Konrad E Bloch

University of Zurich, Zürich, Zurich, Switzerland

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Publications (190)918.54 Total impact

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    ABSTRACT: Bloch, Konrad E., Tsogyal D. Latshang, and Silvia Ulrich. Patients with obstructive sleep apnea at altitude. High Alt Med Biol. 00:000-000, 2015.-Obstructive sleep apnea (OSA) is highly prevalent in the general population, in particular in men and women of older age. In OSA patients sleeping near sea level, the apneas/hypopneas associated with intermittent hypoxemia are predominantly due to upper airway collapse. When OSA patients stay at altitudes above 1600 m, corresponding to that of many tourist destinations, hypobaric hypoxia promotes frequent central apneas in addition to obstructive events, resulting in combined intermittent and sustained hypoxia. This induces strong sympathetic activation with elevated heart rate, cardiac arrhythmia, and systemic hypertension. There are concerns that these changes expose susceptible OSA patients, in particular those with advanced age and co-morbidities, to an excessive risk of cardiovascular and other adverse events during a stay at altitude. Based on data from randomized trials, it seems advisable for OSA patients to use continuous positive airway pressure treatment with computer controlled mask pressure adjustment (autoCPAP) in combination with acetazolamide during an altitude sojourn. If CPAP therapy is not feasible, acetazolamide alone is better than no treatment at all, as it improves oxygenation and sleep apnea and prevents excessive blood pressure rises of OSA patients at altitude.
    High altitude medicine & biology 05/2015; 16(2). DOI:10.1089/ham.2015.0016
  • Pneumologie 05/2015; 69(05). DOI:10.1055/s-0035-1551925
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    ABSTRACT: High altitude pulmonary hypertension (HAPH), a chronic altitude related illness, causes hypoxemia and impaired exercise performance. We evaluated the hypothesis that hemodynamic limitation and hypoxemia in patients with HAPH are associated with impaired cerebral tissue oxygenation (CTO) compared to healthy highlanders (HH) and lowlanders (LL). We studied 36 highlanders with HAPH and 54 HH at an altitude of 3250 m, and 34 LL at 760 m. Mean(±SD), mean pulmonary artery pressures were 34(±3), 22(±5), 16(±4) mmHg, respectively (p<0.05, all comparisons). CTO was monitored by near-infrared spectroscopy along with pulse oximetry (SpO2 ) during quiet breathing of room air (RA) and oxygen for 20 min each, and during hyperventilation with RA and oxygen, respectively. In HAPH, HH and LL breathing RA, SpO2 was 88(±4)%, 92(±2)%, 95(±2)% (p<0.001, all comparisons), CTO was similar in the 3 groups: 68(±3%), 68(±4)% 69(±4)% (P = NS, all comparisons). Breathing oxygen increased SpO2 and CTO significantly more in HAPH than in HH and LL. Hyperventilation (RA) did not reduce CTO in HAPH but in HH and LL; hyperventilation (oxygen) increased CTO in HAPH only. Highlanders with and without HAPH studied at 3250 m have a similar CTO as healthy lowlanders at 760 m even though highlanders were hypoxemic. The physiologic response to hyperoxia and hypocapnia assessed by cerebral NIRS suggests that healthy highlanders and even highlanders with HAPH effectively maintain an adequate CTO. This adaptation may be of particular relevance since an adequate cerebral oxygenation is essential for vital brain functions. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Experimental physiology 05/2015; DOI:10.1113/EP085200
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    ABSTRACT: Introduction: Patients with chronic obstructive pulmonary disease (COPD) might be particularly susceptible to hypoxia-induced autonomic dysregulation. Decreased baroreflex sensitivity (BRS) and increased blood pressure variability (BPV) are markers of impaired cardiovascular autonomic regulation and there is evidence for an association between decreased BRS/increased BPV and high cardiovascular risk. The aim of this study was to evaluate the effect of a short-term exposure to moderate altitude on blood pressure (BP) and measures of cardiovascular autonomic regulation in COPD patients. Methods: Continuous morning beat-to-beat BP was non-invasively measured with a Finometer device during ten minutes atlow altitude (490 m, Zurich) and at two days at moderate altitude (2590 m, Davos Jakobshorn) – the order of altitude exposure was randomized. Outcomes of interest were mean systolic and diastolic BP, BPV expressed as coefficient of variation, and spontaneous BRS. Changes between low altitude and day one and day two at moderate altitude were assessed by analysis of variance (ANOVA) for repeated measurements with Fisher post hoc analysis. Results: 39 patients with moderate to severe COPD (mean±SD age 64±6.2 y, FEV1 1.7±0.7 l, SpO2 93.6±1.8) were included. Systolic morning BP increased by +10.9 mm Hg [95% CI 4.6, 17.2] (p = 0.001) and diastolic morning BP by +6.4 mm Hg [95% CI 2.2, 10.6] (p = 0.004) in response to altitude exposure. BRS significantly and progressively decreased (p = 0.004) at moderate altitude, whereas BPV significantly and progressively increased (p < 0.001) upon exposure to altitude (table 1). Conclusion: Short-term exposure of lowlanders with COPD to moderate altitude is associated with a clinically relevant increase in blood pressure which seems to be related to autonomic dysregulation.
