CT-measured lung air-trapping is associated with higher carotid artery stiffness in individuals with chronic obstructive pulmonary disease

Abstract

Early stages of chronic obstructive pulmonary disease (COPD) are characterized by the loss and narrowing of terminal bronchioles in the lung, resulting in “air-trapping,” often occurring before overt emphysema manifests. Individuals with an airway-predominant phenotype of COPD display extensive lung air-trapping and are at greater cardiovascular disease (CVD) risk than COPD patients with an emphysema-predominant phenotype. We hypothesized that the degree of computed tomography (CT)-quantified lung air-trapping would be associated with greater aortic and carotid artery stiffness and lower endothelial function, known biomarkers of CVD risk. Lung air-trapping was associated with greater aortic stiffness (carotid femoral pulse wave velocity, CFPWV) ( r = 0.60, P = 0.007) and carotid β-stiffness ( r = 0.75, P = 0.0001) among adults with ( n = 10) and without ( n = 9) a clinical diagnosis of COPD and remained significant after adjusting for blood pressure (BP) and smoking history (pack-years) (carotid β-stiffness: r = 0.68, P < 0.01; CFPWV r = 0.53, P = 0.03). The association between lung air-trapping and carotid β-stiffness remained significant after additionally adjusting for age and forced expiratory volume 1(FEV1) ( r = 0.64, P = 0.01). In the COPD group only ( n = 10), lung air-trapping remained associated with carotid β-stiffness ( r = 0.82, P = 0.05) after adjustment for age, pack-years, and FEV1. In contrast, no association was observed between CFPWV and lung air-trapping after adjustment for BP, pack-years, age, and FEV1 ( r = 0.12, P = 0.83). Lung air-trapping was not associated with endothelial function (brachial artery flow-mediated dilation) in the entire cohort ( P = 0.80) or in patients with COPD only ( P = 0.71). These data suggest that carotid artery stiffness may be a mechanism explaining the link between airway-predominant phenotypes of COPD and high CVD risk. NEW & NOTEWORTHY Previous cross-sectional studies have demonstrated greater large elastic artery stiffness and lower endothelium-dependent dilation in chronic obstructive pulmonary disease (COPD) patients compared with controls. Furthermore, COPD patients with emphysema have greater aortic stiffness than non-COPD controls, and the degree of stiffness is associated with emphysema severity. The present study is the first to demonstrate that even before overt emphysema manifests, lung air-trapping is associated with carotid artery stiffness in COPD patients independent of blood pressure, age, or smoking history.

The Role of Oxidative Stress and Antioxidants in Cardiovascular Comorbidities in COPD

“…Numerous studies have found that PWV is abnormally high in COPD patients [ 58 , 59 ]. Arterial stiffness, as measured by PWV, was independently associated with the severity of emphysema [ 60 ] and airway obstruction [ 59 , 61 , 62 , 63 , 64 ]. Furthermore, it was established by studying twins that the link between lung function and arterial stiffness is not genetically determined.…”

Karma of Cardiovascular Disease Risk Factors for Prevention and Management of Major Cardiovascular Events in the Context of Acute Exacerbations of Chronic Obstructive Pulmonary Disease

“…The exact mechanism by which COPD enhances risk of MACEs is not completely clear, but could be explained by airway and systemic inflammation resulting in over spilling of inflammatory cytokines in circulation leading to atherosclerosis. Also, COPD patients frequently demonstrate myocardial inflammation, arterial stiffness and endothelial dysfunction, intensified during acute exacerbations, possibly owing to “blood” inflammation and elastin degradation (5–7). Moreover, patients with COPD experience dynamic (and even static) hyperinflation, which may increase end diastolic pressures in the heart, and impair both right and left ventricular contractility that can further increase CV risk (8).…”