Abstract 12093: Role of Active Valvular Calcification and Inflammation in Patients with Aortic Stenosis
Introduction. The pathophysiology of aortic stenosis is incompletely understood and the relative contributions of active valvular calcification and inflammation to disease progression are unknown.
Hypothesis. PET/CT would elucidate the contribution of inflammation and calcification to the pathophysiology of this condition in a cohort of patients with the full spectrum of disease severity
Methods. Patients with aortic sclerosis and mild, moderate and severe stenosis were prospectively compared to age and sex-matched control subjects. Aortic valve severity was assessed by echocardiography, and active valvular calcification and inflammation by sodium 18-fluoride (Na18F) and 18-fluorodeoxyglucose (18FDG) uptake using PET/CT. Standardized uptake values and tissue to background ratios were calculated for the aortic valve and thoracic aorta.
Results. One hundred and nine subjects (14 controls, 17 aortic sclerosis, and 24 mild, 32 moderate, and 22 severe aortic stenosis) were administered both Na18F and 18FDG. Uptake values for both tracers were higher in patients than control subjects (P<0.001). Valvular Na18F uptake displayed a progressive rise with valve severity (r2=0.516, P<0.001) and uptake values were 34% higher than in the aorta (2.70±0.87 vs 2.01±0.33; p<0.001). Valvular 18FDG uptake was lower than Na18F (P<0.001) and there was only a weak correlation between these two tracers (r2= 0.13, P<0.001). Valvular 18FDG activity displayed a modest association with valve severity (r2=0.204; P<0.001) and, in contrast to Na18F, 18FDG uptake was lower in the valve than the aorta (1.53±0.22 vs 1.79±0.32; P<0.001).
Conclusions. Active calcific and inflammatory processes are prominent in the valves of patients with aortic stenosis, and correlate with disease severity. Valvular calcification appears to be the predominant pathogenetic process that is particular to the valve and disproportionate to the degree of inflammation.
- © 2011 by American Heart Association, Inc.