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PubMed2001

In vitro activity of a novel antimycobacterial compound, N-octanesulfonylacetamide, and its effects on lipid and mycolic acid synthesis.

beta-Sulfonyl carboxamides have been proposed to serve as transition-state analogues of the beta-ketoacyl synthase reaction involved in fatty acid elongation. We tested the efficacy of N-octanesulfonylacetamide (OSA) as an inhibitor of fatty acid and mycolic acid biosynthesis in mycobacteria. Using the BACTEC radiometric growth system, we observed that OSA inhibits the growth of several species of slow-growing mycobacteria, including Mycobacterium tuberculosis (H37Rv and clinical isolates), the Mycobacterium avium complex (MAC), Mycobacterium bovis BCG, Mycobacterium kansasii, and others. Nearly all species and strains tested, including isoniazid and multidrug resistant isolates of M. tuberculosis, were susceptible to OSA, with MICs ranging from 6.25 to 12.5 microg/ml. Only three clinical isolates of M. tuberculosis (CSU93, OT2724, and 401296), MAC, and Mycobacterium paratuberculosis required an OSA MIC higher than 25.0 microg/ml. Rapid-growing mycobacterial species, such as Mycobacterium smegmatis, Mycobacterium fortuitum, and others, were not susceptible at concentrations of up to 100 microg/ml. A 2-dimensional thin-layer chromatography system showed that OSA treatment resulted in a significant decrease in all species of mycolic acids present in BCG. In contrast, mycolic acids in M. smegmatis were relatively unaffected following exposure to OSA. Other lipids, including polar and nonpolar extractable classes, were unchanged following exposure to OSA in both BCG and M. smegmatis. Transmission electron microscopy of OSA-treated BCG cells revealed a disruption in cell wall synthesis and incomplete septum formation. Our results indicate that OSA inhibits the growth of several species of mycobacteria, including both isoniazid-resistant and multidrug resistant strains of M. tuberculosis. This inhibition may be the result of OSA-mediated effects on mycolic acid synthesis in slow-growing mycobacteria or inhibition via an undescribed mechanism. Our results indicate that OSA may serve as a promising lead compound for future antituberculous drug development.

Acetamides↗

PubMed2006

Left ventricular geometry in patients with obstructive sleep apnea coexisting with treated systemic hypertension.

BACKGROUND: Left ventricular (LV) hypertrophy is a common consequence of systemic hypertension (SH) and obstructive sleep apnea (OSA). However, little is known about the degree of LV involvement in patients with OSA coexisting with treated SH. OBJECTIVES: Our study was designed in order to assess the prevalence of distinct types of LV geometry in treated hypertensive OSA patients. METHODS PATIENTS: 183 patients with treated SH were enrolled to the study. Group 1 consisted of 38 patients with newly-diagnosed OSA and ineffectively treated SH. The remaining 145 patients with effectively treated SH were divided into three groups: group 2 - 70 patients with newly-diagnosed OSA, group 3 - 31 patients with OSA treated with continuous positive airway pressure (CPAP), and group 4 - 44 patients without OSA. Overnight sleep studies and M-mode echocardiography were performed. RESULTS: LV mass index did not differ between the study groups. Mean values of LV end-diastolic diameter (LVED) were 55.4 +/- 6.8 mm in group 1 and 53.6 +/- 6.9 mm in group 2 and were significantly increased in comparison to subjects treated with CPAP and controls (49.8 +/- 6.8 mm and 50.1 +/- 64.7 mm, respectively; p = 0.001). LVED correlated positively with the apnea-hypopnea index and desaturation index. LV eccentric hypertrophy was the commonest type of LV geometry in newly-diagnosed OSA patients. CONCLUSIONS: The major finding of our study is the predominance of LV eccentric hypertrophy in newly-diagnosed OSA patients. We suggest that a relatively moderate degree of LV involvement in hypertensive OSA patients may depend on the cardioprotective effect of concomitant antihypertensive therapy, ameliorating OSA-dependent neurohumoral abnormalities.

Antihypertensive Agents↗

PubMed2003

Serum amyloid a in obstructive sleep apnea.

