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Biomedical subjects

H F Becker

Publications and source records attributed to H F Becker.

At least 19 recordsLinked to original sources

[Sleep disorders and sleep-related breathing disorders].

Normal sleep consists of 4-5 sleep cycles including light-, deep- and rapid eye-movement sleep. Restoration of physical and psychological function are the main effects of sleep. In most cases, disturbances of normal sleep become clinically evident as problems of initiating and maintaining sleep and/or as increased daytime sleepiness. Approximately 10% of adults suffer from pronounced insomnia, a similar percentage from markedly increased daytime sleepiness. Sleep disorders cause high socio-economic costs due to increased accident risk, cardiovascular sequelae and sick leave. Most of the 88 distinct diagnoses summarized in the international classification of sleep disorders can be differentiated and managed according to patients history. In patients with severe daytime sleepiness - sleep disordered breathing being the most frequent cause - the diagnostic evaluation and treatment in the sleep laboratory is required. Effective therapeutic strategies are available for many sleep disorders. According to the underlying disorder, treatment includes a variety of measures like life style changes, differentiated medical treatment and the use of nasally applied positive pressure in patients suffering from sleep disordered breathing.

Activities of Daily Living↗

[Relevance of sleep for patients with lung diseases].

Sleep is characterized by a profound change of load and capacity of the respiratory system. Load increases due to a rise in upper and lower airway resistance. Capacity decreases due to reduced chemosensitivity, a decrease in muscle activity and minute ventilation. Whereas these changes do not lead to relevant blood gas changes and do not disturb sleep in healthy subjects, patients with respiratory diseases frequently show the first symptoms of their disease during sleep. Pulmonary diseases in which sleep plays an important role are asthma, COPD, hypercapnic respiratory failure, sleep disordered breathing, the overlap-syndrome and cystic fibrosis. Medical history should include sleep and complaints during the night. In asthmatics peak-flow measurements during the night may provide valuable information. In all other disorders mentioned, nocturnal ambulatory recording of respiration and arterial oxygen saturation often allow the detection of relevant disorders of breathing during sleep. If ambulatory monitoring reveals relevant pathology, then further evaluation and treatment in the sleep laboratory are warranted.

Airway Obstruction↗

Sympathetic activity is reduced by nCPAP in hypertensive obstructive sleep apnoea patients.

There is increasing evidence that nasal continuous positive airway pressure (nCPAP) lowers blood pressure in obstructive sleep apnoea (OSA) patients, not only during sleep but also in the daytime. However, both the mechanisms of blood pressure reduction and the considerable differences in the magnitude of the effect in the studies presented to date are not fully understood. Therefore, the authors prospectively studied the effect of nCPAP on noradrenaline plasma levels (NApl), blood pressure and heart rate (HR) in 10 normotensive and eight hypertensive OSA patients before and after 41.6 +/- 16.9 days of nCPAP therapy. Polysomnography and invasive blood pressure were continuously monitored over 24 h in the supine position before and with nCPAP. NApl were analysed every 15 min. In hypertensives, nCPAP reduced NApl by 36 +/- 25%, lowered mean arterial blood pressure substantially (night-time: -8.89 +/- 14.09 mmHg; daytime: -7.94 +/- 10.47 mmHg) and decreased HR by 6.6 +/- 5.4 beats x min(-1), whereas in normotensives there were only minor changes. The decrease in heart rate was associated with a decrease in mean arterial blood pressure and noradrenaline plasma levels, suggesting a causal effect of nasal continuous positive airway pressure therapy. This nasal continuous positive airway pressure effect occurs mainly in hypertensive obstructive sleep apnoea patients, whereas the effect is small in normotensives. This may explain, at least in part, some of the discrepant results in previous treatment studies.

Adult↗

Automatic CPAP titration with different self-setting devices in patients with obstructive sleep apnoea.