    Annual Meeting of the Swiss Respiratory Society, Lugano, Switzerland; 04/2015
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    ABSTRACT: Introduction: Patients with obstructive sleep apnea (OSA) suffer from cognitive impairment and are at increased risk of stroke. Suspected underlying mechanisms include cerebral hypoxia related to repetitive arterial oxygen desaturation and impaired cerebrovascular autoregulation. Using a randomized controlled CPAP withdrawal protocol, we evaluated the hypothesis that patients with untreated OSA experience clinically relevant nocturnal cerebral hypoxia which may be prevented by CPAP therapy. Methods: OSA patients established on CPAP treatment taking part in a trial on the effects of CPAP withdrawal on myocardial perfusion were included. Patients were randomized to either continue therapeutic CPAP or to withdraw it for two weeks by using a subtherapeutic CPAP-device. Nocturnal polygraphy including continuous monitoring of regional cerebral tissue oxygenation(CTO) by near infrared spectroscopy (NIRS) with optodes placed on the skin of the forehead was performed at baseline and after two weeks of either therapeutic or subtherapeutic CPAP. Outcomes of interest were the mean nocturnal CTO, the cerebral oxygen desaturation index (cerebral ODI, ≥3% dips) associated with apneas/hypopneas, and the number of patients experiencing a major fall in CTO of ≥13% which has been associated with neurophysiological signs of severe cerebral ischemia in neurosurgical patients [Al-Rawi, Stroke 2006]. Analyses were adjusted for baseline differences. Results: 21 patients (mean±SD: age = 63.0±8.9 yrs, apnea/hypopnea-index at diagnosis = 50.3±19.1/h) were enrolled. CPAP withdrawal led to a recurrence of OSA (increase in apnea/hypopnea index by +40.7/h; 95% CI:+31.1,+50.4/h, p < 0.001). This was associated with a reduced mean arterial and cerebral oxygenation and cyclic drops in CTO (increase in cerebral ODI by +37.0/h; 95% CI:+25.3,+48.7/h, p < 0.001). A major fall of CTO by ≥13% was observed in 4/9 patients treated with subtherapeutic CPAP but in none of the patients on therapeutic CPAP (chi square = 6.6, p = 0.01). Conclusions: CPAP therapy withdrawal – and thus recurrence of OSA – results in intermittent and sustained nocturnal cerebral tissue deoxygenation to a degree reported to cause cerebral dysfunction. These findings suggest that patients with untreated OSA are at increased risk of nocturnal cerebral damage, a threat than can be prevented by CPAP therapy.
    Annual Meeting of the Swiss Respiratory Society, Lugano, Switzerland; 04/2015
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    ABSTRACT: This work investigates the performance of cardiorespiratory analysis detecting periodic breathing (PB) in chest wall recordings in mountaineers climbing to extreme altitude. The breathing patterns of 34 mountaineers were monitored unobtrusively by inductance plethysmography, ECG and pulse oximetry using a portable recorder during climbs at altitudes between 4497 and 7546 m on Mt. Muztagh Ata. The minute ventilation (VE) and heart rate (HR) signals were studied, to identify visually scored PB, applying time-varying spectral, coherence and entropy analysis. In 411 climbing periods, 30–120 min in duration, high values of mean power (MPVE) and slope (MSlopeVE) of the modulation frequency band of VE, accurately identified PB, with an area under the ROC curve of 88 and 89 %, respectively. Prolonged stay at altitude was associated with an increase in PB. During PB episodes, higher peak power of ventilatory (MPVE) and cardiac (MP LFHR) oscillations and cardiorespiratory coherence (MP LFCoher), but reduced ventilation entropy (SampEnVE), was observed. Therefore, the characterization of cardiorespiratory dynamics by the analysis of VE and HR signals accurately identifies PB and effects of altitude acclimatization, providing promising tools for investigating physiologic effects of environmental exposures and diseases.