BACKGROUND: Patients with severe obstructive sleep apnea (OSA) may have increased risk for cardiovascular and cerebrovascular diseases. Serum amyloid A (SAA) protein has recently been linked to the development of atherosclerosis, stroke, diabetes, and dementia. We tested the hypothesis that plasma SAA levels are increased in otherwise healthy subjects with OSA. METHODS AND RESULTS: Plasma SAA levels were measured in 10 male patients with moderate to severe OSA before sleep, after 5 hours of untreated OSA, and in the morning after effective continuous positive airway pressure treatment. SAA levels were also measured in 10 closely matched control subjects at similar time points. Baseline plasma SAA levels before sleep were strikingly higher in patients with moderate to severe OSA than in controls (18.8+/-2.6 versus 7.2+/-2.6 microg/mL, respectively; P=0.005) and remained unchanged in both groups throughout the night. SAA levels in 10 male patients with mild OSA were comparable with controls (P=0.46). Plasma SAA in 7 female patients with moderate to severe OSA was also markedly higher compared with matched control female subjects (24.1+/-2.4 versus 10.2+/-2.4 microg/mL, respectively; P=0.0013) but was not different from male patients with moderate to severe OSA (P=0.3). There was a significant positive correlation between SAA and apnea-hypopnea index (r=0.40, P=0.03). CONCLUSIONS: Plasma SAA levels are more than 2-fold greater in patients with moderate to severe OSA compared with subjects with mild OSA or healthy controls regardless of gender. Elevated SAA may contribute to any increased risk for cardiovascular and neuronal dysfunction in patients with OSA.

Enzyme-Linked Immunosorbent Assay↗

PubMed1999

Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea.

BACKGROUND: The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. METHODS AND RESULTS: We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43+/-4 versus 21+/-3 bursts per minute; P<0. 001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=0.02), heart rate (10+/-1 versus 7+/-1 bpm; P=0.03), and mean arterial pressure (7+/-2 versus 0+/-2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106+/-20%) was greater than in control subjects (52+/-23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24+/-6%) than in control subjects (7+/-5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects. CONCLUSIONS: OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.

Adult↗

PubMed1994

Ventilatory responses during wakefulness in children with obstructive sleep apnea.

The pathophysiology of the obstructive sleep apnea syndrome (OSAS) is not fully understood. In children, airway obstruction secondary to tonsilloadenoidal hypertrophy is the leading cause of OSAS. However, not all children with tonsilloadenoidal hypertrophy develop OSAS. Thus, other factors, including abnormalities in ventilatory control, may contribute to the etiology of OSAS. To test this, we performed polysomnography and hypercapnic and hypoxic ventilatory response testing in 20 children and adolescents with OSAS (mean age, 8 +/- 3 [SD] yr) and 19 control subjects. Only two children with OSAS were obese. Children with OSAS had an apnea index of 16 +/- 20, peak PETCO2 of 54 +/- 5 mm Hg, and SaO2 nadir of 84 +/- 13% during polysomnography. Ventilatory responses were performed by rebreathing techniques. The slope of the hypercapnic ventilatory responses, corrected for body surface area, was 1.74 +/- 0.79 L/min/m2/mm Hg PETCO2 in children with OSAS and 1.45 +/- 0.58 L/min/m2/mmHg PETCO2 in control subjects (NS). Hypoxic ventilatory responses, corrected for body surface area, were -0.94 +/- 0.49 L/min/m2/% SaO2 in children with OSAS and -0.95 +/- 0.45 L/min/m2/% SaO2 in control subjects (NS); however, the sample size was small. There was a weak inverse correlation between the slope of the hypercapnic ventilatory response and the duration of hypoventilation during polysomnography (r = -0.44, p < 0.05). We conclude that children with OSAS have normal ventilatory responses to hypercapnia, and they may have normal ventilatory responses to hypoxia. We speculate that abnormal central ventilatory drive plays little if any role in the pathogenesis of pediatric OSAS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoids↗

PubMed1996

The association of sudden unexpected infant death with obstructive sleep apnea.

