Abstract 18627: Monocyte Subsets in Patients With Severe Aortic Valve Stenosis Undergoing TAVI

Abstract

Introduction: Aortic valve stenosis (AVS) shares profound similarities with atherosclerotic plaque progression, including the presence of macrophages in the valve tissue. Monocytes are the precursor of macrophages and various studies have shown associations of individual monocyte subsets with cardiovascular risk. Therefore, we assessed the hypotheses that monocyte subsets differ in the presence of severe AVS compared to an AVS-free setting and change by intervention of the AVS. Methods: Classical (CD14++CD16-), intermediate (CD14++CD16+) and non-classical (CD14+CD16++) CD86 positive monocyte subsets and monocyte activation (median fluorescent intensity of CD11b) were determined by flow cytometry in peripheral blood from patients with severe AVS (n=32) and matched AVS-free controls (n=28). A follow-up evaluation of monocyte subsets and activation was performed in AVS patients undergoing transcutaneous valve implantation (TAVI) 3 months after the procedure (n=9). Results: There were no significant differences in the absolute monocyte counts between AVS patients and controls. In contrast, AVS patients exhibited a shift towards CD16+ monocytes subsets with significant higher proportion of the intermediate monocyte subset compared to controls (median [IQR] 7.0% [5.5-8.7%] versus 5.8% [4.7-6.6%]; p=0.015). Classical and non-classical monocyte subsets and monocyte activation did not differ significantly between the groups. There was no significant change in the distribution of monocyte subsets or in monocyte activation 3 months after TAVI compared to baseline. Conclusions: We found preliminary evidence for a significant difference in the distribution of monocyte subsets in patients with severe AVS compared to AVS-free controls indicating an involvement of monocyte subsets in the pathogenesis of AVS. Monocyte subsets and activation did not change after treatment of AVS by TAVI.