    Medical & Biological Engineering 03/2015; 53(8). DOI:10.1007/s11517-015-1275-x
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    ABSTRACT: Intact postural control is essential for safe performance of mountain sports, operation of machinery at altitude, and for piloting airplanes. We tested whether exposure to hypobaric hypoxia at moderate altitude impairs the static postural control of healthy subjects. In 51 healthy men, median age 24 y (quartiles 20;28), static control was evaluated on a balance platform in Zurich, 490 m, and during a 4-day sojourn in Swiss mountain villages at 1630 m and 2590 m, 2 days each. The order of altitude exposure was randomized. Total center of pressure path length (COPL) and sway amplitude measured in two directions by a balance platform, and pulse oximetry were recorded. Data were compared between altitudes. Median (quartiles) COPL during standing on both legs with eyes open at 490 m and in the evenings on the first and second days at 1630 and 2590 m, respectively were: 50 (45;57), 55 (48;62), 56 (49;61), 53 (47;59), 54 (48;60) cm, P<0.001 ANOVA. Corresponding arterial oxygen saturation was 97% (96;97), 95% (94;96), 95%(94;96), 92%(90;93), 93%(91;93), P<0.001. Anterior-posterior sway amplitudes were larger at 1630 and 2590 m compared to 490 m, P<0.001. Multiple logistic regression analysis confirmed that higher altitudes (1630 and 2590m) were independently associated with increased COPL when controlled for the order of altitude exposure and age (P=0.001). Exposure to 1630 and 2590m was associated with impaired static postural control even when visual references were available. ClinicalTrials.gov NCT01130948.
    PLoS ONE 02/2015; 10(2):e0116695. DOI:10.1371/journal.pone.0116695
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    ABSTRACT: Arterial and thromboembolic pulmonary hypertension (PH) lead to arterial hypoxaemia. To investigate whether cerebral tissue oxygenation (CTO) in patients with PH is reduced and whether this is associated with reduced exercise tolerance. 16 patients with PH (mean pulmonary arterial pressure ≥25 mmHg, 14 arterial, 2 chronic thromboembolic) and 15 controls underwent right heart catheterisation with monitoring of CTO at rest, during maximal bicycle exercise and during inhalation of oxygen and NO. The 6 min walk distance (6MWD) was measured. Median CTO in PH-patients at rest was 62 % (quartiles 53; 71), during exercise 60 % (53; 65); corresponding values in controls were 65 % (73; 73) (P = NS) and 68 % (66; 70) (p = .013 vs. PH). Inhalation of NO and oxygen improved CTO in PH. In multivariate regression analysis CTO at maximal exercise predicted the work load achieved when controlled for age, pulmonary vascular resistance and mixed venous oxygen saturation (R (2) = .419, p < .000); in addition, the 6MWD was predicted by CTO (adjusted R (2) = .511, p < .000). In PH-patients but not in controls CTO decreased during exercise. Since CTO was an independent predictor of the work load achieved and the 6MWD cerebral hypoxia may contribute to exercise limitation in PH. Clinicaltrials.gov: NCT01463514.
    Beiträge zur Klinik der Tuberkulose 11/2014; 193(1). DOI:10.1007/s00408-014-9667-5
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    ABSTRACT: Several studies showed beneficial effects of sleep on memory performance. Slow waves, the electroencephalographic characteristic of deep sleep, reflected on the neuronal level by synchronous slow oscillations, seem crucial for these benefits. Traveling to moderate altitudes decreases deep sleep. In a randomized cross-over design healthy male subjects performed a visuo-motor learning task in Zurich (490 m) and at Davos Jakobshorn (2590 m) in random order. Memory performance was assessed immediately after learning, before sleep, and in the morning after a night of sleep. Sleep EEG recordings were performed during the nights. Our findings show an altitude induced reduction of sleep dependent memory performance. Moreover, this impaired sleep dependent memory performance was associated with reduced slow wave derived measures of neuronal synchronization. Our results are consistent with a critical role of slow waves for the beneficial effects of sleep on memory that is susceptible to natural environmental influences.
