Impact of mental health and personality traits on the incidence of chronic cough in the Canadian Longitudinal Study on Aging

BACKGROUND: Chronic cough is a common troublesome condition, but risk factors for developing chronic cough are poorly understood. The aim of this study was to understand the relationship between mental health disorders, personality traits and chronic cough. METHODS: The Canadian Longitudinal Study on Aging is a prospective, nationally generalisable, random sample of adults aged 45–85 years at baseline recruited between 2011 and 2015, and followed-up 3 years later. Chronic cough was defined as a daily cough over the last 12 months. Incident chronic cough was defined as those participants who reported new-onset chronic cough between baseline and follow-up 1. Current depressive symptoms and psychological distress were assessed using the Center for Epidemiologic Study Short Depression Scale (CESD-10) and Kessler Psychological Distress Scale (K-10), respectively. The “Big Five” personality traits were assessed using the Ten-Item Personality Inventory. Relative risks are reported using a multivariate mutually adjusted model. RESULTS: At follow-up 1, 2506 participants (11.1%) reported new-onset chronic cough during the ∼3-year interval. Depressive symptoms (CESD-10 ≥10: relative risk 1.22 (95% CI 1.03–1.44)) and psychological distress (K-10 ≥22: relative risk 1.20 (95% CI 1.07–1.36)) at baseline were both independent predictors of a higher risk of incident chronic cough. Prevalent and incident chronic cough were also independently associated with an increased risk of developing depressive symptoms and psychological distress. Personality traits did not influence the development of chronic cough but did increase the risk of depressive symptoms and psychological distress. CONCLUSIONS: This study shows that there is a bidirectional relationship between chronic cough, and depressive symptoms and psychological distress, and personality traits do not independently influence the development of chronic cough

Language and geographical location influence the incidence of chronic cough in the Canadian Longitudinal Study on Aging

French speakers have a 4% lower incidence of chronic cough than English speakers in the CLSA, but English speakers from Quebec, Newfoundland and Labrador, and Nova Scotia also have a lower risk of developing chronic cough https://bit.ly/3qAd3M

Exercise testing in the assessment of impairment/disability

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Contribution of Respiratory Muscle Oxygen Consumption to Breathing Limitation and Cyspnea

During exercise, the sustainable activity of large muscle groups is limited by oxygen delivery. The purpose of this study was to see whether the oxygen consumption of the respiratory muscles reaches a similar critical value under maximal resistive loading and hyperventilation. A secondary objective was to see whether dyspnea (estimated discomfort experienced with breathing using the Borg 0-10 scale) and the oxygen consumption of the respiratory muscles are closely related across conditions. This would be expected if intramuscular sensory nerve fibres stimulated as a consequence of metabolic events contributed to this sensation. In six normal subjects the respiratory muscles were progressively activated by the addition of incremental inspiratory resistive loads to a maximum of 300 cm H20×s/L (SD=66.4), and incremental dead space to a maximum of 2638 mL (SD=452), associated with an increase in ventilation to 75.1 L/min (SD=29.79). Each increment was maintained for 5 mins to allow the measurement of oxygen uptake in a steady state. During resistive loading total oxygen consumption increased from 239 mL/min (SD=38.2) to 299 mL/min (SD=52.3) and dyspnea increased to "very severe" (Borg scale 7.5, SD=1.55). During dead space loading total oxygen consumption increased from 270 mL/min (SD=20.2) to 426 mL/min (SD=81.9) and dyspnea increased to "very severe" (7.1, SD=0.66). Oxygen cost of inspiratory muscle power was 25 mL/watt (95% confidence limits 16.7 to 34.3) with dead space loading and 91 mL/watt (95% confidence limits 54 to 128) with resistive loading. Oxygen consumption did not reach a critical common value in the two types of loading, 60 mL/min (SD 22.3) during maximal resistive loading and 156 mL/min (SD 82.4) during maximal dead space loading (P<0.05). Physiological factors limiting the respiratory muscles are not uniquely related to oxygen consumption and appear to be expressed through the activation of sensory structures, perceptually manifested as dyspnea

Effects of cigarette smoke exposure on pulmonary physiology, muscle strength and exercise capacity in a retrospective cohort with 30,000 subjects.

BACKGROUND: The effects of long-term cigarette smoke exposure on pulmonary physiology and how those effects lead to reduced exercise capacity are not well established. METHODS: We retrospectively analyzed the spirometry, single-breath gas transfer (DLCO), peripheral muscle strength, and maximum exercise capacity data in patients referred to McMaster University Medical Centre for cardiopulmonary exercise testing between 2000 and 2012. RESULTS: 29,441 subjects underwent CPET and had a recorded smoking history [58% male, mean age 51.1 years (S.D.±19.6), BMI 27.4 kg/m2(±5.8)]. 7081 (24%) were current or former smokers and were divided into 4 categories by packs years (mean ±S.D.): 40 (53.9±12.8). Patients with greater cigarette smoke exposure had lower expiratory flow rates (FEV1, FEF50, FEF75, PEFR), DLCO, and maximum power output (MPO) during exercise. There was no association between smoke exposure and muscle strength. Modeling MPO (kpm/min) output as a function of demographic and physiologic variables showed that the data are well explained by muscle strength (kg), FEV1 (L), and DLCO (mmHg/min/mL) in similar magnitude (MPO = 42.7*Quads0.34*FEV10.34 * DLCO0.43; r = 0.84). CONCLUSIONS: Long-term cigarette smoke exposure is associated with small airway narrowing and impaired diffusion capacity but not with peripheral muscle weakness. The effects of smoking, age, and gender on maximum power output are mediated by reductions in FEV1, muscle strength and DLCO. Exercise capacity in smokers may benefit from therapies targeting all 3 variables

Prevalence and contribution of respiratory viruses in the community to rates of emergency department visits and hospitalizations with respiratory tract infections, chronic obstructive pulmonary disease and asthma

BACKGROUND: The individual and combined contribution of viral prevalence in the community to Emergency Department (ED) visits and hospitalizations with respiratory tract infections (RTIs), chronic obstructive pulmonary disease (COPD) and asthma is unclear. METHODS: A retrospective analysis on daily viral positive tests and daily ED visits and hospitalizations between 01/01/2003 to 31/12/2013 in Ontario, Canada. Viral data was collected from the Centre for Immunization and Respiratory Infectious Diseases (CIRID). The Canadian Institute for Health Information reports daily ED visits and hospitalizations for RTIs, COPD and asthma as a primary diagnosis. RESULTS: There were 4,365,578 ED visits with RTIs of which 321,719 (7.4%) were admitted to hospital; 817,141 ED visits for COPD of which 260,665 (31.9%) were admitted and 649,666 ED visits with asthma of which 68,626 (10.6%) were admitted. The percentage of positive tests to influenza A and B, respiratory syncytial virus (RSV), parainfluenza and adenovirus prevalence explained 57.4% of ED visits and 63.8% of hospitalizations for RTI, 41.4% of ED visits and 39.2% of hospitalizations with COPD but only 1.5% of ED visits and 2.7% of hospitalizations for asthma. The further addition of human metapneumovirus, rhinovirus and coronavirus over the final 3 years accounted for 66.7% of ED visits and 74.4% of hospitalizations for RTI, 52.5% of visits and 48.2% of hospitalizations for COPD, and only 13.3% of visits and 10.4% of hospitalizations for asthma. CONCLUSIONS: Community respiratory viral epidemics are major drivers of ED visits and hospitalizations with RTIs and COPD but only a modest contributor to asthma