The speed of blood pressure fluctuations in patients with chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) has been associated with increased risk for cardiovascular disease but mechanisms underlying this association are incompletely understood. The speed of beat-to-beat changes in systolic blood pressure (vSBP) was found to be pronounced in patients with elevated cardiovascular risk. Although increased vSBP may thus be a contributing mechanism to cardiovascular morbidity, no data exist on vSBP in patients with COPD. Therefore, the purpose of this study was to evaluate whether there is an association between severity of COPD and vSBP. METHODS: Resting beat-to-beat blood pressure was recorded during 5 min. vSBP was assessed by calculating the slopes of oscillatory fluctuations in SBP for different inter-beat intervals (IBI). Univariate and multivariate analyses were performed to evaluate the association between forced expiratory volume in 1 s (FEV1) and vSBP. RESULTS: This study comprised 60 patients with COPD (24 females) with a mean [SD] FEV1 of 45.4 [22.7] %predicted and 34 healthy controls. Short-term fluctuations in SBP were more pronounced in patients with COPD compared to healthy controls. There was a significant inverse correlation between FEV1 and vSBP (r=-0.41, p=0.001). Even after adjustment for covariates in multivariate analysis, FEV1 was found to be independently associated with vSBP. CONCLUSIONS: Patients with COPD are characterised by steeper blood pressure changes than healthy controls. The speed of fluctuations in SBP is associated with the severity of airflow limitation. Increased vSBP may be a mechanism underpinning the association between COPD and cardiovascular disease.

The effects of simulated obstructive apnea and hypopnea on arrhythmic potential in healthy subjects.

Preliminary evidence supports an association between OSA and cardiac dysrhythmias. Negative intrathoracic pressure, as occurring during OSA, may provoke cardiac dysrhythmias. Thus, we aimed to study the acute effects of simulated apnea and hypopnea on arrhythmic potential and measures of cardiac repolarization [QT(C) and T (peak) to T (end) intervals [TpTec]) in humans. In 41 healthy volunteers, ECG was continuously recorded prior, during and after simulated obstructive hypopnea (inspiration through a threshold load), simulated apnea (Mueller maneuver), end-expiratory central apnea and normal breathing in randomized order. The number of subjects with premature beats was significantly higher during inspiration through a threshold load (n = 7), and the Mueller maneuver (n = 7) compared to normal breathing (n = 0) (p = 0.008 for all comparisons), but not during end-expiratory central apnea (n = 3, p = 0.125). Inspiration through a threshold load was associated with a non-significant mean (SD) increase of the QT(C) interval [+5.4 (22.4) ms, 95 %CI -1.7 to +12.4 ms, p = 0.168] and a significant increase of the TpTcc interval [+3.7 (8.9) ms, 95 %CI +0.9 to +6.6 ms, p = 0.010]. The Mueller maneuver induced a significant increase of the QT(C) interval [+8.3 (23.4) ms, 95 %CI 0.9 to +15.6 ms, p = 0.035] and the TpTec interval (+4.2 (8.2) ms, 95 %CI +1.6 to +6.8 ms, p = 0.002). There were no significant changes of the QT(C) and TpTec intervals during central end-expiratory apnea. These data indicate that simulated obstructive apnea and hypopnea are associated with an increase of premature beats and prolongation of QT(C) and TpTec intervals. Therefore, negative intrathoracic pressure changes may be a contributory mechanism for the association between OSA and cardiac dysrhythmias.

[Obstructive Sleep Apnea Syndrome]. / Obstruktives Schlafapnoe-Syndrom.

Obstructive Sleep Apnea Syndrome Abstract. The obstructive sleep apnea syndrome (OSAS) is a disorder of the control of breathing in which repetitive collapse of the upper airway during sleep leads to frequent apneas/hypopneas with cyclic oxygen desaturation and arousals. Sleep is fragmented and unrefreshing. The affected patients suffer from an increased tendency to fall asleep, impaired concentration and a reduced quality of life. The consequences of OSAS also include an increased risk of accidents caused by falling asleep as well as cardiovascular diseases. The diagnosis of OSAS is based on a typical history and clinical examination. Overweight, a large neck circumference and a narrow throat are conditions that may suggest an OSAS. The diagnosis is confirmed by sleep examination. The most important treatment for OSAS is the nightly application of continuous positive pressure (CPAP) via a nasal or mouth-nose mask, which usually leads to a rapid improvement of the symptoms. Patients who do not tolerate CPAP therapy can be successfully treated with a mandibular advancement device. Supporting measures are regular and sufficiently long sleeping times, avoidance of smoking and alcohol consumption in the evening as well as weight reduction for obese patients.

