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A case of obstructive sleep apnea (OSA) is presented which led to cor pulmonale. The diagnosis was based on polysomnography (PSG) which demonstrated OSA periods with hypoxemia. The patient was qualified for uvulopalitopharyngoplasty. Also CPAP is being considered.
Obstructive sleep apnea syndrome (OSAS) is a complex disorder characterized by a sleep-related collapse of the upper airway. The most likely candidate for the common pathway linking various abnormalities casually associated with OSAS (such as adenotonsillar hypertrophy, obesity, retro- or micrognathia, acromegaly, or more subtle structural anomalies) is an abnormally small upper airway lumen. Symptoms of OSAS that appear during sleep include snoring, abnormal motor activity, disturbed nocturnal sleep, a sensation of choking, heartburn, nocturia, nocturnal enuresis, and heavy sweating. Daytime waking symptoms are dominated by often profound sleepiness, which may secondarily be associated with automatic behavior, retrograde amnesia, hypnagogic hallucinations, personality changes, sexual difficulties, and headaches. Careful evaluation, both sleeping and waking, are essential to select appropriate treatment. Treatments include nasal continuous positive airway pressure, tracheostomy, weight loss, uvulopalatopharyngoplasty, mandibular advancement, and so forth.
Hypersomnia in obstructive sleep apnea syndrome (OSAS) is due to sleep fragmentation caused by arousals related to repeated episodes of apnea. Arousals may also be triggered by other non-apneic respiratory events (NAREs). The contribution of NARE to sleep disruption and nocturnal desaturation has been assessed by evaluating the polysomnograms of 58 consecutive OSAS patients. We studied 28 cases (25 men) presenting more than 5 NAREs/hour of sleep in addition to apneic events. Mean age was 48.8 +/- 14 years, mean body mass index was 38.1 +/- 10.2 kg/m2 and mean oxygen saturation at baseline, before the polysomnogram, was 94.0 +/- 2.5%. The following NARE categories were identified: incomplete apnea, paradoxical breathing, periodic breathing, hypoventilation and snore-arousals. All respiratory arousals were tabulated as indexes (number/hours of sleep). Although the number of apneic arousals was significantly greater, the NARE arousal index, both in REM and non-REM sleep reached the sleep disruption range (around 20 arousals/hour). Apneic desaturations were greater than non-apneic ones, during both REM and non-REM sleep. We conclude that NARE significantly contribute to sleep fragmentation in nearly half the patients with OSAS.
11 patients with obstructive sleep apnea (OSA) and maxillary and mandibular characteristics participated. All patients received nCPAP therapy for at least 3 months. The surgical treatment principle consists of 10 mm maxillary and mandibulary advancement. Cardiorespiratory polysomnography (cPSG) control was assessed 3 months after surgical treatment. The daytime vigilance was investigated using a 90-min 4-choice reaction-time test. Patients reports of excessive daytime sleepiness (EDS) were confirmed by pre-treatment vigilance testing. Accordingly, daytime vigilance, respiratory and polysomnography patterns were improved with nCPAP and surgical treatment in a likewise manner. The tolerance to monotonous situations increased distinctly with nCPAP as well as after osteotomy. Surgical treatment of OSA in carefully selected cases has positive effects on sleep and daytime vigilance. There were no significant differences in the cPSG nor in vigilance tests with regard to nCPAP therapy.
Apneas generally reappear in patients with obstructive sleep apnea (OSA) when treatment with continuous positive airway pressure (CPAP) is interrupted. However, a single-night treatment interruption may be associated with a lesser severity of sleep apneas than before treatment. We hypothesized that this decrease in severity of sleep apneas reflects changes in the respiratory response to upper airway obstruction. Therefore, we compared indexes of respiratory effort during sleep in 25 patients with OSA before and after 1 year of CPAP treatment. Respiratory effort was assessed by means of an esophageal balloon. After 1 year of CPAP treatment, there was a decrease in the maximal end-apneic esophageal pressure swings (Pes) (from 56.7 +/- 5.4 to 30.3 +/- 2.6 cm H2O; p = 0.000; mean +/- SEM), in the overall increase in Pes during an apnea (35.2 +/- 3.6 vs 16.5 +/- 1.5 cm H2O; p = 0.000), as well as the rate of increase in Pes (1.1 +/- 0.1 vs 0.6 +/- 0.1 cm H2O/s; p = 0.000). Although body mass index (BMI) did not change significantly, the individual changes in BMI significantly correlated with the changes in respiratory effort after 1 year of CPAP treatment. Apnea duration and apnea-related oxygen desaturation also decreased significantly. We conclude that long-term CPAP treatment induces changes in respiratory control that persist at least on the first night of treatment interruption.
