Individual monocyte subsets have been associated with atherosclerotic disease, but their distribution has not been evaluated in aortic valve stenosis (AS) so far. In the present study, we have asked whether levels of the circulating intermediate monocyte subset are increased in AS. Classical (CD14++CD16-), intermediate (CD14++CD16+), and non-classical (CD14+CD16++) CD86-positive monocytes and monocyte activation (intensity of CD11b expression) were determined by flow cytometry in peripheral blood of patients with severe AS (n = 100) and matched AS-free controls (n = 75). AS patients exhibited significantly higher levels of circulating intermediate monocytes, while levels of circulating classical and non-classical monocytes or monocyte activation did not differ compared to controls. The difference in levels of intermediate monocytes between groups was independent of age, gender, BMI, LDL-C, NT-proBNP, NYHA functional class, or creatinine levels. The present pilot study provides evidence of an association of severe AS with increased levels of circulating intermediate monocytes. Further studies need to clarify whether this finding is related to the inflammatory status and hemodynamic disturbances associated with severe AS.
Aortic valve stenosis (AS) is a chronic inflammatory disease. We have previously shown that severe AS is associated with increased levels of circulating intermediate monocytes. Haemodynamics are considered to influence levels of circulating monocyte subsets; we therefore hypothesized that aortic valve replacement may result in changes in the distribution of circulating monocyte subsets. In the present study, we evaluated levels of circulating monocyte subsets in patients with severe AS undergoing surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR). Levels of classical (CD14++CD16–), intermediate (CD14++CD16+), and non-classical (CD14+CD16++) CD86-positive monocytes were determined by flow cytometry in peripheral blood of patients with severe AS before (baseline) and at 3- and 6-month follow-ups (FUP) after SAVR (n = 25 patients) or TAVR (n = 44 patients). Absolute and relative levels of circulating intermediate monocytes decreased from median 39.9/µL (interquartile range [IQR]: 31.7–53.6/µL) and 6.7% (5.6–8.1%) at baseline to 31.6/µL (24.3–42.4/µL; p < 0.001) and 5.4% (4.4–6.7%; p < 0.001) at 6-month FUP after aortic valve replacement, respectively. The decrease in levels of circulating intermediate monocytes appeared earlier (between baseline and 3-month FUP) in the TAVR group compared with the SAVR group (between 3- and 6-month FUP). In conclusion, levels of circulating intermediate monocytes decrease after SAVR or TAVR in patients with severe AS.
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.
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