Actigraphy of Wrist and Ankle for Measuring Sleep Duration in Altitude Travelers.

Latshang, Tsogyal Daniela, Daniela Juliana Mueller, Christian Maurizio Lo Cascio, Anne-Christin Stöwhas, Katrin Stadelmann, Noemi Tesler, Peter Achermann, Reto Huber, Malcolm Kohler, and Konrad Ernst Bloch. Actigraphy of wrist and ankle for measuring sleep duration in altitude travelers. High Alt Med Biol. 17:194-202, 2016-Aims: Actigraphy might be convenient to assess sleep disturbances in altitude field studies. Therefore, we evaluated whether actigraphy accurately measures sleep duration in healthy subjects traveling to altitude. METHODS: Fifty-one healthy men, aged mean ± standard deviation (SD) 27 ± 9 years, were studied during one night at Zurich (490 m), two nights at Davos Wolfgang (1630 m), and two nights at Jakobshorn (2590 m), in randomized order. Sleep duration measured by actigraphy, using a one-axis device at the wrist (n = 51), a three-axis device at the other wrist, and a three-axis device at the ankle (n = 22), was compared with corresponding total sleep time (TST) measured by polysomnography. RESULTS: During 255 polysomnographic overnight studies, 449 paired actigraphic recordings were obtained. The median polysomnographic-derived TST ranged from 397 to 408 minutes. Actigraphic mean TST from wrists with one-axis and three-axis devices, and from ankle agreed well with polysomnographic values with a bias of +1, -7, +6 minutes, respectively. Corresponding limits of agreement (±2 SD of bias) were ±51, ±60, and ±59 minutes. Limits of agreement of mean TST over five nights by actigraphy and polysomnography were similar to the coefficient of repeatability (2 SD of mean) of polysomnographic TST, that is, ±31, ±38, and ±36 minutes versus ±34 minutes. CONCLUSIONS: Actigraphy of the wrist or ankle by a one-axis or a three-axis device accurately estimates mean TST in groups of subjects and mean TST over several nights in individuals traveling to altitude. Therefore, actigraphy is valuable for assessing effects of altitude and other environmental influences on sleep duration during field studies over extended periods.

Are nocturnal breathing, sleep, and cognitive performance impaired at moderate altitude (1,630-2,590 m)?

STUDY OBJECTIVES: Newcomers at high altitude (> 3,000 m) experience periodic breathing, sleep disturbances, and impaired cognitive performance. Whether similar adverse effects occur at lower elevations is uncertain, although numerous lowlanders travel to moderate altitude for professional or recreational activities. We evaluated the hypothesis that nocturnal breathing, sleep, and cognitive performance of lowlanders are impaired at moderate altitude. DESIGN: Randomized crossover trial. SETTING: University hospital at 490 m, Swiss mountain villages at 1,630 m and 2,590 m. PARTICIPANTS: Fifty-one healthy men, median (quartiles) age 24 y (20-28 y), living below 800 m. INTERVENTIONS: Studies at Zurich (490 m) and during 4 consecutive days at 1,630 m and 2,590 m, respectively, 2 days each. The order of altitude exposure was randomized. Polysomnography, psychomotor vigilance tests (PVT), the number back test, several other tests of cognitive performance, and questionnaires were evaluated. MEASUREMENTS AND RESULTS: The median (quartiles) apnea-hypopnea index at 490 m was 4.6/h (2.3; 7.9), values at 1,630 and 2,590 m, day 1 and 2, respectively, were 7.0/h (4.1; 12.6), 5.4/h (3.5; 10.5), 13.1/h (6.7; 32.1), and 8.0/h (4.4; 23.1); corresponding values of mean nocturnal oxygen saturation were 96% (95; 96), 94% (93; 95), 94% (93; 95), 90% (89; 91), 91% (90; 92), P < 0.05 versus 490 m, all instances. Slow wave sleep on the first night at 2,590 m was 21% (18; 25) versus 24% (20; 27) at 490 m (P < 0.05). Psychomotor vigilance and various other measures of cognitive performance did not change significantly. CONCLUSIONS: Healthy men acutely exposed during 4 days to hypoxemia at 1,630 m and 2,590 m reveal a considerable amount of periodic breathing and sleep disturbances. However, no significant effects on psychomotor reaction speed or cognitive performance were observed. CLINICAL TRIALS REGISTRATION: Clinicaltrials.gov: NCT01130948.