Autotitrating continuous positive airway pressure (CPAP) devices automatically adjust the pressure according to upper airway obstructions. The aim of this study was to compare the treatment effects of different automatic CPAP devices (AutoSet, Horizon and Virtuoso) with conventional CPAP in patients with obstructive sleep apnoea independently of financial manufacturer support. Twelve male patients with obstructive sleep apnoea were submitted to a crossover study protocol with overnight polysomnography for 6 consecutive nights. After diagnostic polysomnography, the CPAP pressure was manually titrated. Over the next 4 nights, the patients were treated with any one of the three automatic CPAP devices or fixed CPAP in random order. The apnoea/hypopnoea index on the diagnostic night was 67.3+/-21.7 events h(-1), and was significantly reduced to 0.7+/-1.2, 3.0+/-2.9, 2.3+/-2.5 and 12.0+/-13.6 events x h(-1) with the fixed CPAP, AutoSet, Horizon and Virtuoso devices respectively. An apnoea/ hypopnoea index of <5 events h(-1), an indicator of optimal treatment, was achieved in all patients with fixed CPAP and in 10 patients using the Autoset and Horizon devices, but in only six of the 12 using the Virtuoso. The mean pressure was significantly lower with the AutoSet and Virtuoso devices, but not with the Horizon as compared to fixed CPAP. The maximum pressure was significantly higher with the Horizon. It is concluded that automatic continuous positive airway pressure devices produce a significant reduction in apnoea/hypopnoea index; however, there is considerable difference in the efficacy of the various devices.

Adult↗

[Why is obstructive sleep apnea (OSA) a cardiovascular risk factor?].

Patients with obstructive sleep apnea (OSA) frequently suffer from cardiovascular diseases. Mechanisms like intrathoracic pressure variations, changes in blood gases (hypoxia), arousals and neurohumeral adaptation mechanisms, combined with breathing disorders are causing these cardiovascular sequelae. In particular repetitive hypoxemia and activation of the sympathetic nervous system have to be considered as stressors for the cardiovascular system. Special clinical findings should take OSA into consideration as a differential diagnosis. A systematic anamnesis with questions to daytime conditions (hypersomnia, decrease of performance), snoring and apneas while sleeping is easy to ascertain, and will lead to the correct diagnosis in more than 90% of cases. The extent and need for therapy should be assessed by three criteria: 1) daytime symptoms, 2) the extent of breathing disorder and 3) cardiovascular comorbidity.

Arousal↗

[Measuring hypoxic and hypercapnic respiratory response in patients with obstructive sleep apnea].

The gas composition of breathing air is a very important stimulus for the control of breathing. The different partial pressures of O2 and CO2 independently trigger individually different reactions (respiratory response), which can be measured as a change of respiratory minute volume. Investigations of the respiratory control in patients with obstructive sleep apnoea (OSA) have up to now been restricted to an analysis of the breathing patterns at night. Therefore we have developed a computer-controlled device which allows a flexible composition of the air to be inhaled using a regulated feet-back circle. With this system it is possible to produce a hypercapnia test as well as a hyperoxia and an isocapnic hypoxia test. The simultaneous recording of all relevant respiratory parameters (AF, AMV, ETCO2, SpO2, FiO2) and the parallel recording of continuous blood pressure allow a quantitative description of the respiratory regulation of patients with OSA with exactly defined tests.

Airway Resistance↗

[Dependence of nocturnal bronchial obstruction on sleep position].

Patients with bronchial obstructions often have problems to stay asleep at night. The interaction between sleep position and bronchial obstructions has not been investigated until now. A total of 20 patients was included in this study. All patients were recorded one night in our sleep laboratory with a parallel recording of lung sounds using a commercial Pulmotrack 1010 system. The bronchial obstructions were lower in lateral position than in supine position for both tracheal and chest sounds (p = 0,083 and p = 0,036; n.s.). This effect seemed to be especially high in patients with many obstruction episodes. From our results we can conclude that there is a small dependence of bronchial obstructions from sleep position. Further investigations are needed to verify this result.

Adult↗

Effect of sleep position and sleep stage on the collapsibility of the upper airways in patients with sleep apnea.

Collapsibility of the upper airways has been identified as an important pathogenic factor in obstructive sleep apnea (OSA). Objective measures of collapsibility are pharyngeal critical pressure (Pcrit) and resistance of the upstream segment (Rus). To systematically determine the effects of sleep stage and body position we investigated 16 male subjects suffering from OSA. We compared the measures in light sleep, slow-wave sleep, REM sleep and supine vs. lateral positions. The pressure-flow relationship of the upper airways has been evaluated by simultaneous readings of maximal inspiratory airflow (Vimax) and nasal pressure (p-nCPAP). With two-factor repeated measures ANOVA on those 7 patients which had all 6 situations we found a significant influence of body position on Pcrit (p<0.05) whereas there was no significant influence of sleep stage and no significant interaction between body position and sleep stage. When comparing the body positions Pcrit was higher in the supine than in the lateral positions. During light sleep Pcrit decreased from 0.6 +/- 0.8 cm H2O (supine) to -2.2 +/- 3.6 cm H2O (lateral) (p<0.01), during slow-wave sleep Pcrit decreased from 0.3 +/- 1.4 cm H2O (supine) to -1.7 +/- 2.6 (lateral) (p<0.05) and during REM sleep it decreased from 1.2 +/- 1.5 cm H2O to -2.0 +/- 2.2 cm H2O (p<0.05). Changes in Rus revealed no body position nor sleep-stage dependence. Comparing the different body positions Rus was only significantly higher in the lateral position during REM sleep (p<0.05). The results indicate that collapsibility of the upper airways is not mediated by sleep stages but is strongly influenced by body position. As a consequence lower nCPAP pressure is needed during lateral positions compared to supine positions.