We studied the relationship of sudden unexpected infant death/apparent life-threatening events (ALTE) to obstructive sleep apnea (OSA) in 74 index probands who had either sleep-laboratory-confirmed OSA or a clinical diagnosis of OSA requiring treatment, 62 matched control probands, and their spouses and first- and second-degree relatives. Sleep was monitored in the home overnight, and OSA was defined by respiratory disturbance indices (number of apneas/hypopneas per hour of sleep) corrected for normal increases with age. Information on sudden unexpected infant death/ALTE was obtained by questionnaire and was corroborated. For living relatives, data were obtained by questionnaire, examination, or study (cephalometric radiographs, ventilatory responsiveness to hypercapnia and hypoxia). Eight index families had 10 infants with sudden unexpected infant death/ALTE; two control families had three infants with sudden death (p = 0.11). All told, 91 of the 136 families (index plus control) included members with OSA, and all 10 infant death/ALTE families were among these (versus zero of 45 families with no OSA; p = 0.03). The sudden infant death/ALTE families had a greater frequency of two or more members with OSA (p = 0.06), reported more respiratory disease or allergy, were more frequently brachycephalic (p = 0.05), and had a smaller mean posterior nasal spine-basion distance (p = 0.0001) and ratio of anterior mandibular/anterior maxillary dental height (p < 0.05). Ventilatory responses to hypoxia were reduced in members of families with OSA (p = 0.008), with a trend toward the greatest blunting in subjects from families with OSA plus sudden unexpected infant death/ALTE. Thus, OSA in adults and sudden unexpected infant death/ALTE in their biologic relatives appear to be related. Familial factors influencing this association may include the degree of the predilection for OSA, liability for respiratory illness or allergy, dimensions of the oral-pharyngeal airway, and ventilatory response to hypoxia.

Case-Control Studies↗

PubMed2001

Chemical control stability in patients with obstructive sleep apnea.

The role of chemical control instability in the pathogenesis of obstructive sleep apnea (OSA) is not clear. We studied 32 patients with OSA during sleep while their upper airway was stabilized with continuous positive airway pressure. Twelve patients had repetitive OSA whenever they were asleep, regardless of body position or sleep stage, and were classified as having severe OSA (apnea-hypopnea index [AHI] = 88 +/- 19). The remaining 20 patients had sporadic OSA or repetitive OSA for only part of the time (mild/moderate OSA; AHI = 27 +/- 16). Susceptibility to periodic breathing (PB) was assessed by gradually increasing controller gain, using proportional assist ventilation. The increase in loop gain (LG) at each assist level was quantified from the ratio of assisted tidal volume (VT) to the VT obtained during single-breath reloading tests (VT amplification factor [VTAF]). Nine of 12 patients with severe OSA developed PB, with recurrent central apneas, whereas only six of 20 patients in the mild/moderate group developed PB (p < 0.02). This difference was observed despite the subjection of the mild/moderate group to greater amplification of LG; the highest values of VTAF in the mild/moderate and severe groups were 2.7 +/- 1.0 and 1.9 +/- 0.7, respectively (p < 0.01). We conclude that the chemical control system is more unstable in patients with severe OSA than in patients with milder OSA. We speculate that this may contribute to the severity of OSA, at least in some patients.

Chemoreceptor Cells↗

PubMed2006

Elevated morbidity and health care use in children with obstructive sleep apnea syndrome.

RATIONALE: Health care use, a reliable measure of morbidity, is noticeably higher 1 yr before obstructive sleep apnea syndrome (OSAS) diagnosis in preschool children. It is not clear at what age OSAS-related morbidity becomes expressed. OBJECTIVE: To explore morbidity and health care use among children with OSAS starting from first year of life. METHODS: Case-control study, starting from the first year of life to date of OSAS diagnosis, among 156 patients (age range, 3-5 yr) and their pair-matched healthy control subjects, by age, sex, primary care physician, and geographic location. MEASUREMENTS: Patients with OSAS underwent nocturnal polysomnography studies. Medical records during hospital visits were reviewed for diagnosis. Variables of health care use were obtained from computerized databases of Clalit Health Care Services, the largest health maintenance organization in Israel. MAIN RESULTS: From the first year of life to date of OSAS diagnosis, children with OSAS had 40% more (p = 0.048) hospital visits, 20% more repeated (two or more) visits (p < 0.0001), and higher consumption of antiinfective and respiratory system drugs (p < 0.0001). Referrals of children with OSAS to otolaryngology surgeons and pediatric pulmonologists were higher from Year 1 (p < 0.0001) to date of OSAS diagnosis, especially in Year 4 (odds ratio, 9.4; 95% confidence interval, 4.2-21.1). The 215% elevation (p < 0.0001) in health care use of the OSAS group was due mainly to higher occurrence of respiratory tract morbidity (p < 0.0001). CONCLUSIONS: Practitioners should be aware that starting in Year 1 until date of diagnosis, children with OSAS have higher health care use, mostly related to respiratory diseases.