Although obstructive sleep apnea (OSA) occurs in the pediatric population, diagnostic criteria have not been established. Since criteria for adult OSA are well established, we asked whether commonly used adult criteria, such as the apnea index (based on the number of obstructive apnea [OA] events per hour), would identify children with serious sleep-related upper airway obstruction. Polysomnographic data were analyzed from 20 children (ages 8 months to 16 yr) with clinical evidence of upper airway obstruction during sleep (loud snoring and labored breathing) and who had cyclic oscillations of oxyhemoglobin saturation (SaO2) during sleep. The overnight studies included sleep state (EEG, EOG, and EMG), SaO2, ECG, nasal (end-tidal CO2) and oral (thermistor) airflow, chest and abdominal movement (inductance plethysmography), and video camera and behavioral observations. Measurements included the number of obstructive events > or = 10 s, the number of desaturations (> or = 5% decrease lasting > or = 5 s), the number of desaturation episodes to < 90%, < 85%, and < 80% lasting > 5 s, and the percentage of sleep time with SaO2 values < 90%. Gas exchange was impaired as evidenced by cyclic decreases in SaO2 and elevated PETCO2 values (maximum value 58 +/- 6 mm Hg). The children experienced 175 +/- 168 (range 6 to 609) episodes of decreased SaO2 > 5%, with an average minimum SaO2 of 66 +/- 13% (range 30 to 85%). The average number of apnea events was only 1.9 +/- 3.2 events/h (range 0 to 10.4).(ABSTRACT TRUNCATED AT 250 WORDS)
In a 27-year-old patient with a severe obstructive sleep apnea syndrome documented by a polysomnographic study, an oral dose of 15 mg midazolam caused life-threatening obstructive apnea and excessive sedation. Therapy with nasal CPAP eliminated the pharyngeal obstruction, but marked central hypoventilation persisted. Benzodiazepines are known to aggravate the obstructive sleep apnea syndrome. Dangerous central hypoventilation occurring after this medication during treatment with nasal CPAP has not yet been reported. Excessive susceptibility to depression of chemoresponsiveness to pCO2 is suspected. The potentially dangerous and life-threatening side effects of sedatives in patients with obstructive sleep apnea syndrome are discussed.
BACKGROUND: Hypoglossal nerve stimulation has been demonstrated to relieve upper airway obstruction acutely, but its effect on obstructive sleep apnea is not known. OBJECTIVE: To determine the response in obstructive sleep apnea to electrical stimulation of the hypoglossal nerve. METHODS: Eight patients with obstructive sleep apnea were implanted with a device that stimulated the hypoglossal nerve unilaterally during inspiration. Sleep and breathing patterns were examined at baseline before implantation and after implantation at 1, 3, and 6 months and last follow-up. RESULTS: Unilateral hypoglossal nerve stimulation decreased the severity of obstructive sleep apnea throughout the entire study period. Specifically, stimulation significantly reduced the mean apnea-hypopnea indices in non-rapid eye movement (mean +/- SD episodes per hour, 52.0 +/- 20.4 for baseline nights and 22.6 +/- 12.1 for stimulation nights; P<.001) and rapid eye movement (48.2 +/- 30.5 and 16.6 +/- 17.1, respectively; P<.001) sleep and reduced the severity of oxyhemoglobin desaturations. With improvement in sleep apnea, a trend toward deeper stages of non-rapid eye movement sleep was observed. Moreover, all patients tolerated long-term stimulation at night and did not experience any adverse effects from stimulation. Even after completing the study protocol, the 3 patients who remained free from stimulator malfunction continued to use this device as primary treatment. CONCLUSION: The findings demonstrate the feasibility and therapeutic potential for hypoglossal nerve stimulation in obstructive sleep apnea.