    Physiology & Behavior 11/2014; 139. DOI:10.1016/j.physbeh.2014.11.033
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    ABSTRACT: Pulmonary hypertension (PH) due to COPD has dismal prognosis. We reviewed the long-term effect of PH-target therapy in severe PH-COPD.
    Beiträge zur Klinik der Tuberkulose 10/2014; DOI:10.1007/s00408-014-9650-1
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    ABSTRACT: Background Obstructive sleep apnoea (OSA) is a risk factor for hypertension and associated with increased cardiovascular risk. Continuous positive airway pressure (CPAP) is presumed to be an everyday therapy and has been shown to reduce blood pressure and improve other measures of vascular risk. It is not known whether short-term CPAP withdrawal results in impaired myocardial perfusion and thus, might increase the risk for myocardial ischemia. Objective We assessed the effect of a short-term CPAP withdrawal on myocardial perfusion in patients with OSA. Methods 45 patients with moderate to severe OSA, currently on CPAP, were randomised to either continue or withdraw CPAP (subtherapeutic CPAP) for two weeks. Sleep studies and cardiac positron emission tomography to assess myocardial perfusion were performed at baseline and at two weeks. Results CPAP withdrawal led to a recurrence of OSA (mean difference in AHI between groups +39.7/h, 95%CI 32.7 to 46.7/h, p<0.001). In comparison to continuing CPAP, subtherapeutic CPAP led to a statistically significant increase in morning blood pressure; mean difference in systolic blood pressure +10.8mmHg (95%CI 5.2 to 16.4mmHg) and diastolic blood pressure +7.5mmHg (95%CI 3.5 to 11.5mmHg, both p<0.001), but was not associated with deterioration of myocardial perfusion (mean difference in hyperaemic myocardial blood flow -0.09ml/min/g, 95%CI -0.17 to -0.36ml/min/g, p=0.907). Conclusions Although short-term CPAP therapy withdrawal leads to a considerable increase in blood pressure, it is not associated with impaired myocardial perfusion. Thus, short-term discontinuation of CPAP does not seem to increase the risk of myocardial ischemia.
    Annual Congress of the European Respiratory Society (ERS), Munich, Germany; 09/2014
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    ABSTRACT: Background Based on meta-analyses, the blood pressure (BP) lowering effect of continuous positive airway pressure (CPAP) in obstructive sleep apnoea (OSA) is reported to be 2mmHg. This figure is derived from trials often limited by poor CPAP compliance, thus, underestimating the effect of CPAP treatment. We analysed BP data from randomised-controlled CPAP withdrawal trials which included only optimally CPAP compliant patients. Methods 145 OSA patients on CPAP were randomised to continue therapeutic (n=62) or to withdraw CPAP (n=83) for two weeks. Morning BP was measured at home before and in hospital after sleep studies. Results CPAP withdrawal was associated with a return of OSA (apnoea-hypopnoea index (AHI) at baseline 2.8/h, at follow-up 33.2/h). Systolic office BP increased in the CPAP withdrawal group compared to CPAP continuation by +6.5mmHg (95%CI 2.6-10.4mmHg, p=0.001) and systolic home BP by +9.7mmHg (95%-CI 6.3-13.0mmHg, p<0.001); diastolic office BP increased by +5.0mmHg (95%CI 2.4-7.6mmHg, p<0.001) and diastolic home BP by +7.9mmHg (95%CI 5.6-10.3mmHg, p<0.001). AHI, baseline systolic BP, statins, gender and number of antihypertensive drugs were independently associated with systolic BP change in multivariate analysis controlled for age, BMI, smoking, diabetes, and sleepiness. Change in diastolic BP was independently predicted by AHI, baseline diastolic BP, and statins. Conclusions Short-term CPAP withdrawal results in a clinically relevant increase in BP, which is considerably higher than in conventional CPAP trials and may be underestimated if only office BP values are used. OSA severity and baseline BP seem to be predictors of BP response to CPAP.
