Association of Snoring and Daytime Sleepiness With Subsequent Incident Hypertension: A Population-Based Cohort Study.

BACKGROUND: There is a strong association between obstructive sleep apnea and hypertension, but the effects of obstructive sleep apnea symptoms on the risk of incident hypertension are not well documented. The aim of this prospective study was to examine whether snoring and sleepiness are associated with incident hypertension. METHODS: Data from the French population-based CONSTANCES cohort were analyzed. Normotensive participants, aged 18 to 69 years, were included between 2012 and 2016 and screened for snoring, morning fatigue, and daytime sleepiness in 2017 using items of the Berlin Questionnaire. We used Cox models, adjusted for multiple potential confounders, including body mass index, baseline blood pressure, sleep duration, and depressive symptoms, to compute hazards ratios of incidentally treated hypertension. RESULTS: Among 34 727 subjects, the prevalence of self-reported habitual snoring, morning fatigue, and excessive daytime sleepiness (≥3× a week for each) was 23.6%, 16.6%, and 19.1%, respectively. During a median follow-up of 3.1 years (interquartile range, 3.0-3.5), the incidence of treated hypertension was 4.1%. The risk of de novo treated hypertension was higher in participants who reported habitual snoring (adjusted hazard ratio, 1.17 [95% CI, 1.03-1.32]) and excessive daytime sleepiness (adjusted hazard ratio, 1.42 [95% CI, 1.24-1.62]), and increased with the weekly frequency of symptoms, with a dose-dependent relationship (Ptrend≤0.02 for all symptoms). CONCLUSIONS: Self-reported snoring and excessive daytime sleepiness are associated with an increased risk of developing hypertension. Identification of snoring and daytime sleepiness may be a useful public health screening tool in primary care for hypertension prevention.

Metrology of two wearable sleep trackers against polysomnography in patients with sleep complaints.

Sleep trackers are used widely by patients with sleep complaints, however their metrological validation is often poor and relies on healthy subjects. We assessed the metrological validity of two commercially available sleep trackers (Withings Activité/Fitbit Alta HR) through a prospective observational monocentric study, in adult patients referred for polysomnography (PSG). We compared the total sleep time (TST), REM time, REM latency, nonREM1 + 2 time, nonREM3 time, and wake after sleep onset (WASO). We report absolute and relative errors, Bland-Altman representations, and a contingency table of times spent in sleep stages with respect to PSG. Sixty-five patients were included (final sample size 58 for Withings and 52 for Fitbit). Both devices gave a relatively accurate sleep start time with a median absolute error of 5 (IQR -43; 27) min for Withings and -2.0 (-12.5; 4.2) min for Fitbit but both overestimated TST. Withings tended to underestimate WASO with a median absolute error of -25.0 (-61.5; -8.5) min, while Fitbit tended to overestimate it (median absolute error 10 (-18; 43) min. Withings underestimated light sleep and overestimated deep sleep, while Fitbit overestimated light and REM sleep and underestimated deep sleep. The overall kappas for concordance of each epoch between PSG and devices were low: 0.12 (95%CI 0.117-0.121) for Withings and VPSG indications 0.07 (95%CI 0.067-0.071) for Fitbit, as well as kappas for each VPSG indication 0.07 (95%CI 0.067-0.071). Thus, commercially available sleep trackers are not reliable for sleep architecture in patients with sleep complaints/pathologies and should not replace actigraphy and/or PSG.

NKX2.1 (TTF1) germline mutation associated with pulmonary fibrosis and lung cancer.

Germline surfactant-associated genes mutations are associated with ILD and increased risk of lung cancer https://bit.ly/3CkkXgD.

Anti-parietal cell autoimmunity is associated with an accelerated decline of lung function in IPF patients.

BACKGROUND: Autoantibodies against lung epithelial antigens are often detected in patients with Idiopathic Pulmonary Fibrosis (IPF). Anti-Parietal Cell Antibodies (APCA) target the H+/K+ATPase (proton pump). APCA prevalence and lung H+/K+ATPase expression was never studied in IPF patients. METHODS: We retrospectively collected clinical, lung function and imaging data from APCA positive patients (APCA+IPF) and compared them with APCA negative IPF patients matched on the date of diagnostic assessment. H+/K+ATPase expression was assessed with immunohistochemistry and PCR. RESULTS: Among 138 IPF patients diagnosed between 2007 and 2014 and tested for APCA, 19 (13.7%) APCA+ patients were identified. APCA+IPF patients were 16 men and 3 women, mean age 71 years. The median titer of APCA was 1:160. A pernicious anemia was present in 5 patients and preceded the fibrosis in 3 cases. With a mean follow up of 31 months, 2 patients had an exacerbation and 7 patients died. As compared with 19 APCA- IPF patients, APCA+IPF patients had a less severe disease with better DLCO (57% vs 43% predicted), preserved PaO2 (85 ± 8 mmHg vs 74 ± 11 mmHg), a lower rate of honeycombing on HRCT (58% vs 89%), but they experienced an accelerated decline of FVC (difference 61.4 ml/year; p = .0002). The H+/K+ATPase was strongly expressed by hyperplastic alveolar epithelial cells in the fibrotic lung. CONCLUSION: Anti-parietal cell autoimmunity is detected in some IPF patients and is associated with an accelerated decline of lung function. Anti-parietal cell autoimmunity may promote lung fibrosis progression.

Dysfunctional lung anatomy and small airways degeneration in COPD.

Chronic obstructive pulmonary disease (COPD) is characterized by incompletely reversible airflow obstruction. Direct measurement of airways resistance using invasive techniques has revealed that the site of obstruction is located in the small conducting airways, ie, bronchioles with a diameter < 2 mm. Anatomical changes in these airways include structural abnormalities of the conducting airways (eg, peribronchiolar fibrosis, mucus plugging) and loss of alveolar attachments due to emphysema, which result in destabilization of these airways related to reduced elastic recoil. The relative contribution of structural abnormalities in small conducting airways and emphysema has been a matter of much debate. The present article reviews anatomical changes and inflammatory mechanisms in small conducting airways and in the adjacent lung parenchyma, with a special focus on recent anatomical and imaging data suggesting that the initial event takes place in the small conducting airways and results in a dramatic reduction in the number of airways, together with a reduction in the cross-sectional area of remaining airways. Implications of these findings for the development of novel therapies are briefly discussed.