Assessment of Calcification and Inflammation with Positron Emission Tomography in Aortic Stenosis and Atherosclerosis

Background Calcifi cation and infl ammation are key pathological processes in aortic stenosis and atherosclerosis.Using combined positron emission tomography and computed tomography (PET/CT), we sought to investigate their contribution to disease progression in aortic stenosis and to help identify vulnerable atherosclerotic plaque.Methods In the fi rst part of the study patients with calcifi c aortic valve disease stenosis were prospectively compared with age-matched and sex-matched controls with normal valves.Aortic valve severity was determined at baseline and 1 year by echocardiography and CT calcium scoring.Calcifi cation and infl ammation in the valve were assessed by sodium 18-fl uoride (NaF) and 18-fl uorodeoxyglucose (FDG) uptake with PET.In the second part of the study NaF and FDG activity was assessed in the coronary arteries both in patients with stable coronary disease and in patients after myocardial infarction.Findings 101 patients with aortic stenosis were compared with 20 controls.Tracer activity (target to background ratio [TBR]) was higher in patients with aortic stenosis than in controls (mean NaF 2•87 [SD 0•82] vs 1•55 [0•17], FDG 1•58 [0•21] vs 1•30 [0•13]; both p<0•01).NaF uptake displayed a progressive rise with valve severity (r²=0•540) with a more modest increase observed for FDG (r²=0•218).Baseline NaF correlated closely with alkaline phosphatase staining on immunohistochemistry (r²=0•79) and was a better predictor of disease progression at 1 year (r²=0•44, n=20) than was FDG (r²=0•02) or baseline calcium score (r²=0•36, current best predictor).Increased NaF activity was observed in 45 (42%) of 106 patients with stable coronary atherosclerosis and was localised to individual coronary plaques.These patients had higher rates of previous major adverse cardiovascular events (p=0•016) and higher Framingham risk scores (p=0•011) than did patients without increased uptake .In patients after myocardial infarction (n=15) intense NaF activity was observed at the site of the culprit lesion, with increased uptake compared with the maximum uptake elsewhere in the coronary arteries (TBR median 1•56 [IQR 1•49-1•82] vs 1•23 [1•15-1•48], p=0•02).Interpretation In the valve, NaF holds promise in predicting aortic stenosis progression.In the coronary arteries it identifi es culprit plaque post myocardial infarction and stable patients at elevated cardiac risk.