Assessment of Valvular Calcification and Inflammation by Positron Emission Tomography in Patients with Aortic Stenosis
Background—The pathophysiology of aortic stenosis is incompletely understood and the relative contributions of valvular calcification and inflammation to disease progression are unknown.
Methods and Results—Patients with aortic sclerosis and mild, moderate and severe stenosis were prospectively compared to age and sex-matched control subjects. Aortic valve severity was determined by echocardiography. Calcification and inflammation in the aortic valve were assessed by sodium 18-fluoride (18F-NaF) and 18-fluorodeoxyglucose (18F-FDG) uptake using positron emission tomography. One hundred and twenty one subjects (20 controls; 20 aortic sclerosis; 25 mild, 33 moderate and 23 severe aortic stenosis) were administered both 18F-NaF and 18F-FDG. Quantification of tracer uptake within the valve demonstrated excellent inter-observer repeatability with no fixed or proportional biases and limits of agreement of ±0.21 (18F-NaF) and ±0.13 (18F-FDG) for maximum tissue-to-background ratios (TBR). Activity of both tracers was higher in patients with aortic stenosis than control subjects (18F-NaF:2.87±0.82 vs 1.55±0.17; 18F-FDG: 1.58±0.21 vs 1.30±0.13; both P<0.001).18F-NaF uptake displayed a progressive rise with valve severity (r2=0.540, P<0.001) with a more modest increase observed for 18F-FDG (r2=0.218; P<0.001). Amongst patients with aortic stenosis, 91% had increased 18F-NaF (>1.97) and 35% increased 18F-FDG (>1.63) uptake. A weak correlation between the activities of these tracers was observed (r2= 0.174, P<0.001).
Conclusions—Positron emission tomography is a novel, feasible and repeatable approach to thee valuation of valvular calcification and inflammation in patients with aortic stenosis. The frequency and magnitude of increased tracer activity correlates with disease severity, and is strongest for 18F-NaF.
Clinical Trial Registration Information—ClinicalTrials.gov; Reference Number: NCT01358513
- Received June 29, 2011.
- Accepted October 11, 2011.
- Copyright © 2011, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited