Left ventricular volume and wall stress are linked to lung function impairment in COPD

Cardiovascular comorbidities are common in chronic obstructive pulmonary disease (COPD). We examined the association between airflow limitation, hyperinflation and the left ventricle (LV).

Patients from the COPD cohort COSYCONET underwent evaluations including forced expiratory volume in 1 s (FEV₁), forced vital capacity (FVC), effective airway resistance (R_eff), 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".

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".

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.