Adult↗

Low-flow oxygen and bilevel ventilatory support: effects on ventilation during sleep in cystic fibrosis.

We measured ventilation in all sleep stages in patients with cystic fibrosis (CF) and moderate to severe lung disease, and compared the effects of low-flow oxygen (LFO2) and bilevel ventilatory support (BVS) on ventilation and gas exchange during sleep. Thirteen subjects, age 26 +/- 5.9 yr (mean +/- 1 SD), body mass index (BMI) 20 +/- 3 kg/m2, FEV1 32 +/- 11% predicted, underwent three sleep studies breathing, in random order, room air (RA), LFO2, and BVS +/- O2 with recording of oxyhemoglobin saturation (SpO2) (%) and transcutaneous carbon dioxide (TcCO2) (mm Hg). During RA and LFO2 studies, patients wore a nasal mask with a baseline continuous positive airway pressure (CPAP) of 4 to 5 cm H2O. Minute ventilation (V I) was measured using a pneumotachograph in the circuit and was not different between wake and non-rapid eye movement (NREM) sleep on any night. However, V I was reduced on the RA and LFO2 nights from awake to rapid eye movement (REM) (p < 0.01) and from NREM to REM (p < 0.01). On the BVS night there was no significant difference in V I between NREM and REM sleep. Both BVS and LFO2 improved nocturnal SpO2, especially during REM sleep (p < 0.05). The rise in TcCO2 seen with REM sleep with both RA and LFO2 was attenuated with BVS (p < 0.05). We conclude that BVS leads to improvements in alveolar ventilation during sleep in this patient group.

Adult↗

Relations among hypoxemia, sleep stage, and bradyarrhythmia during obstructive sleep apnea.

BACKGROUND: Obesity, apneic hypoxemia, and rapid eye movement (REM) sleep are supposed to be the major causes for bradyarrhythmia in patients with obstructive sleep apnea. The aims of this study were to compare clinical findings and diagnoses in patients with obstructive sleep apnea with and without nocturnal bradyarrhythmia and to analyze the relations among hypoxemia, sleep stage, and bradyarrhythmia. METHODS: During a 17-month period 239 patients were found to have sleep apnea in an ambulatory study. Patients with nocturnal bradyarrhythmia were hospitalized for 3 days and polysomnographies were performed over 2 successive nights. A Holter electrocardiogram was recorded for 48 hours. RESULTS: Nocturnal episodes of bradyarrhythmia were identified in 17 (7%) of 239 patients. Body mass index (39 +/- 7 vs 31 +/- 5 kg/m(2)) and respiratory disturbance index (90 +/- 36 per hour vs 24 +/- 24 per hour) were significantly different (P <.01) between patients with (n = 17) and without bradyarrhythmia (n = 222). Bradyarrhythmia occurred significantly more often during REM than non-REM sleep (P <.01). There was a significant difference in end-apneic oxygen saturation in apnea/hypopnea episodes with and without bradyarrhythmia (71% +/- 9% vs 75% +/- 10%; P <.01). A linear relation between end-apneic oxygen saturation and number of sinus arrests and heart blocks could not be found. CONCLUSIONS: Patients with apnea-associated bradyarrhythmia are more overweight than patients without bradyarrhythmia. The higher respiratory disturbance index measurements found in these patients may be caused by this difference. Bradyarrhythmia occurs predominantly during REM sleep and occurred independently from decrease in oxygen saturation; a threshold value as an upper limit could not be found.

Adolescent↗

Sleep-apnea in patients with end-stage renal disease and objective results.