Case-Control Studies↗

PubMed1991

Octenylsuccinic aciduria in children fed protein-hydrolysate formulas containing modified cornstarch.

The excretion of 2-(2'-octenyl)succinic acid (OSA) and several metabolites of OSA was studied by gas chromatography/mass spectrometry in 17 infants and children fed one of three proprietary elemental or protein-hydrolysate formulas that use OSA-modified cornstarch as an emulsifying agent. Variable but often large amounts (up to 2500 mg/g creatinine) of the fatty acid-like OSA and its metabolites were found in the urine of these children, and levels of OSA in their blood ranged from 9.5 to 57.9 mumol/L. Apparently secondary abnormalities, such as increased urinary levels of glutaric acid and 2-ketoglutaric acid, were also found in more than half of the urine specimens. The molecular weight and mass fragmentation patterns of the nine compounds associated with the excretion of OSA are consistent with the proposal that OSA is metabolized in human infants and children by a combination of omega-, omega-1-, and beta-oxidation steps, similar to the metabolism of another branched-chain fatty acid, valproic acid. The urinary organic acid pattern of children fed elemental formulas containing OSA-modified starch often was dominated by OSA and its metabolites, and in several children the OSA-related changes were mistaken for a primary metabolic disease. Physicians and laboratories evaluating children for suspected metabolic diseases should be aware of the possibility of abnormal organic acid studies associated with OSA-containing formulas.

Child↗

PubMed2000

Endogenous digitalislike factors in obstructive sleep apnea.

Recent studies have provided evidence that hypoxia may stimulate the release of endogenous digitalislike factors (EDLF). Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia during sleep and may be associated with sympathetic activation and a high risk of developing hypertension. This study was designed to measure EDLF in the plasma of patients with OSA diagnosed by polysomnography, with patients being classified by the number of apneic-hypopneic episodes/h sleep (apnea-hypopnea index, AHI). Plasma was obtained in the morning from 8 male normotensive OSA patients (OSA-N) (AHI 70+/-6), 2 untreated hypertensive OSA patients (OSA-HT), and 11 age-matched healthy male controls (C). EDLFs of different hydrophobicities were separated from the same plasma sample by solid-state C18-cartridges with 25% acetonitrile (ACN) (EDLF-1) followed by 40% ACN (EDLF-2). This procedure recovered ouabain in the first fraction and digoxin and digoxigenin in the second. EDLF was quantified in pM ouabain-equivalents by a human placenta radioreceptor assay. EDLF-1 levels were similar for OSA-N and C (231+/-55 vs. 258+/-58), whereas EDLF-2 levels were increased in OSA-N (244+/-51 vs. 110+/-25 in C, p=0.02). Norepinephrine was increased in apneics. The two OSA-HT had EDLF and norepinephrine levels similar to OSA-N. These preliminary results suggest that OSA is associated with an increase in the more hydrophobic EDLF levels in both normotensive and hypertensive states. No significant increase was found for the less hydrophobic ouabain-like EDLF.

Adult↗

PubMed2006

Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury.

BACKGROUND: Childhood obstructive sleep apnea (OSA) is associated with neuropsychological deficits of memory, learning, and executive function. There is no evidence of neuronal brain injury in children with OSA. We hypothesized that childhood OSA is associated with neuropsychological performance dysfunction, and with neuronal metabolite alterations in the brain, indicative of neuronal injury in areas corresponding to neuropsychological function. METHODS AND FINDINGS: We conducted a cross-sectional study of 31 children (19 with OSA and 12 healthy controls, aged 6-16 y) group-matched by age, ethnicity, gender, and socioeconomic status. Participants underwent polysomnography and neuropsychological assessments. Proton magnetic resonance spectroscopic imaging was performed on a subset of children with OSA and on matched controls. Neuropsychological test scores and mean neuronal metabolite ratios of target brain areas were compared. Relative to controls, children with severe OSA had significant deficits in IQ and executive functions (verbal working memory and verbal fluency). Children with OSA demonstrated decreases of the mean neuronal metabolite ratio N-acetyl aspartate/choline in the left hippocampus (controls: 1.29, standard deviation [SD] 0.21; OSA: 0.91, SD 0.05; p = 0.001) and right frontal cortex (controls: 2.2, SD 0.4; OSA: 1.6, SD 0.4; p = 0.03). CONCLUSIONS: Childhood OSA is associated with deficits of IQ and executive function and also with possible neuronal injury in the hippocampus and frontal cortex. We speculate that untreated childhood OSA could permanently alter a developing child's cognitive potential.