Effects of acute exposure to moderate altitude on vascular function, metabolism and systemic inflammation.

BACKGROUND: Travel to mountain areas is popular. However, the effects of acute exposure to moderate altitude on the cardiovascular system and metabolism are largely unknown. OBJECTIVES: To investigate the effects of acute exposure to moderate altitude on vascular function, metabolism and systemic inflammation. METHODS: In 51 healthy male subjects with a mean (SD) age of 26.9 (9.3) years, oxygen saturation, blood pressure, heart rate, arterial stiffness, lipid profiles, low density lipoprotein (LDL) particle size, insulin resistance (HOMA-index), highly-sensitive C-reactive protein and pro-inflammatory cytokines were measured at 490 m (Zurich) and during two days at 2590 m, (Davos Jakobshorn, Switzerland) in randomized order. The largest differences in outcomes between the two altitudes are reported. RESULTS: Mean (SD) oxygen saturation was significantly lower at 2590 m, 91.0 (2.0)%, compared to 490 m, 96.0 (1.0)%, p<0.001. Mean blood pressure (mean difference +4.8 mmHg, p<0.001) and heart rate (mean difference +3.3 bpm, p<0.001) were significantly higher at 2590 m, compared to 490 m, but this was not associated with increased arterial stiffness. At 2590 m, lipid profiles improved (median difference triglycerides -0.14 mmol/l, p=0.012, HDL +0.08 mmol/l, p<0.001, total cholesterol/HDL-ratio -0.25, p=0.001), LDL particle size increased (median difference +0.45 nm, p=0.048) and hsCRP decreased (median difference -0.18 mg/l, p=0.024) compared to 490 m. No significant change in pro-inflammatory cytokines or insulin resistance was observed upon ascent to 2590 m. CONCLUSIONS: Short-term stay at moderate altitude is associated with increased blood pressure and heart rate likely due to augmented sympathetic activity. Exposure to moderate altitude improves the lipid profile and systemic inflammation, but seems to have no significant effect on glucose metabolism. TRIAL REGISTRATION: ClinicalTrials.gov NCT01130948.

The effect of simulated obstructive apnea and hypopnea on aortic diameter and BP.

BACKGROUND: Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation. The mechanisms through which OSA may promote thoracic aortic dilatation are incompletely understood. Therefore, we studied the acute effects of simulated apnea and hypopnea on aortic diameter and BP in humans. METHODS: The diameter of the aortic root was measured in 20 healthy volunteers by echocardiography, and peripheral BP was continuously recorded prior, during, and immediately after simulated obstructive hypopnea (inspiration through threshold load), simulated obstructive apnea (Müller maneuver), end-expiratory central apnea, and normal breathing in randomized order. RESULTS: Proximal aortic diameter increased significantly during inspiration through a threshold load (+6.48%; SE, 3.03; P = .007), but not during Müller maneuver (+3.86%; SE, 2.71; P = .336) or end-expiratory central apnea (+0.62%; SE, 2.94; P = .445). Maneuver-induced changes in mean BP were observed during inspiration through a threshold load (-10.5 mm Hg; SE, 2.2; P < .001), the Müller maneuver (-8.8 mm Hg; SE, 2.4; P < .001), and end-expiratory central apnea (-4.2 mm Hg; SE, 1.4; P = .052). There was a significant increase in mean BP on release of threshold load inspiration (+8.1 mm Hg; SE, 2.9 mm Hg; P = .002), Müller maneuver (+10.7 mm Hg; SE, 2.9; P < .001), and end-expiratory central apnea (+10.6 mm Hg; SE, 2.5; P < .001). CONCLUSIONS: Simulated obstructive hypopnea/apnea and central apnea induced considerable changes in BP, and obstructive hypopnea was associated with an increase in proximal aortic diameter. Further studies are needed to investigate effects of apnea and hypopnea on transmural aortic pressure and aortic diameter to define the role of OSA in the pathogenesis of aortic dilatation.