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Published on: February 16, 2016
Atherosclerotic calcification in major vessel beds in chronic obstructive pulmonary disease: The Rotterdam Study
Lies Lahousse1, Daniel Bos2, Sara R A Wijnant3
1Department of Bioanalysis, Ghent University, Ghent, Belgium; Department of Epidemiology, Erasmus MC, Rotterdam, the Netherlands.
Insights
Chronic obstructive pulmonary disease (COPD) is linked to atherosclerosis, particularly in extracranial carotid arteries. This study found COPD is associated with increased calcification in multiple arteries, suggesting a role in systemic atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Pulmonology
- Epidemiology
Background:
- Chronic obstructive pulmonary disease (COPD) is a known risk factor for cardiovascular disease.
- The specific impact of COPD on atherosclerosis in different arterial locations, including intracranial arteries, remains unclear.
- Understanding these relationships is crucial for managing cardiovascular risks in COPD patients.
Purpose of the Study:
- To investigate the association between COPD and atherosclerosis in various major arteries.
- To determine if COPD influences the presence and volume of calcification in coronary, aortic, extracranial carotid, and intracranial carotid arteries.
Main Methods:
- A population-based cohort study of 2187 elderly participants from the Rotterdam Study.
- Computed tomography was used to quantify calcification in coronary arteries (CAC), aortic arch (AAC), extracranial carotid arteries (ECAC), and intracranial carotid arteries (ICAC).
- Logistic and linear regression analyses were performed to assess the association of COPD (defined by FEV1/FVC < 70%) with calcification presence and volume, adjusting for age and smoking.
Main Results:
- Prevalence of CAC, AAC, and ECAC was significantly higher in individuals with COPD.
- COPD remained significantly associated with the presence of ECAC (OR 1.46) after adjusting for age and smoking.
- COPD was associated with larger calcification volumes across all four assessed arterial beds in individuals with existing calcification.
Conclusions:
- COPD is implicated in the initiation of atherosclerosis in the extracranial carotid arteries.
- The findings suggest COPD contributes to the aggravation of systemic atherosclerosis.
- Further research into the mechanisms linking COPD and cardiovascular atherosclerosis is warranted.
Background And Aims:
COPD is associated with an increased risk of cardiovascular morbidity and mortality, potentially by mechanisms of atherosclerosis. Insight into location-specific vulnerability to atherosclerosis in COPD, including intracranial arteries, is lacking. We aimed to investigate the relation between COPD and atherosclerosis in multiple vessel beds within a large population-based cohort study.
Methods:
From 2003 to 2006, a random sample of 2187 elderly participants (mean age, 69.6 ± 6.8 years; 50.9% female; 11.7% COPD) from the population-based Rotterdam Study underwent computed tomography to quantify atherosclerotic coronary artery calcification (CAC), aortic arch calcification (AAC), extracranial carotid artery calcification (ECAC), and intracranial carotid artery calcification (ICAC). We investigated the association of COPD [ratio of forced expiratory volume in the first second to forced vital capacity (FEV1/FVC) < 70%] with the presence of calcification and with calcification volumes in each vessel bed using logistic and linear regression, with adjustments for cardiovascular risk factors including smoking.
Results:
The prevalence of CAC, AAC and ECAC was significantly higher in subjects with COPD compared to those without. After adjusting for age and smoking, COPD remained associated with the presence of ECAC (odds ratio 1.46 [95% confidence interval, 1.02-2.07, p = 0.037]). COPD was significantly associated with larger calcification volumes in all four vessel beds in people in whom calcification was present.
Conclusions:
The results of this study suggest that COPD plays a role in extracranial carotid artery atherosclerosis initiation and systemic atherosclerosis aggravation.