Adolescent↗

PubMed1995

Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children.

STUDY OBJECTIVE: To determine whether primary snoring (PS) could be distinguished from childhood obstructive sleep apnea syndrome (OSAS) by clinical history. DESIGN: Retrospective study of clinical history of 83 children with snoring and/or sleep disordered breathing who were referred for polysomnography. SETTING: Tertiary referral center; pediatric pulmonary sleep apnea clinic. MEASUREMENTS: We evaluated the ability of a clinical obstructive sleep apnea (OSA) score and other questions about sleep, breathing, and daytime symptoms to distinguish PS from OSAS in children. Parents were asked about the child's snoring, difficulty breathing, observed apnea, cyanosis, struggling to breathe, shaking the child to "make him or her breathe," watching the child sleep, afraid of apnea, the frequency and loudness of snoring, and daytime symptoms such as excessive daytime sleepiness (EDS). RESULTS: Based on polysomnography results, 48 patients were classified as PS and 35 as OSAS. Peak endtidal CO2 (49 +/- 3.2 vs 55 +/- 8.2 [SD] mm Hg); lowest arterial oxygen saturation measured by pulse oximetry (95 +/- 1.9 vs 82 +/- 14%); and apnea/hypopnea index (0.27 +/- .3 vs 8.4 +/- 6 events/h) indicated that the diagnostic criteria for PS versus OSA were reasonable. There were no differences between PS and OSA patients with respect to age, sex, race, failure to thrive, obesity, history of EDS, snoring history, history of cyanosis during sleep, or daytime symptoms except for mouth breathing. There were no significant differences in sleep variables between PS patients and those with any severity of OSAS. The OSA score misclassified about one of four patients. Comparing PS and OSA patients, significant findings were daytime mouth breathing (61 vs 85%; p = 0.024); observed apnea (46 vs 74%; p = 0.013); shaking the child (31 vs. 60%; p = 0.01); struggling to breathe (58 vs 89%; p = 0.003); and afraid of apnea (71 vs 91%; p = 0.028). However, none of these were sufficiently discriminatory to predict OSAS. CONCLUSION: We conclude that PS in children cannot be reliably distinguished from OSAS by clinical history alone.

Case-Control Studies↗

PubMed1991

Obstructive sleep apnea syndrome in male hypertensives, refractory to drug therapy. Nocturnal automatic blood pressure measurements--an aid to diagnosis?

Sixteen therapy resistant hypertensive males and 16 responders to antihypertensive drug treatment, matched for age, gender and body mass index, were examined by means of Static Charge Sensitive Bed (SCSB) and oximetry for the presence of obstructive sleep apnea syndrome (OSAS). In borderline cases, polysomnography was performed. The prevalence of OSAS among therapy resistant patients was 56%, as compared to 19% in the control group (p less than 0.05). This higher prevalence of OSAS in a weight-matched group of subjects with severe hypertension supports the notion of a causal connexion between hypertension and OSAS. In 10 OSAS patients and 10 hypertensives with normal respiration during sleep, ambulatory noninvasive monitoring (ABPM) of arterial pressure (AP) and heart rate (HR) was also performed. The OSAS patients had a higher nocturnal variability of HR, systolic blood pressure (both p less than 0.05), and diastolic blood pressure (p less than 0.01) in 8 half-hourly single ABPM measurements. Contrary to the non-OSAS subjects they also had a higher HR variability during sleep than they had in the waking state (p less than 0.05). For subjects less than 60 yrs a range/median value of greater than 0.32 for nocturnal diastolic pressure was found to predict OSAS with a sensitivity of 87.5% and a specificity of 100%. It is concluded that therapy-resistant male hypertensives have a high prevalence of OSAS. As this may be a deleterious combination, screening for OSAS is highly indicated in such patients. A high variability of HR and AP in nocturnal ABPM suggests OSAS.