Undiagnosed obstructive sleep apnea (OSA) can contribute to hypertension, cardiovascular disease, stroke, and detract from overall quality of life. Dentists can play an important role in detecting, making recommendations for, and treating OSA with oral appliances (OAs). A survey of 18 questions of knowledge and opinion of, educational background for, and clinical experience with OSA and OAs was mailed to 500 general practice dentists in Indiana, United States. Two hundred survey returns produced 192 valid responses. Responders reported strong positive opinions toward OSA and OAs. However, 58% of dentists could not identify common signs and symptoms of OSA, and 55% of dentists did not know the mechanism for mandibular advance devices. Only 39% of dentists could identify snoring, mild OSA, and intolerance to continuous positive airway pressure as possible indications for OA treatment. Respondents reported a general lack of education about both OSA and OAs. Only 31 (16%) were taught about this issue in dental school; 77 (40%) knew little or nothing about OA treatment for OSA patients; 57 (30%) learned from postgraduate training. Cooperation and referrals between dentists and physicians were rated as "poor." Of the responders, 54% never consulted with physicians for a suspected OSA patient in their practice; 75% of dentists reported they have never been referred patients by physicians; and 80% of dentists never or less than five times prescribed OAs to OSA patients. Results suggest a need for increased education and training regarding OSA and OAs in dental school, as well as increased cooperation between dentists and physicians for better patient care.
Obstructive sleep apnea syndrome (OSAS) is associated with mild to severe cardiovascular risks. The most common standard treatment for OSAS, continuous positive airway pressure, was found to have beneficial effects on cardiovascular sequelae of OSAS. Additionally, commercial companies promote nonprescription treatments for OSAS. These products frequently lack scientific support for their efficacy and need further research. We report an objective test of magnetic therapy, one such product, in a patient with OSAS and cardiovascular comorbidities. Two nights of polysomnographic recording using the split-night protocol did not reveal any consistent differences in OSAS symptoms whether the patient slept with or without the magnetic equipment. It was concluded that magnetic treatment was unsuccessful in reducing OSAS symptoms in our patient and may even increase possible cardiovascular and stroke risks by preventing the patient from pursuing an adequate medical treatment, such as continuous positive airway pressure.
Obstructive sleep apnea (OSA) has emerged as a major public health problem and increasing evidence indicates that untreated OSA can lead to the development of various cardiovascular disorders. One important mechanism by which OSA may promote cardiovascular diseases is intermittent hypoxia, in which patients are subjected to repeated episodes of brief oxygen desaturation in the blood, followed by reoxygenation. Such cycles of hypoxia/reoxygenation may result in the generation of reactive oxygen species. Some studies have demonstrated the presence of oxidative stress in OSA patients as well as in animals subjected to intermittent hypoxia. Further, modulations of nitric oxide and biothiol status might also play important roles in the pathogenesis of OSA-associated diseases. Reactive oxygen species and redox events are also involved in the regulation of signal transduction for oxygen-sensing mechanisms. This review summarizes currently available information on the evidence for and against the occurrence of oxidative stress in OSA and the role of reactive oxygen species in cardiovascular changes associated with OSA.
BACKGROUND AND PURPOSE: Obstructive sleep apnea syndrome (OSAS) is a chronic disease ranging from innocuous to life-threatening and causes brain alterations manifested by neuropsychiatric symptoms. Neuron-specific enolase (NSE) and the astrocytic protein S100B are established sensitive peripheral biochemical markers of brain injury. In the present work we measured the serum levels of S100B and NSE in order to evaluate the deleterious effects of OSAS to the brain. PATIENTS AND METHODS: We studied 29 male patients with OSAS and 17 male asymptomatic control subjects with an apnea-hypopnea index (AHI) less than five events per hour. Patients and control subjects were evaluated by full-night polysomnography (PSG) and by Mini International Neuropsychiatric Interview (MINI) for the presence of neuropsychiatric symptoms. In the morning following the PSG, blood was collected and serum levels of S100B and NSE were measured using standard techniques. RESULTS: The AHI in the OSAS group was (mean+/-SD) 27+/-25 AH/h, ranging from 5 to 99 AH/h. S100B was higher in OSAS (0.15+/-0.09 microg/l) than in the control group (0.08+/-0.06 microg/l; P<0.01). Serum NSE was similar in both groups (17.5+/-12.2 vs. 15.8+/-6.8ng/ml). CONCLUSIONS: We report elevated serum S100B levels in OSAS patients in this study.