    Annual Congress of the European Respiratory Society (ERS) 2014, Munich, Germany; 09/2014
  • European Respiratory Journal 09/2014; 44(3):578-84. DOI:10.1183/09031936.00109314
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    ABSTRACT: Background:Sleep-disturbed breathing (SDB) is common in patients with pre-capillary pulmonary hypertension (PH). Nocturnal oxygen therapy (NOT) and acetazolamide improve SDB in PH-patients and NOT improves exercise capacity. We investigated the effect of NOT and acetazolamide on nocturnal cardiac conduction, repolarization and arrhythmias in patients with PH and SDB. Methods:In a randomized, placebo-controlled, double-blind, cross-over trial 23 patients with arterial (n=16) or chronic thromboembolic PH (n=7) and SDB defined as a mean nocturnal oxygen saturation (SpO2)<90% or dips(>3%)>10/h with daytime PaO2≥7.3kPa were studied. Participants received NOT (3l/min), acetazolamide tablets (2x250mg), and sham-NOT/placebo each during one week separated by a one-week washout period. Three-lead electrocardiography was recorded during overnight polysomnography at the end of each treatment period. Repolarization indices were averaged over three cardiac cycles at late evening and at early morning and nocturnal arrhythmias were counted. Results:NOT was associated with a lower overnight (68±10 vs. 72±9bpm, p=0.010) and early morning heart rate compared with placebo. At late evening, the PQc-time was increased under acetazolamide compared with placebo (mean difference 10ms, 95%CI 0 to 20ms, p=0.042). In the morning under NOT, the QTc-interval was decreased compared with placebo (mean difference -25ms, 95%CI -45 to -6ms, p=0.007) and the TpTec-interval shorter compared with acetazolamide (mean difference -11ms, 95%CI -21 to -1ms, p=0.028). Arrhythmias were rare and similar with all treatments. Conclusions:In PH-patients with SDB, NOT reduces nocturnal heart rate and QTc in the morning thus favorably modifying prognostic markers. Clinical Trial Registration:This trial is registered at clinicalTrials.gov: NTC-01427192.
    Chest 07/2014; DOI:10.1378/chest.14-0495
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    ABSTRACT: Sleep disordered breathing may impair cerebral oxygenation in patients with obstructive sleep apnea syndrome (OSA), in particular during altitude travel. We studied cerebral tissue oxygenation (CTO) in OSA patients at low and moderate altitude, and evaluated whether acetazolamide improved CTO. 18 OSA patients living at <600m discontinued CPAP therapy during studies in Zurich (490m) and during 2 sojourns of 3 days in the Swiss Alps (2 days at 1860m, 1 day at 2590 m) separated by a 2-week washout period at <600m. Patients received acetazolamide (2x250mg/d) or placebo at altitude in a randomized, double-blind, cross-over design. Nocturnal polysomnography including CTO-monitoring by near-infrared spectroscopy(NIRS) was performed. At 490m, medians of CTO, pulse oximetry (SpO2), and apnea/hypopnea index were 65%, 93%, and 57.3/h. At 2590m, on placebo, corresponding values were 59%, 86%, 86.4/h (P<0.05, all corresponding comparisons). Acetazolamide increased CTO and SpO2 at 2590m by mean values (95% CI) of 2% (0-4) and 2% (1-3), and reduced the apnea/hypopnea index by 23.4/h (14.0-32.8) (P<0.05, all changes). Cerebral total hemoglobin concentration, a NIRS-derived surrogate reflecting regional cerebral blood volume, increased by a similar degree in response to apneas at 490m and 2590m, and during acetazolamide and placebo treatment. In OSA patients staying at altitude nocturnal cerebral and arterial oxygenation were reduced in association with exacerbated sleep apnea. Acetazolamide partially improved CTO, SpO2 and sleep apnea without impairing the cerebral blood flow response to apneas. www.clinicaltrials.gov: NCT00714740.
    Chest 05/2014; 146(2). DOI:10.1378/chest.13-2967
  • Pneumologie 05/2014; 68(05). DOI:10.1055/s-0034-1375918
  • Pneumologie 05/2014; 68(05). DOI:10.1055/s-0034-1375917
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    ABSTRACT: Duchenne muscular dystrophy (DMD) leads to progressive paresis, respiratory failure and premature death. Long-term positive pressure ventilation can improve quality of life and survival, but previously unrecognized complications may arise. We analyzed the characteristics of severe metabolic acidosis occurring in 8 of 55 DMD patients, of 20-36 years of age, observed over a 5-year period. All patients were on positive pressure ventilation and were being treated for chronic constipation. Before admission, they had had a reduced intake of fluids and food. Upon examination, they were severely ill, dyspneic and suffering from abdominal discomfort. Metabolic acidosis with a high anion gap was noted in 5 of the 8 patients and with a normal anion gap in the other 3. They all recovered after the administration of fluids and nutrition, the regulation of bowel movements and treatment with antibiotics, as appropriate. Metabolic acidosis is a life-threatening, potentially preventable complication in older DMD patients. Early recognition, subsequent administration of fluids, nutrition and antibiotics and regulation of bowel movements seem to be essential. © 2014 S. Karger AG, Basel.