Aged↗

PubMed2000

[Obstructive sleep apnea and risk factors for coronary artery disease].

STUDY AIM: Obstructive sleep apnoea (OSA) is strongly associated with obesity, especially abdominal obesity. Obesity in turn is a well-known risk factor for coronary artery disease (CAD). The aim of our study was to evaluate the relationship between OSA severity and CAD risk factors. MATERIAL AND METHODS: The sample consisted of 73 subjects (mean age +/- SE, 46.7 +/- 1 years) referred to a sleep laboratory. Subjects were either: 1. obese with OSA (O-OSA group n = 35; body mass index, BMI ł 30 kg/m2; apnoea/hypopnoea index, AHI > 35), 2. non-obese with OSA (BO-OSA group n = 14; BMI < 27 kg/m2; AHI > 35), or 3. obese without OSA (O-Z group n = 24; BMI ł 30 kg/m2; AHI < 5). All subjects underwent full overnight polysomnography. Blood samples were taken from all subject, for fasting levels of insulin (INS), glucose (GLU), total, HDL and LDL cholesterol, triglyceride (TG) and uric acid (UA). RESULTS: O-OSA had significantly higher INS and UA levels (p < 0.05) compared to BO-OSA and O-Z. GLU and lipid levels were comparable in the studied groups. GLU level correlated (p < 0.05) negatively to minimum oxyhemoglobin saturation (SAT-MIN) and positively to neck circumference. TG and UA levels were correlated (p < 0.05) positively to AHI and negatively to SAT-MIN. UA level was also positively correlated (p < 0.05) to BMI, waist/hip circumference ratio (WHR), and INS level. INS level correlated (p < 0.05) positively to AHI, T90, WHR and UA, and negatively to SAT-MIN and mean oxyhemoglobin saturation. After adjusting for the influence of OSA and obesity (multiple regression analysis), we found independent negative correlations (p < 0.05) between: GLU level and SAT-MIN, UA level and SAT-MIN, and INS level and SAT-MIN. An independent, positive correlation (p < 0.05) was found between TG level and AHI. CONCLUSIONS: Results of our study suggest that OSA increases the risk of coronary artery disease by increasing plasma levels of glucose, triglyceride and insulin, independent of obesity.

Adolescent↗

PubMed2004

Cardiac autonomic activity in obstructive sleep apnea: time-dependent and spectral analysis of heart rate variability using 24-hour Holter electrocardiograms.

To analyze the function of cardiac autonomic regulation in patients with obstructive sleep apnea syndrome (OSAS), we enrolled 36 patients with OSAS and divided them according to the apnea hypopnea index (AHI) into 2 groups: Group I (n=19) had mild OSAS (AHI < 20) and Group II (n=17) had severe OSAS (AHI > or = 20). The findings were compared with those of 24 healthy control subjects who were matched for age, sex, blood pressure, and body mass index. All participants underwent 24-hour Holter monitoring, with continuous time-dependent and spectral analysis of heart rate variability. In addition, we performed arrhythmia analysis. Frequent or repetitive ventricular arrhythmias (> or = 30 premature ventricular beats/hour) were detected in 15 (42%) patients with OSAS and in 6 (25%) members of the control group. In both mild and severe OSAS, SDNN was significantly lower than in controls, and SDANN findings were similar. In mild OSAS, RMSSD values were not significantly lower than in controls, but in severe OSAS they were. The ULF, VLF, LF and LF/HF values of both groups of OSAS patients were significantly higher than those of controls, but their HF values were lower. The mean LF/HF ratio during the same period was significantly higher in Group II than in Group I and the control group. Our results suggest that cardiac autonomic activity may be altered in patients with OSAS throughout a 24-hour period, that this alteration occurs even in the absence of hypertension, heart failure, or other disease states, and that it is linked to the severity of OSAS.

Adult↗

PubMed2004

Night and day proteinuria in patients with sleep apnea.

