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

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.

Blood Pressure Profile and Hypertensive Organ Damage in COPD Patients and Matched Controls. The RETAPOC Study.

BACKGROUND: Several studies suggest that there is a pathogenic link between chronic obstructive pulmonary disease (COPD) and cardiovascular diseases. On the other hand, increased sympathetic tone has been described in several respiratory diseases. Our objective was to determine whether hypertension mediated by sympathetic overactivity is a mechanism that explains the association between COPD and cardiovascular diseases. METHODS: Prospective nested case-control observational study; 67 COPD patients were matched 1:1 by sex and age to controls with smoking history. 24 hour-blood pressure monitoring, urinary catecholamines and their metabolites measurement, echocardiography, carotid ultrasound examination, nocturnal oximetry and retinography were performed. FINDINGS: classic cardiovascular risk factors and comorbidities were similarly distributed between cases and controls. No significant differences for blood pressure variables (difference for mean systolic blood pressure: -0·13 mmHg; 95% CI: -4·48,4·20; p = 0·94; similar results for all blood presssure variables) or catecholamines values were found between both groups. There was a tendency for lower left ventricle ejection fraction in the COPD cases, that approached statistical significance (64·8 ± 7·4 vs 67·1 ± 6·2, p = 0·05). There were no differences in the retinal arteriovenous ratio, the carotid intima-media thickness, or the number of carotid plaques, between cases and controls. Fibrinogen values were higher in the COPD group (378·4 ± 69·6 vs 352·2 ± 45·6 mg/dL, p = 0·01) and mean nocturnal oxygen saturation values were lower for COPD patients (89·0 ± 4·07 vs 92·3 ± 2·2%, p < 0·0001). INTERPRETATION: Hypertension induced by sympathetic overactivity does not seem to be a mechanism that could explain the association between COPD and cardiovascular disease.