BACKGROUND: A high prevalence of sleep apnea syndrome (SAS) of 54%-80% has been reported in patients with end-stage renal disease (ESRD). However, these studies were either done in highly selected small patient groups or without objective data using questionnaires only. PATIENTS AND METHODS: We, therefore, studied the prevalence of SAS in a large, unselected group of patients with ESRD. During a 6-month period 77 out of 84 unselected patients with ESRD filled out the sleep apnea questionnaire of the University of Marburg and the Epworth Sleepiness Scale. In 55 of these patients, snoring sounds, heart rate, body position and transcapillary arterial oxygen saturation were recorded with an ambulatory device during the night after hemodialysis. RESULTS: In the questionnaires, 70.3% of the patients reported of an excessive day-time sleepiness, 40.5% of unwillingly falling asleep during the daytime and 35.2% rated their ability to concentrate as decreased. 30.9% (40% male/15% female) of the patients showed evidence of sleep-disordered breathing with an apnea-hypopnea-index (AHI) equal or more than 5/hour. 16.4% (20% male/10% female) of the patients met the diagnostic criteria of SAS. Neither dialysis and biochemical data nor anamnestic parameters measured by the questionnaires correlated significantly with sleep-disordered breathing. CONCLUSION: The prevalence of SAS in this large unselected patient group was not as high as previously reported, but it is still considerably higher than in the general population. Objective recordings are essential, as questionnaires overestimate the prevalence of SAS in patients with ESRD. As SAS promotes hypertension and impairs quality of life, ESRD patients might benefit from a treatment of concomitant SAS.

Female↗

Inosine and N1-methylinosine within a synthetic oligomer mimicking the anticodon loop of human tRNA(Ala) are major epitopes for anti-PL-12 myositis autoantibodies.

Sera of some patients afflicted with the inflammatory disease myositis contain antibodies of the anti-PL-12 type. A fraction of these polyclonal autoantibodies specifically precipitates the fully matured human tRNA(Ala) bearing the anticodon IGC (PL-12 antigen). Earlier work (Bunn & Mathews, 1987, Science 238:116-119) had shown that the epitopes are located entirely within the anticodon stem-loop of the tRNA(Ala). Here we demonstrate that human anti-tRNA(Ala) autoantibodies immunoprecipitate a synthetic polyribonucleotide containing inosine (I) and N1-methylinosine (m1I) separated by 2 nt as in the anticodon stem-loop of human tRNA(Ala). The shortest polyribonucleotide that can be immunoprecipitated corresponds to the pentanucleotide IpGpCpm1IpUp, which corresponds to part of the anticodon loop of human tRNA(Ala) and lacks the stem-loop structure. The efficiency of immunoprecipitation was about four times greater with longer polyribonucleotides capable of forming a stem-loop structure, and was abolished by altering the relative positions of I and m1I within the synthetic polynucleotide. Synthetic oligodeoxyribonucleotide analogs of the tRNA(Ala) stem-loop, containing the sequence dIpdGdCdm1Ip, are not antigenic. Our results show that human anti-tRNA(Ala) autoantibodies selectively recognize chemical details of modified nucleotides (the 6-keto group of inosine-34 and the 6-keto group and the N1-methyl groups of N1-methylinosine-37) within an anticodon loop structure of a tRNA molecule. We also describe the chemical synthesis of the phosphoramidite derivatives corresponding to N1-methylinosine and N1-methyl-2'-deoxyinosine for use in the automatic chemical synthesis of oligonucleotides containing N1-methylinosine and N1-methyl-2'-deoxyinosine.

Antibodies, Antiphospholipid↗

Breathing during sleep in patients with nocturnal desaturation.

The mechanisms leading to hypoxemia during sleep in patients with respiratory failure remain poorly understood, with few studies providing a measure of minute ventilation (V I) during sleep. The aim of this study was to measure ventilation during sleep in patients with nocturnal desaturation secondary to different respiratory diseases. The 26 patients studied had diagnoses of chronic obstructive pulmonary disease (COPD) (n = 9), cystic fibrosis (CF) (n = 2), neuromusculoskeletal disease (n = 4), and obesity hypoventilation syndrome (OHS) (n = 11). Also reported are the results for seven normal subjects and seven patients with effectively treated obstructive sleep apnea (OSA) without desaturation during sleep. Ventilation was measured with a pneumotachograph attached to a nasal mask. In the treated patients with OSA and in the normal subjects, only minor alterations in V I were observed during sleep. In contrast, mean V I for the group with nocturnal desaturation decreased by 21% during non-rapid-eye-movement (NREM) sleep and by 39% during rapid-eye-movement (REM) sleep as compared with wakefulness. This reduction was due mainly to a decrease in tidal volume (V T). Hypoventilation was most pronounced during REM sleep, irrespective of the underlying disease. These data indicate that hypoventilation may be the major factor leading to hypoxia during sleep, and that reversal of hypoventilation during sleep should be a major therapeutic strategy for these patients.

Adult↗