Key result
Usual COPD linked to ~27% higher aortic stiffness and greater aortic inflammation versus smoking controls.
Why the study?
COPD is associated with increased cardiovascular disease, but the mechanisms such as aortic inflammation and stiffness contributing to vascular risk are not well defined.
Does the presence of COPD increase aortic inflammation and stiffness compared to healthy never-smokers and smokers without COPD?
Cross-Sectional (n=121)
Yes
Does the presence of COPD increase aortic inflammation and stiffness compared to healthy never-smokers and smokers without COPD?
Absolute Event Rate: 1.9% vs 1.74%
p-value: p=<0.05
COPD is associated with increased aortic inflammation and stiffness regardless of smoking history, suggesting potential mechanisms for the increased cardiovascular risk observed in these patients.
Aortic inflammation and stiffness may mediate excess CV risk in COPD; hypothesis-generating for vascular imaging in risk stratification.
Chronic obstructive pulmonary disease (COPD) is a complex inflammatory condition in which an important extra-pulmonary manifestation is cardiovascular disease. We hypothesized that COPD patients would have increased aortic inflammation and stiffness, as candidate mechanisms mediating increased cardiovascular risk, compared to two negative control groups: healthy never-smokers and smokers without COPD. We also studied patients with COPD due to alpha − 1 antitrypsin deficiency (α 1 ATD) as a comparator lung disease group. Participants underwent 18 F-Fluorodeoxyglucose (FDG) positron emission tomography imaging to quantify aortic inflammation as the tissue-to-blood-ratio (TBR) of FDG uptake. Aortic stiffness was measured by carotid-femoral aortic pulse wave velocity (aPWV). Eighty-five usual COPD (COPD due to smoking), 12 α 1 ATD-COPD patients and 12 each smokers and never-smokers were studied. There was no difference in pack years smoked between COPD patients and smokers (45 ± 25 vs 37 ± 19, p = 0.36), but α 1 ATD patients smoked significantly less (19 ± 11, p < 0.001 for both). By design, spirometry measures were lower in COPD and α 1 ATD-COPD patients compared to smokers and never-smokers. Aortic inflammation and stiffness were increased in COPD (TBR: 1.90 ± 0.38, aPWV: 9.9 ± 2.6 m/s) and α 1 ATD patients (TBR: 1.94 ± 0.43, aPWV: 9.5 ± 1.8 m/s) compared with smokers (TBR: 1.74 ± 0.30, aPWV: 7.8 ± 1.8 m/s, p < 0.05 all) and never-smokers (TBR: 1.71 ± 0.34, aPWV: 7.9 ± 1.7 m/s, p ≤ 0.05 all). In this cross-sectional prospective study, novel findings were that both usual COPD and α1ATD-COPD patients have increased aortic inflammation and stiffness compared to smoking and never-smoking controls, regardless of smoking history. These findings suggest that the presence of COPD lung disease per se may be associated with adverse aortic wall changes, and aortic inflammation and stiffening are potential mechanisms mediating increased vascular risk observed in COPD patients.
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Fisk et al. (2018) conducted a cross-sectional in Chronic obstructive pulmonary disease (COPD) (n=121). Chronic obstructive pulmonary disease (COPD) vs. Healthy smokers and never-smokers was evaluated on Aortic inflammation (tissue-to-blood-ratio [TBR] of FDG uptake) (p=<0.05). Patients with usual COPD had significantly increased aortic inflammation (TBR 1.90 vs 1.74) and aortic stiffness (aPWV 9.9 vs 7.8 m/s) compared to smoking controls.
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