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Subclinical Carotid Atherosclerosis in COPD Cases and Control Smokers: Analysis in Relation with COPD Exacerbations and Exacerbation-like Episodes

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Abstract

Purpose

It remains unclear whether there is a pathogenic link between chronic obstructive pulmonary disease (COPD) and cardiovascular diseases. Subclinical carotid atherosclerosis is a predictor of future cardiovascular events. Exacerbations increase all-cause mortality in COPD, and exacerbation-like episodes have been described in subjects without COPD. Our objectives were as follows: (1) to confirm the independent association between COPD and carotid atherosclerosis and (2) to asses the possible relationship between COPD exacerbations or exacerbation-like episodes and a higher risk of atherosclerosis.

Methods

127 COPD subjects and 80 control subjects with smoking history were studied. Carotid ultrasound examination was carried out in all subjects. Univariate and multivariate logistic regression analyses were performed in order to assess the relationship between both COPD diagnosis and previous COPD exacerbations (or exacerbation-like episodes in non-COPD subjects) and the presence of carotid atherosclerosis.

Results

The prevalence of carotid atherosclerosis was higher in COPD group (65.3 vs. 47.5%, p = 0.01; OR 2.18, 95% CI 1.23–3.88, p < 0.01). Diagnosis of COPD was not independently associated with atherosclerosis, after adjusting for potential confounders. Neither COPD exacerbations nor exacerbation-like episodes in control subjects were associated with a higher risk of atherosclerosis.

Conclusion

There is a higher prevalence of carotid atherosclerosis in COPD than in control smokers or ex-smokers, but the differences seem to be related to shared risk factors. We have not found evidence for an increased risk of atherosclerosis associated with COPD exacerbations or exacerbation-like events. Further longitudinal studies should be carried out to confirm these findings.

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Authors contributions

RG: study concept and design; analysis and interpretation of data; had full access to all of the data in the study and took responsibility for the integrity of the data and the accuracy of the data analysis; and drafting of the manuscript. A M-C: study concept and design; acquisition of data; study supervision; analysis and interpretation of data and drafting of the manuscript. C G-J: acquisition of data and drafting of the manuscript. A T-F: acquisition of data and critical revision of the manuscript for important intellectual content. N D-P: acquisition of data and critical revision of the manuscript for important intellectual content. FJ M-V: acquisition of data and critical revision of the manuscript for important intellectual content.

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Authors and Affiliations

  1. Respiratory Service, Servicio de Neumología. Unidad Administrativa 4-A, Hospital Universitario Lucus Agusti, C/ Dr Ulises Romero no 1, 27003, Lugo, Spain

    Rafael Golpe

  2. Internal Medicine Service, Hospital Universitario Lucus Agusti, Lugo, Spain

    Alfonso Mateos-Colino & Nuria Domínguez-Pin

  3. Cardiology Service, Hospital Universitario Lucus Agusti, Lugo, Spain

    Carlos González-Juanatey & Ana Testa-Fernández

  4. EOXI Lugo, Cervo e Monforte de Lemos, Servizo Galego de Saúde, Lugo, Spain

    Francisco J. Martín-Vázquez

Authors
  1. Rafael Golpe
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  2. Alfonso Mateos-Colino
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  3. Carlos González-Juanatey
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  4. Ana Testa-Fernández
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  5. Nuria Domínguez-Pin
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  6. Francisco J. Martín-Vázquez
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Corresponding author

Correspondence to Rafael Golpe.

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Conflict of interest

The authors do not declare any conflict of interest.

Ethical Approval

The study was performed in accordance with the 1964 Declaration of Helsinki and its later amendments and it was approved by our ethical committee (Comité Autonómico de Ética de la Investigación de Galicia, registry number 2010/228).

Informed Consent

Informed written consent was obtained from all the subjects.

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Golpe, R., Mateos-Colino, A., González-Juanatey, C. et al. Subclinical Carotid Atherosclerosis in COPD Cases and Control Smokers: Analysis in Relation with COPD Exacerbations and Exacerbation-like Episodes. Lung 195, 185–191 (2017). https://doi.org/10.1007/s00408-017-9986-4

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  • DOI: https://doi.org/10.1007/s00408-017-9986-4

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