# Subclinical Carotid Atherosclerosis Is Present from Early COPD Stages, Being in a Close Relationship with Systemic Inflammation

## TL;DR

This study shows that early stages of COPD are linked to carotid atherosclerosis, which is closely tied to systemic inflammation.

## Contribution

The study reveals that subclinical atherosclerosis is present early in COPD and is strongly associated with inflammatory biomarkers.

## Key findings

- Carotid intima–media thickness increases with COPD severity, especially in early stages.
- Inflammatory biomarkers are significantly associated with higher carotid wall thickness.
- Patients with two positive inflammatory markers show worse outcomes in age, exercise tolerance, and symptoms.

## Abstract

Background: Several cohort studies have demonstrated a link between subclinical carotid atherosclerosis and obstructive chronic airflow limitation. These conditions exhibit common risk factors associated with unhealthy lifestyles, as well as analogous pathophysiological mechanisms, including chronic low-degree systemic inflammation. Purpose: The aim of this study was to investigate the association between airflow obstruction and carotid intima–media thickness (c-IMT), together with the influence of inflammatory biomarkers on this relationship, in patients diagnosed with chronic obstructive pulmonary disease (COPD). Methods and Patients: This study is cross-sectional and includes 106 patients with stable COPD. All patients underwent evaluation through spirometry, carotid ultrasound, and assessment of inflammatory biomarkers, including C-reactive protein, fibrinogen, and erythrocyte sedimentation rate. The relationship between carotid subclinical atherosclerosis and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage of COPD was assessed. Additionally, we compared patients with two positive biomarkers of inflammation with those who had no positive inflammatory biomarkers. Results: Significant statistical differences were observed in carotid intima–media thickness values associated with the severity of airflow obstruction, with measurements of 1.03 mm in COPD stage 1–2 GOLD, 1.07 mm in COPD GOLD 3, and 0.96 mm in GOLD 4 (p = 0.04). However, no direct correlation with forced expiratory volume in the first second (FEV1) was identified. The post hoc analysis revealed a notable increase in carotid wall thickness for the early stages of COPD. C-IMT demonstrated a significant association with inflammation parameters, muscle dysfunction, body composition, and lipid profile. The comparison of groups exhibiting two positive inflammatory biomarkers with those with no positive inflammatory markers revealed significant differences in age, c-IMT, exercise tolerance, and COPD symptoms. Conclusions: Subclinical carotid atherosclerosis is evident from the early stages of obstructive airflow limitation. Carotid intima–media thickness is significantly higher in patients with positive inflammatory biomarkers.