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Published on: June 12, 2019
High risk of subclinical atherosclerosis in COPD exacerbator phenotype
Adolfo Domenech1, Ana Muñoz-Montiel2, Natalia García-Casares3
1Pulmonology Service, Regional University Hospital of Malaga, Malaga, Spain.
Insights
COPD exacerbations significantly increase the risk of subclinical atherosclerosis, particularly in younger patients. Intensifying vascular risk factor control is crucial for exacerbator phenotypes.
Area of Science:
- Cardiology
- Pulmonology
- Vascular Medicine
Background:
- Chronic Obstructive Pulmonary Disease (COPD) is linked to increased vascular risk.
- The specific contribution of COPD exacerbations to this vascular risk remains unclear.
Purpose of the Study:
- To prospectively evaluate the association between COPD exacerbator phenotypes and subclinical atherosclerosis.
- To determine if exacerbations independently predict vascular risk.
Main Methods:
- 127 COPD patients underwent assessment including blood tests, lung function tests, cardiovascular risk scores, and EcoDoppler.
- Carotid intima-media thickness (c-IMT) and ankle-brachial index (ABI) were measured.
- Patients were classified as exacerbators or non-exacerbators based on exacerbation history.
Main Results:
- The exacerbator phenotype was independently associated with increased c-IMT (OR ~3), irrespective of COPD severity or global cardiovascular risk.
- This association was more pronounced in patients younger than 65.
- No significant difference in ABI was noted between groups.
Conclusions:
- Subclinical atherosclerosis, indicated by high c-IMT, is independently linked to the COPD exacerbator phenotype.
- Younger patients with exacerbator phenotypes show a more significant increase in c-IMT.
- Intensified management of vascular risk factors is recommended for COPD patients with frequent exacerbations.
Abstract:
It is not known whether COPD exacerbations contribute to an increased vascular risk already associated with the disease. For this reason, we prospectively evaluated 127 patients referred for a monographic COPD consultation. We classify as exacerbators those who had experienced two or more moderate exacerbations in the previous year, or who had had a hospital admission. All underwent a blood analysis, respiratory function tests, global cardiovascular and coronary risk estimates (with four of the most frequently used scores, and the Chronic Obstructive Pulmonary Disease Coronaropathy Risk (COPDCoRi) score, respectively); and an EcoDoppler to measure carotid intima-media thickness and the ankle-brachial index. Finally, we included 50 patients with exacerbator phenotypes and 57 with non-exacerbator phenotypes, ranging from 63 ± 7 years old, 74% of whom were male. The exacerbator phenotype increased the risk of carotid intima-media thickness above the 75th percentile range by a factor of almost three, independently of the severity of COPD and global cardiovascular risk. The association between the exacerbator phenotype and high c-IMT was more evident in patients under 65. In conclusion, the presence of subclinical atherosclerosis is independently associated with the exacerbator phenotype, with more pronounced differences in younger patient; which suggests that we should intensify control of vascular risk factors in these groups of patients.
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