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Published on: February 4, 2021
Mon2-monocytes and increased CD-11b expression before transcatheter aortic valve implantation are associated with
C Pfluecke1, S Wydra1, K Berndt2
1Technische Universität Dresden, Heart Center Dresden, University Hospital, Germany.
Insights
Elevated Mon2 monocytes and high monocyte activation before Transcatheter aortic valve implantation (TAVI) predict early mortality. Chronic inflammation is a key risk factor for TAVI patients.
Area of Science:
- Cardiology
- Immunology
- Inflammation Research
Background:
- Transcatheter aortic valve implantation (TAVI) is associated with unfavorable outcomes in a significant number of patients within three months.
- Inflammatory responses post-TAVI are suspected contributors to adverse events, but mechanisms remain unclear.
Purpose of the Study:
- To investigate the impact of monocyte subpopulations on clinical outcomes following TAVI.
- To assess the degree of monocyte activation and its correlation with inflammation and platelet activation markers.
Main Methods:
- Flow cytometry was used to analyze peripheral blood monocytes (defined by CD14 and CD16 expression) in 120 TAVI patients before and after the procedure.
- Monocyte activation was quantified by CD11b expression, and pro-inflammatory cytokines (IL-6, IL-8) and C-reactive protein (CRP) were measured.
Main Results:
- Higher levels of Mon2 monocytes (CD14++CD16+) and elevated CD11b expression before TAVI were independently linked to 3-month mortality.
- Mon2 monocytes exhibited the highest CD11b expression, which correlated with platelet activation and systemic inflammation markers.
- Pre-TAVI levels of CRP and IL-8 also predicted mortality, whereas post-TAVI inflammation did not correlate with early death.
Conclusions:
- Increased Mon2 monocytes and heightened monocyte activation preceding TAVI are significant predictors of early mortality.
- Chronic inflammation in aging patients appears to be a critical risk factor influencing outcomes after TAVI.
Background:
In the first three months after Transcatheter aortic valve implantation (TAVI), a remarkable number of patients have an unfavorable outcome. An inflammatory response after TAVI is suspected to have negative effects. The exact mechanisms remain unclear. We examined the influence of monocyte subpopulations on the clinical outcome, along with the degree of monocyte activation and further parameters of inflammation and platelet activation.
Methods:
Flow-cytometric quantification analyses of peripheral blood were done in 120 consecutive patients who underwent TAVI (one day before TAVI and on day 1 and 7 after TAVI). Monocyte-subsets were defined by their CD14 and CD16 expression, monocyte-platelet-aggregates (MPA) by CD14/CD41 co-expression. The extent of monocyte activation was determined by quantification of CD11b-expression (activation epitope). Additionally, pro-inflammatory cytokines such as interleukin (IL)-6, IL-8, C-reactive protein were measured with the cytometric bead array method or standard laboratory tests.
Results:
Elevated Mon2 (CD14++CD16+) - monocytes (38 vs. 62 cells/μl, p < 0.001) and a high expression of CD11b prior to TAVI (MFI 50.1 vs. 84.6, p < 0.05) were independently associated with death 3 months after TAVI. Mon2 showed the highest CD11b-expression and CD11b correlated with platelet activation and markers of systemic inflammation. Even CRP and IL-8 before TAVI were associated with death after TAVI. In contrast, a systemic inflammation response shortly after TAVI was not associated with early death.
Conclusions:
Elevated Mon2-monocytes and a high level of monocyte activation before TAVI are associated with early mortality after TAVI. Chronic inflammation in aging patients seems to be an important risk factor after TAVI.
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