Abstract

Aims

The pathophysiology of aortic stenosis shares many similarities with atherosclerosis and skeletal bone formation. Using non-invasive imaging, we compared aortic valve calcification and inflammation activity with that measured in atherosclerosis and bone.

Methods and results

Positron emission and computed tomography was performed using 18F-sodium fluoride (18F-NaF, calcification) and 18F-fluorodeoxyglucose (18F-FDG, inflammation) in 101 patients with calcific aortic valve disease (81 aortic stenosis and 20 aortic sclerosis). Calcium scores and positron emission tomography tracer activity (tissue-to-background ratio; TBR) were measured in the aortic valve, coronary arteries, thoracic aorta, and bone. Over 90% of the cohort had coexistent calcific atheroma, yet correlations between calcium scores were weak or absent (valve vs. aorta r2 = 0.015, P = 0.222; valve vs. coronaries r2 = 0.039, P = 0.049) as were associations between calcium scores and bone mineral density (BMD vs. valve r2 = 0.000, P = 0.766; vs. aorta r2 = 0.052, P = 0.025; vs. coronaries r2 = 0.016, P = 0.210). 18F-NaF activity in the valve was 28% higher than in the aorta (TBR: 2.66 ± 0.84 vs. 2.11 ± 0.31, respectively, P < 0.001) and correlated more strongly with the severity of aortic stenosis (r2 = 0.419, P < 0.001) than 18F-NaF activity outwith the valve (valve vs. aorta r2 = 0.167, P < 0.001; valve vs. coronary arteries r2 = 0.174, P < 0.001; valve vs. bone r2 = 0.001, P = 0.806). In contrast, 18F-FDG activity was lower in the aortic valve than the aortic atheroma (TBR: 1.56 ± 0.21 vs. 1.81 ± 0.24, respectively, P < 0.001) and more closely associated with uptake outwith the valve (valve vs. aorta r2 = 0.327, P < 0.001).

Conclusion

In patients with aortic stenosis, disease activity appears to be determined by local calcific processes within the valve that are distinct from atherosclerosis and skeletal bone metabolism.

Trial Registration: ClinicalTrials.gov number: NCT01358513

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