (95% CI 1.40 to 3.42, P=0.0006). CONCLUSIONS: The novel finding of this study is that a strong association exists between OSA and AF, such that OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases. The coinciding epidemics of obesity and AF underscore the clinical importance of these results.

Aged↗

PubMed2000

Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea.

BACKGROUND: Patients with obstructive sleep apnea (OSA) experience repetitive episodic hypoxemia with consequent sympathetic activation and marked blood pressure surges, each of which may impair endothelial function. We tested the hypothesis that patients with OSA have impaired endothelium-dependent vasodilation, even in the absence of overt cardiovascular disease. METHODS AND RESULTS: We studied 8 patients with OSA (age 44+/-4 years) and 9 obese control subjects (age 48+/-3 years). Patients with OSA were newly diagnosed, never treated for OSA, on no medications, and free of any other known diseases. All obese control subjects underwent complete overnight polysomnographic studies to exclude occult OSA. Resistance-vessel function was tested by use of forearm blood flow responses to intra-arterial infusions of acetylcholine (a vasodilator that stimulates endothelial release of nitric oxide), sodium nitroprusside (an exogenous nitric oxide donor), and verapamil (a calcium channel blocker). Conduit-vessel function was also evaluated by ultrasonography. Brachial artery diameter was measured under baseline conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent vasodilator). Patients with OSA had a blunted vasodilation in response to acetylcholine (P:<0.007), but responses to sodium nitroprusside and verapamil were not significantly different from those of control subjects. No significant difference in conduit-vessel dilation was evident between OSA patients and obese control subjects. CONCLUSIONS: Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation. This may be implicated in the pathogenesis of hypertension and heart failure in this condition.

Acetylcholine↗

PubMed1998

Sympathetic activity in obese subjects with and without obstructive sleep apnea.

BACKGROUND: Obese humans are reported to have increased muscle sympathetic nerve activity (MSNA). Obstructive sleep apnea (OSA) may also be accompanied by increased MSNA. Because there is a high prevalence of OSA in obese humans, it is possible that high MSNA reported in obese subjects may in fact reflect the presence of OSA in these subjects. We tested the hypothesis that obesity, per se, in the absence of OSA, is not accompanied by increased MSNA. METHODS AND RESULTS: We measured MSNA in 25 healthy normal-weight subjects and 30 healthy sedentary obese subjects. All subjects were screened by history and examination to exclude subjects with OSA or hypertension. OSA was further excluded by overnight polysomnographic studies. Despite careful screening, polysomnography revealed that 1 of 25 normal-weight subjects and 9 of 30 obese subjects had occult OSA (P=0.015). MSNA was similar in normal-weight subjects (41+/-3 bursts per 100 heartbeats) and obese subjects without sleep apnea (42+/-3 bursts per 100 heartbeats, P=0.99). MSNA in the 9 obese subjects with occult OSA was 61+/-8 bursts per 100 heartbeats, which was higher than MSNA in normal-weight subjects without sleep apnea (P=0.02) and higher than MSNA in obese subjects without sleep apnea (P=0.02). CONCLUSIONS: Obesity alone, in the absence of OSA, is not accompanied by increased sympathetic activity to muscle blood vessels.

Adult↗

PubMed1997

Cerebral metabolism in sleep apnea. Evaluation by magnetic resonance spectroscopy.

Repeated apneic episodes during sleep may lead to cerebral damage in patients with obstructive sleep apnea (OSA). We performed proton magnetic resonance (MR) spectroscopic studies to examine cerebral metabolism in patients with OSA. We studied 15 healthy subjects and 23 patients with OSA who displayed no anatomical abnormalities on MR imaging. The patients were classified into two groups based on the results of polysomnography: mild OSA (11 patients) or moderate to severe OSA (12 patients). All the subjects were examined with two-dimensional chemical shift imaging. The N-acetylaspartate (NAA)/choline (Cho), NAA/creatine (Cre), and Cho/Cre ratios for cerebral cortex and white matter were calculated separately. A statistically significant intergroup difference was found for the NAA/Cho ratio in cerebral white matter (p < 0.005). This ratio was significantly lower in patients with moderate to severe OSA than in patients with mild OSA (p < 0.01) and healthy subjects (p < 0.01). Our findings indicate that cerebral metabolic changes occur in normal-appearing brain tissue in patients with moderate to severe OSA. The findings of a decreased NAA/Cho ratio suggests the presence of cerebral damage, probably caused by repeated apneic episodes. Proton MR spectroscopy may be useful for evaluating cerebral damage in patients with OSA.

Adult↗