Introduction:
COPD is associated with increased cardiovascular events, even after adjusting for traditional risk factors. We hypothesised that this relates to aortic inflammation and stiffness, both surrogates of higher cardiac risk. For comparison, we also measured these parameters in A1ATD patients with emphysema and controls.
Methods:
Sixty subjects (24 COPD, 12 A1ATD, 12 smokers, 12 never smokers (controls)) were recruited. Aortic stiffness was estimated by aortic pulse wave velocity (aPWV). Aortic and carotid wall inflammation was measured by FDG PET/CT, with FDG uptake quantified as the target to blood ratio (TBR).
Results:
COPD and A1ATD subjects had both 1) increased aPWV compared to healthy smokers and controls (Table 1, p=0.01) and 2) more aortic inflammation, particularly in the abdominal aorta (p=0.0001, 24% and 29% difference to controls, respectively, Figure 1). FDG uptake was also higher in the carotid arteries of COPD but not A1ATD subjects (p=0.0001). There was no difference in stiffness between healthy smokers and controls (p=1.0), but arterial inflammation in the abdominal aorta was greater in smokers than controls (p=0.0001).
Conclusions:
COPD is associated with both increased aortic inflammation and stiffness. These mechanisms might explain the unexplained heightened cardiovascular risk in COPD patients and are potential therapeutic targets. A1ATD subjects also have increased aortic inflammation and stiffness suggestive of increased cardiovascular risk. Susceptibility to smoke injury in the lungs and vasculature, or systemic inflammation associated with lung disease, are possible explanations.