THE PRIMARY TREATMENT for obstructive sleep apnea (OSA) has been continuous positive airway pressure (CPAP) therapy, but the minimum acceptable number of hours of nightly CPAP use remains unclear. INTEGRATED SOFT TISSUE and bone surgery may be a viable alternative for patients who have rejected CPAP as a treatment option. Formal sleep testing has shown that surgery and CPAP therapy are equally successful at resolving OSA. REPEAT SLEEP TESTING conducted several years after patients have undergone combined soft tissue and bone surgery has demonstrated consistent and reliable surgical results. Patients with OSA should be offered surgery as an alternative to life-long CPAP treatment or as an option when CPAP therapy has not been successful.
Obstructive sleep apnea (OSA) is a sleep-related breathing disorder that can cause left ventricular (LV) dysfunction. In patients with OSA, the LV dysfunction is usually evaluated by echocardiography. The purpose of this study was to evaluate whether the use of breathhold cine MRI for the study of LV dysfunction would be feasible and well tolerated by patients with OSA. Six volunteers and five patients underwent a breathhold cine MRI study of the LV using a 1.5 Tesla MR imager. Cine MRI was performed using a breathhold k-space segmented TurboFLASH technique during end-expiration. Systolic thickening of the LV septal wall was 49% +/- 16% in normals vs. 25% +/- 10.5% in patients (p < 0.05). Systolic thickening of the LV free wall was 42% +/- 12% in normals vs. 22% +/- 9% in patients (p < 0.05). There was a significant difference in end-diastolic wall thickness between the two groups. All patients tolerated the procedure well. The total duration of each study was relatively short (less than 11 min). Breathhold MRI techniques can be used to study LV dysfunction in patients with respiratory disability such as OSA.
BACKGROUND: Patients with obstructive sleep apnea syndrome (OSAS) have an increased risk of cardiovascular events including myocardial infarction and stroke. OBJECTIVE: To determine whether in vivo platelet activation and the generation of procoagulant platelet-derived microparticles (PMP) are increased during sleep in patients with OSAS. METHODS: In vivo platelet activation and PMP formation was determined using flow cytometry in 12 patients with untreated OSAS during and after sleep (4 and 7 a.m.). To study the effect of treatment with continuous positive airway pressure (CPAP), the measurements were repeated at the same time points after initiation of CPAP therapy. Healthy volunteers served as controls (n = 6). RESULTS: Patients with OSAS had an increased percentage of platelets positive for the activation-dependent epitopes CD63 and CD62P during sleep (4 a.m.) compared to controls (4.8 +/- 0.8 vs. 1.9 +/- 0.4% for CD63, p < 0.01, and 2.0 +/- 0.5 vs. 1.1 +/- 0.3% for CD62P, p < 0.05). In OSAS patients, the amount of CD63- and CD62P-positive platelets was significantly elevated at 4 compared to 7 a.m. (4.8 +/- 0.8 vs. 2.6 +/- 0.4% for CD63 and 2.0 +/- 0.5 vs. 1.1 +/- 0.2% for CD62P, p < 0.05), but not in the control group. The levels of PMP were similar in patients with OSAS and controls at 4 and 7 a.m. After 1 night of CPAP therapy, there was a trend to reduced levels of CD63- and CD62P-positive platelets at 4 a.m. CONCLUSIONS: Patients with OSAS have increased in vivo platelet activation during sleep, which may contribute to the increased incidence of cardiovascular events in patients with OSAS.
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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.
Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality; however, some patients with OSA do not develop cardiovascular disease even in the presence of severe nocturnal oxygen desaturations. Vascular endothelial growth factor (VEGF) is a hypoxia-sensitive glycoprotein stimulating neoangiogenesis. We hypothesized that VEGF production is increased in OSA because of repetitive nocturnal hypoxia. Three different groups were investigated: 10 OSA patients with severe nighttime hypoxia (Group A), 10 OSA patients with moderate hypoxia (Group B), and 10 healthy volunteers (Group C). Serum levels of VEGF were measured by ELISA from peripheral venous blood samples obtained at 7 AM. Group A had significantly (p < 0.01) increased VEGF serum levels when compared with Group B and Group C (mean +/- SEM: 410 +/- 77 pg/ml versus 224 +/- 38 pg/ml and 245 +/- 61 pg/ml). The degree of nocturnal oxygen desaturation in OSA significantly correlated with the VEGF concentrations (r = 0.67, p < 0.01). In conclusion, serum levels of VEGF are elevated in severely hypoxic patients with OSA and are related to the degree of nocturnal oxygen desaturation. This might constitute an adaptive mechanism to counterbalance the emergence of OSA-related cardiovascular disease.