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We executed the presented retrospective cohort study with the purpose of probing the risk of severe acute respiratory infection (SARI) following influenza in patients with sleep apnea.
We executed this real-world study by gathering Taiwan National Health Insurance Research Database (NHIRD) data. From a database containing 1 million individuals sampled at random from the NHIRD, we identified all patients aged 20 years or older with a sleep apnea diagnosis between 1997 and 2013 as the study group. We established a comparison cohort of individuals without sleep apnea by randomly matching patients with respect to monthly income, gender, urbanization level, and age at a 14 ratio. Follow-up was performed until death or the end of 2015 for both groups. We determined the study outcome to be the occurrence of influenza-associated SARI.
We enrolled 6508 and 26,032 patients into the study and comparison groups, respectively. A significantly higher cumulative incidence of influenza-associated SARI was discovered in the study group (
< 0.001). In our multivariate analysis, sleep apnea, chronic obstructive pulmonary disease, and coronary artery disease were independent risk factors for influenza-associated SARI. The hazard ratio of sleep apnea for influenza-associated SARI was 1.98 (95% CI 1.26-3.10) after adjustment for all comorbidities, gender, age, monthly income, and urbanization level.
Sleep apnea increased the risk of influenza-associated SARI. We suggest that physicians be cautious about the development of severe influenza illness in patients with sleep apnea. Vaccination and early oseltamivir administration should be actively considered in this group of patients.
Sleep apnea increased the risk of influenza-associated SARI. We suggest that physicians be cautious about the development of severe influenza illness in patients with sleep apnea. Vaccination and early oseltamivir administration should be actively considered in this group of patients.
We hypothesize the association between sleep duration and cardiovascular disease (CVD) risk varies with age category; however, evidence for the relationship between sleep duration and CVD risk among young and middle-aged adults remains scarce. This research aims to assess the association between night sleep duration and cardiovascular risk by sex among young and middle-aged Chinese adults.
We used the baseline data of a cohort of adults for physical examination by stratified cluster sampling. The Framingham risk score and the Pittsburgh Sleep Quality Index were used to measure CVD risk and sleep duration, respectively. Demographic characteristics, lifestyle factors, height, weight, total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C) were collected. We performed multiple logistic regressions to examine the association between night sleep duration and the predicted cardiovascular risk.
We included 27,547 participants aged 18-64 years free of CVD, cerebral stroke, and not taking lipid-lowering agents. Overall, 12.7%, and 20.4% were at medium and high predicted CVD risk, respectively; 11.9% and 12.3% reported short and long sleep, respectively. Short sleep was independently associated with 23% (95% CI 1.08-1.40) increased odds of medium-to-high CVD risk and 26% (95% CI 1.11-1.45) increased odds of high CVD risk among females. Whereas long sleep was independently associated with 17% (95% CI 0.71-0.98) decreased odds of medium-to-high CVD risk among males.
Among young and middle-aged adults, long sleep was associated with decreased odds of CVD risk in males, whereas short sleep was associated with increased odds of cardiovascular risk in females.
Among young and middle-aged adults, long sleep was associated with decreased odds of CVD risk in males, whereas short sleep was associated with increased odds of cardiovascular risk in females.
Pulmonary arterial hypertension (PAH) is a rare disease characterised by limited survival despite remarkable improvements in therapy. The causes, clinical burden and outcomes of patients admitted to the intensive care unit (ICU) remain poorly characterised. The aim of this study was to describe patient characteristics, causes of ICU hospitalisation, and risk factors for ICU and 1-year mortality.
Data from patients enrolled in the Johns Hopkins Pulmonary Hypertension Registry were analysed for the period between January 2010 and December 2020. Clinical, functional, haemodynamic and laboratory data were collected.
102 adult patients with 155 consecutive ICU hospitalisations were included. The leading causes for admission were right heart failure (RHF, 53.3%), infection (17.4%) and arrhythmia (11.0%). ICU mortality was 27.1%. Mortality risk factors included Na <136 mEq·mL
(OR 3.10, 95% CI 1.41-6.82), elevated pro-B-type natriuretic peptide (proBNP) (OR 1.75, 95% CI 1.03-2.98), hyperbilirubinaemia (OR 1.40, 95% CI 1.09-1.80), hyperlactaemia (OR 1.42, 95% CI 1.05-1.93), and need for vasopressors/inotropes (OR 5.29, 95% CI 2.28-12.28), mechanical ventilation (OR 3.76, 95% CI 1.63-8.76) and renal replacement therapy (OR 5.57, 95% CI 1.25-24.76). Mortality rates at 3, 6 and 12 months were 17.5%, 27.6% and 39.0%, respectively. Connective tissue disease-associated PAH has lower 1-year survival compared to idiopathic PAH (51.4%
79.8%, log-rank test p=0.019).
RHF is the most common cause for ICU admission. In-hospital and 1-year mortality remain exceedingly high despite improved ICU care. Recognising specific risk factors on admission can help identifying patients at risk for poor outcomes.