    Respiration 04/2014; 87(6). DOI:10.1159/000358439
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    ABSTRACT: 1) To investigate the impact of acetazolamide, a drug commonly prescribed for altitude sickness, on cortical oscillations in patients with obstructive sleep apnea syndrome (OSAS). 2) To examine alterations in the sleep EEG after short-term discontinuation of continuous positive airway pressure (CPAP) therapy. Data from two double-blind, placebo-controlled randomized cross-over design studies were analyzed. Polysomnographic recordings in sleep laboratory at 490 m and at moderate altitudes in the Swiss Alps: 1630 or 1860 m and 2590 m. Study 1: 39 OSAS patients. Study 2: 41 OSAS patients. Study 1: OSAS patients withdrawn from treatment with CPAP. Study 2: OSAS patients treated with autoCPAP. Treatment with acetazolamide (500-750 mg) or placebo at moderate altitudes. An evening dose of 500 mg acetazolamide reduced slow-wave activity (SWA; approximately 10%) and increased spindle activity (approximately 10%) during non-REM sleep. In addition, alpha activity during wake after lights out was increased. An evening dose of 250 mg did not affect these cortical oscillations. Discontinuation of CPAP therapy revealed a reduction in SWA (5-10%) and increase in beta activity (approximately 25%). The higher evening dose of 500 mg acetazolamide showed the "spectral fingerprint" of Benzodiazepines, while 250 mg acetazolamide had no impact on cortical oscillations. However, both doses had beneficial effects on oxygen saturation and sleep quality.
    PLoS ONE 04/2014; 9(4):e93931. DOI:10.1371/journal.pone.0093931
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    ABSTRACT: Abstract Kriemler, Susi, Flavia Bürgi, Christian Wick, Birgit Wick, Melanie Keller, Urs Wiget, Christian Schindler, Beat A. Kaufmann, Malcolm Kohler, Konrad Bloch, and Hans-Peter Brunner-La Rocca. Prevalence of acute mountain sickness at 3500 m within and between families: A prospective cohort study. High Alt Biol Med 15:000-000, 2014.-Aim: To investigate symptoms, prevalence and associated factors of acute mountain sickness (AMS) in families upon a fast ascent to 3450 m. Methods: 87 children, 70 adolescents, and 155 parents (n=312) were assessed for AMS 8-10 and 20-24 hours after fast passive ascent by the Lake Louise Score (LLS). Pain sensitivity and oxygen saturation (SO2) were measured and familial clustering was assessed. Results: AMS prevalence was significantly lower in children (21%) compared to adolescents (34%) and adults (39%) on day 1 (p<0.05), but not on day 2 (18% vs. 19% and 25%). Cumulative prevalence of AMS was 30, 37, and 45% in children, adolescents, and adults, respectively (p<0.001). Familial clustering of AMS was consistent and explained 25%-50% of variability in AMS. Pain sensitivity significantly increased from low to high altitude and was higher at low altitude in those with compared to those without AMS. SO2 at high altitude was not related to the presence of AMS. Conclusions: After fast ascent to 3500 m, AMS prevalence was lower in children than in adolescents and adults on day 1, but not on day 2. Thus, children may travel at least as safely to an altitude of 3500 m as adolescents and adults, even if risk factors (pain sensitivity and heredity) are present.
    High altitude medicine & biology 02/2014; 15(1). DOI:10.1089/ham.2013.1073

Publication Stats

3k Citations
918.54 Total Impact Points

Institutions

  • 1991–2015
    • University of Zurich
      • • Center for Integrative Human Physiology
      • • Internal Medicine Unit
      • • Ophthalmology Unit
      • • Pneumologie
      Zürich, Zurich, Switzerland
  • 1997–2009
    • University Hospital Zürich
      Zürich, Zurich, Switzerland
  • 1991–1994
    • University of Miami
      كورال غيبلز، فلوريدا, Florida, United States