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 [QTC and T peak to T end intervals ( $$T_{\text{p}} T_{{{\text{e}}_{\text{c}} }}$$ )] 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 QTC interval [+5.4 (22.4)ms, 95%CI −1.7 to +12.4ms, p=0.168] and a significant increase of the $$T_{\text{p}} T_{{{\text{e}}_{\text{c}} }}$$ interval [+3.7 (8.9)ms, 95%CI +0.9 to +6.6ms, p=0.010]. The Mueller maneuver induced a significant increase of the QTC interval [+8.3 (23.4)ms, 95%CI 0.9 to +15.6ms, p=0.035] and the $$T_{\text{p}} T_{{{\text{e}}_{\text{c}} }}$$ interval (+4.2 (8.2)ms, 95%CI +1.6 to +6.8ms, p=0.002). There were no significant changes of the QTC and $$T_{\text{p}} T_{{{\text{e}}_{\text{c}} }}$$ 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 QTC and $$T_{\text{p}} T_{{{\text{e}}_{\text{c}} }}$$ intervals. Therefore, negative intrathoracic pressure changes may be a contributory mechanism for the association between OSA and cardiac dysrhythmia

Obstruktives Schlafapnoe-Syndrom

Das obstruktive Schlafapnoe-Syndrom (OSAS) ist eine Atemregulationsstörung, bei der ein repetitiver Kollaps der oberen Atemwege während des Schlafes zu gehäuften Apnoen/Hypopnoen mit zyklischen Sauerstoffdesaturationen und Weckreaktionen führt. Der Schlaf wird dadurch fragmentiert und ist nicht erholsam. Die betroffenen Patienten leiden unter vermehrter Einschlaftendenz, Konzentrationsstörungen und einer beeinträchtigten Lebensqualität. Zu den Folgen des OSAS gehören zudem ein erhöhtes Risiko, Unfälle durch Einschlafen zu verursachen, sowie Herz- und Kreislauferkrankungen. Die Diagnose des OSAS beruht auf einer typischen Anamnese und der klinischen Untersuchung. Übergewicht, ein grosser Halsumfang und enge Rachenverhältnisse können auf ein OSAS hinweisen. Die Diagnose wird durch eine Schlafuntersuchung bestätigt. Die wichtigste Behandlung des OSAS ist die nächtliche Anwendung von kontinuierlichem Überdruck (CPAP) über eine Nasen- oder Mund-Nasen-Maske, was in der Regel zur raschen Besserung der Symptome führt. Patienten, die eine CPAP-Therapie nicht tolerieren, können mit einer Unterkieferprotrusionsschiene erfolgreich behandelt werden. Unterstützende Massnahmen sind regelmässige und genügend lange Schlafzeiten, das Vermeiden von Rauchen und abendlichem Alkoholkonsum und die Gewichtsreduktion bei Adipositas

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 5min. 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 1s (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

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

Effects of moderate altitude on LDL diameter.

<p>Scatterplot showing individual median low density lipoprotein (LDL) diameter in Zurich (490 m) and Davos Jakobshorn (2590 m) during day 1 and day 2. Black lines represent medians. LDL diameter was larger on both days at 2590 m compared to 490 m. *p<0.05 vs 490 m.</p

Effects of moderate altitude on C-reactive protein.

<p>Scatterplot showing individual highly sensitive C-reactive protein (hsCRP) blood levels in Zurich (490 m) and Davos Jakobshorn (2590 m). Black lines represent medians. HsCRP levels were lower on day 1 at 2590 m compared to 490 m. *p<0.05 vs 490 m.</p