RHF is the most common cause for ICU admission. In-hospital and 1-year mortality remain exceedingly high despite improved ICU care. Recognising specific risk factors on admission can help identifying patients at risk for poor outcomes.Single nucleotide polymorphisms (SNPs) in various genes have been shown to associate with COPD, suggesting a role in disease pathogenesis. Sulfatase modifying factor (SUMF1) is a key modifier in connective tissue remodelling, and we have shown previously that several SNPs in SUMF1 are associated with COPD. The aim of this study was to investigate the association between SUMF1 SNPs and advanced lung function characteristics. Never-, former and current smokers with (n=154) or without (n=405) COPD were genotyped for 21 SNPs in SUMF1 and underwent spirometry, body plethysmography, diffusing capacity of the lung for carbon monoxide (D LCO) measurement and impulse oscillometry. C1632 in vivo Four SNPs (rs793391, rs12634248, rs2819590 and rs304092) showed a significantly decreased odds ratio of having COPD when heterozygous for the variance allele, together with a lower forced expiratory volume in 1 s (FEV1) and FEV1/forced vital capacity (FVC) ratio and an impaired peripheral resistance and reactance. Moreover, individuals homozygous for the variance allele of rs3864051 exhibited a strong association to COPD, a lower FEV1/FVC, FEV1 and D LCO, and an impaired peripheral resistance and reactance. Other SNPs (rs4685744, rs2819562, rs2819561 and rs11915920) were instead associated with impaired lung volumes and exhibited a lower FVC, total lung capacity and alveolar volume, in individuals having the variance allele. Several SNPs in the SUMF1 gene are shown to be associated with COPD and impaired lung function. These genetic variants of SUMF1 may cause a deficient sulfation balance in the extracellular matrix of the lung tissue, thereby contributing to the development of COPD.
What is the impact of the duration of cough monitoring on its accuracy in detecting changes in the cough frequency?
This is a statistical analysis of a prospective cohort study. Participants were recruited in the city of Pamplona (Northern Spain), and their cough frequency was passively monitored using smartphone-based acoustic artificial intelligence software. Differences in cough frequency were compared using a one-tailed Mann-Whitney U test and a randomisation routine to simulate 24-h monitoring.
616 participants were monitored for an aggregated duration of over 9 person-years and registered 62 325 coughs. This empiric analysis found that an individual's cough patterns are stochastic, following a binomial distribution. When compared to continuous monitoring, limiting observation to 24 h can lead to inaccurate estimates of change in cough frequency, particularly in persons with low or small changes in rate.
Detecting changes in an individual's rate of coughing is complicated by significant stochastic variability within and between days. Assessing change based solely on intermittent sampling, including 24-h, can be misleading. This is particularly problematic in detecting small changes in individuals who have a low rate and/or high variance in cough pattern.
Detecting changes in an individual's rate of coughing is complicated by significant stochastic variability within and between days. Assessing change based solely on intermittent sampling, including 24-h, can be misleading. This is particularly problematic in detecting small changes in individuals who have a low rate and/or high variance in cough pattern.Vitamin D supplementation at the current UK recommended level (400 IU·day-1) or enhanced supplementation (1000 IU·day-1) failed to achieve adequate levels of vitamin D (>75 nmol·L-1) in vitamin-D-insufficient children with acute wheeze https//bit.ly/3J43Ouo.
The success of pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH) is usually evaluated by performing a right heart catheterisation (RHC). Here, we investigate whether residual pulmonary hypertension (PH) can be sufficiently excluded without the need for a RHC, by making use of early post-operative haemodynamics, or N-terminal pro-brain natriuretic peptide (NT-proBNP), cardiopulmonary exercise testing (CPET) and transthoracic echocardiography (TTE) 6 months after PEA.
In an observational analysis, residual PH after PEA measured by RHC was related to haemodynamic data from the post-operative intensive care unit time and data from a 6-month follow-up assessment including NT-proBNP, TTE and CPET. After dichotomisation and univariate analysis, sensitivity, specificity, positive predictive value, negative predictive value (NPV) and likelihood ratios were calculated.
Thirty-six out of 92 included patients had residual PH 6 months after PEA (39%). Correlation between early post-operative and 6-month follow-up mean pulmonary artery pressure was moderate (Spearman rho 0.465, p<0.001). Early haemodynamics did not predict late success. NT-proBNP >300 ng·L
had insufficient NPV (0.71) to exclude residual PH. Probability for PH on TTE had a moderate NPV (0.74) for residual PH. Peak oxygen consumption (
'
) <80% predicted had the highest sensitivity (0.85) and NPV (0.84) for residual PH.
CPET 6 months after PEA, and to a lesser extent TTE, can be used to exclude residual CTEPH, thereby safely reducing the number of patients needing to undergo re-RHC after PEA.
CPET 6 months after PEA, and to a lesser extent TTE, can be used to exclude residual CTEPH, thereby safely reducing the number of patients needing to undergo re-RHC after PEA.
Pulmonary hypertension (PH) in patients with chronic lung disease (CLD) predicts reduced functional status, clinical worsening and increased mortality, with patients with severe PH-CLD (≥35 mmHg) having a significantly worse prognosis than mild to moderate PH-CLD (21-34 mmHg). The aim of this cross-sectional study was to assess the association between computed tomography (CT)-derived quantitative pulmonary vessel volume, PH severity and disease aetiology in CLD.
Treatment-naïve patients with CLD who underwent CT pulmonary angiography, lung function testing and right heart catheterisation were identified from the ASPIRE registry between October 2012 and July 2018. Quantitative assessments of total pulmonary vessel and small pulmonary vessel volume were performed.
90 patients had PH-CLD including 44 associated with COPD/emphysema and 46 with interstitial lung disease (ILD). Patients with severe PH-CLD (n=40) had lower small pulmonary vessel volume compared to patients with mild to moderate PH-CLD (n=50). Patients with PH-ILD had significantly reduced small pulmonary blood vessel volume, compared to PH-COPD/emphysema.