BACKGROUND: Previous studies have suggested an association between obstructive sleep apnea (OSA) and heavy proteinuria. Two recent studies cast doubt on the association between OSA and proteinuria, but neither studied the effect of disordered sleep per se on urinary protein excretion. METHODS: We prospectively studied 75 patients undergoing polysomnography for suspected OSA. We excluded patients with renal insufficiency, diabetes mellitus, and systemic lupus erythematosus and those administered angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Urine protein-creatinine (P/C) ratio was measured on the date of the polysomnography before sleep (awake P/C ratio) and on awakening (asleep P/C ratio). Severity of OSA was stratified by means of the apnea-hypopnea index (AHI). RESULTS: Twenty-six patients (35%) did not have OSA, 25 patients (33%) had mild OSA, 9 patients (12%) had moderate OSA, and 15 patients (20%) had severe OSA. Asleep P/C ratio was less than 0.2 in 96% of patients, and awake P/C ratio was less than 0.2 in 89% of patients. No patient had an asleep P/C ratio greater than 1.0. There was no correlation between log asleep P/C ratio and log AHI ( r = -0.042; P = 0.73) or log awake P/C ratio and log AHI (r = 0.004; P = 0.97). No significant differences could be shown between mean log P/C ratio for either the asleep or awake urine collection across any of the 4 OSA severity strata. CONCLUSION: We found clinically significant proteinuria to be absent in stable outpatients with OSA. Proteinuria in patients with OSA should not be attributed to sleep apnea and warrants further evaluation.

Adult↗

PubMedDate not supplied

Successful treatment of obstructive sleep apnea syndrome improves autonomic nervous system dysfunction.

Autonomic nervous system (ANS) dysfunction may be implicated in the subsequent development of cardiovascular disease in patients with obstructive sleep apnea syndrome (OSAS). To confirm the relation between OSAS and ANS dysfunction, we prospectively investigated ANS function in 7 patients with moderate or severe OSAS; 7 healthy age-matched volunteers were for control. We also studied ANS function before and after treatment in the patients with OSAS to evaluate the effect of OSAS treatment on ANS dysfunction. The body mass index of patients with OSAS was 32.2 (27.4-45) (median [range]) kg/m2. The patients were treated by nasal continuous positive airway pressure (n = 5) or uvulopalatopharyngoplasty (n = 2). The apnea/hypopnea index decreased markedly from 42.1 (30.6-77.2) events/hr of sleep before treatment to 2.3 (1.4-3.8) after treatment. To evaluate ANS function, the coefficient of variation of the RR interval (CV-RR) and corrected QT (QTc) interval on the electrocardiogram at rest and the heart rate (HR) responses to blood pressure (BP) changes during the Valsalva maneuver were studied. Baseline HR of OSAS patients was significantly higher than that of the control subjects (p < .05). The Valsalva ratio (VR), baroreflex sensitivity (BRS), and CV-RR values in patients with OSAS were significantly lower than those of the control subjects (all, p < .005). However, there were no significant differences in systolic and diastolic BP or QTc intervals. After treatment, VR, BRS, and CV-RR values increased significantly compared with those before treatment in patients with OSAS (all, p < .05). There were no significant differences in systolic and diastolic BP, HR, or QTc intervals measured before and after treatment. These results suggest that impaired ANS function is present in patients with OSAS and can be improved by successful treatment of OSAS.

Adult↗

PubMed1991

Causes and consequences of blood pressure alterations in obstructive sleep apnea.

The obstructive sleep apnea (OSA) syndrome has been considered to be a cause of both transient blood pressure elevations during sleep and sustained hypertension during the awake state. The purpose of this review was to examine critically the existing literature regarding (1) the blood pressure alterations associated with OSA, (2) causal mechanisms relating specific blood pressure alterations to OSA, and (3) potential consequences of the systemic circulatory abnormalities associated with OSA. Particular attention was directed at studies that assessed the prevalence of OSA in patients with hypertension and that examined the effects on blood pressure of treatment of OSA. We conclude that patients with OSA have abnormal sleep blood pressure patterns, manifested most frequently by apnea-associated blood pressure elevations. Confounding factors such as obesity and antihypertensive drug therapy, and conflicting evidence regarding changes in daytime blood pressure after therapy for OSA, make it premature to conclude that OSA and daytime hypertension are directly associated. Circumstantial evidence suggests that the blood pressure alterations that occur during sleep could contribute to the high cardiovascular morbidity in patients with OSA. Further research into the relationship between OSA and hypertension should improve the future care of patients with these conditions and enhance our understanding of cardiopulmonary pathophysiology.

Blood Pressure↗