TY - JOUR
T1 - Left ventricular volume and wall stress are linked to lung function impairment in COPD
AU - Alter, Peter
AU - Jorres, Rudolf A.
AU - Watz, Henrik
AU - Welte, Tobias
AU - Glaser, Sven
AU - Schulz, Holger
AU - Bals, Robert
AU - Karch, Annika
AU - Wouters, Emiel F. M.
AU - Vestbo, Jorgen
AU - Young, David
AU - Vogelmeier, Claus F.
PY - 2018/6/15
Y1 - 2018/6/15
N2 - Background: Cardiovascular comorbidities are common in chronic obstructive pulmonary disease (COPD). We examined the association between airflow limitation, hyperinflation and the left ventricle (LV). Methods: Patients from the COPD cohort COSYCONET underwent evaluations including forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), effective airway resistance (Reff), intrathoracic gas volume (ITGV), and echocardiographic LV end-diastolic volume (LVEDV), stroke volume (LVSV), end-systolic volume (LVESV), and end-diastolic and end-systolic LV wall stress. Data from Visit 1 (baseline) and Visit 3 (18 months later) were used. In addition to comparisons of both visits, multivariate regression analysis was conducted, followed by structural equation modelling (SEM) with latent variables "Lung' and "Left heart. Results: A total of 641 participants were included in this analysis. From Visit 1 to Visit 3, there were significant declines in FEV1 and FEV1/FVC, and increases in R-eff, ITGV and LV end-diastolic wall stress, and a borderline significant decrease in LV mass. There were significant correlations of: FEV1 predicted with LVEDV and LVSV; R-eff (with LVSV; and ITGV with LV mass and LV end-diastolic wall stress. The SEM fitted the data of both visits well (comparative fit index: 0.978, 0.962), with strong correlation between "Lung" and "Left heart". Conclusions: We demonstrated a relationship between lung function impairment and LV wall stress in patients with COPD. This supports the hypothesis that LV impairment in COPD could be initiated or promoted, at least partly, by mechanical factors exerted by the lung disorder. (C) 2018 Elsevier B.V. All rights reserved.
AB - Background: Cardiovascular comorbidities are common in chronic obstructive pulmonary disease (COPD). We examined the association between airflow limitation, hyperinflation and the left ventricle (LV). Methods: Patients from the COPD cohort COSYCONET underwent evaluations including forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), effective airway resistance (Reff), intrathoracic gas volume (ITGV), and echocardiographic LV end-diastolic volume (LVEDV), stroke volume (LVSV), end-systolic volume (LVESV), and end-diastolic and end-systolic LV wall stress. Data from Visit 1 (baseline) and Visit 3 (18 months later) were used. In addition to comparisons of both visits, multivariate regression analysis was conducted, followed by structural equation modelling (SEM) with latent variables "Lung' and "Left heart. Results: A total of 641 participants were included in this analysis. From Visit 1 to Visit 3, there were significant declines in FEV1 and FEV1/FVC, and increases in R-eff, ITGV and LV end-diastolic wall stress, and a borderline significant decrease in LV mass. There were significant correlations of: FEV1 predicted with LVEDV and LVSV; R-eff (with LVSV; and ITGV with LV mass and LV end-diastolic wall stress. The SEM fitted the data of both visits well (comparative fit index: 0.978, 0.962), with strong correlation between "Lung" and "Left heart". Conclusions: We demonstrated a relationship between lung function impairment and LV wall stress in patients with COPD. This supports the hypothesis that LV impairment in COPD could be initiated or promoted, at least partly, by mechanical factors exerted by the lung disorder. (C) 2018 Elsevier B.V. All rights reserved.
KW - COPD
KW - Airflow limitation
KW - Hyperinflation
KW - Heart failure
KW - Ventricular wall stress
KW - Dyspnea
KW - Breathing
KW - OBSTRUCTIVE PULMONARY-DISEASE
KW - HEART-FAILURE
KW - MYOCARDIAL-INFARCTION
KW - RESPIRATORY SOCIETY
KW - TRIAL
KW - RISK
KW - STANDARDIZATION
KW - HYPERTROPHY
KW - DYSFUNCTION
KW - TIOTROPIUM
U2 - 10.1016/j.ijcard.2018.02.074
DO - 10.1016/j.ijcard.2018.02.074
M3 - Article
C2 - 29657040
SN - 0167-5273
VL - 261
SP - 172
EP - 178
JO - International Journal of Cardiology
JF - International Journal of Cardiology
ER -