Leukocyte activation after coronary stenting in patients during the subacute phase of a previous ST-elevation myocardial infarction
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Published on: May 28, 2019
Dimitrios A Stakos1, Ioannis Kotsianidis, Dimitrios N Tziakas
1Cardiology Department, Democritus University of Thrace, Alexandroupolis, and 2nd Cardiology Department, Papanikolaou General Hospital, Thessaloniki, Greece. dstakos@med.duth.gr
Insights
Leukocyte activation, specifically CD62L expression, reliably indicates early changes after percutaneous coronary intervention in ST-elevation myocardial infarction patients. This cellular biomarker may predict future events or restenosis.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Interventional Cardiology
Background:
- ST-elevation myocardial infarction (STEMI) requires interventions like percutaneous coronary intervention (PCI).
- Leukocyte activation is a key factor in cardiovascular events post-PCI.
- Understanding early cellular responses is crucial for risk stratification.
Purpose of the Study:
- To investigate leukocyte activation markers following PCI in STEMI patients.
- To assess changes in neutrophil and monocyte activation.
- To identify early cellular biomarkers of PCI-induced inflammation.
Main Methods:
- Flow cytometry assessed CD11b and CD62L expression on neutrophils and monocytes.
- Measurements were taken before and after coronary angiography and PCI.
- Plasma cytokines and C-reactive protein levels were also monitored.
Main Results:
- CD11b expression significantly increased post-PCI and coronary angiography, with a greater increase after PCI.
- CD62L expression decreased significantly after PCI but not after coronary angiography.
- No significant changes were observed in plasma cytokine or C-reactive protein levels.
Conclusions:
- CD62L is a specific and reliable early biomarker of leukocyte activation post-PCI in STEMI patients.
- Further research is needed to determine if CD62L predicts future events or restenosis.
- This finding aids in understanding the inflammatory response to PCI.
Objective:
To study leukocyte activation after percutaneous coronary intervention in patients with previous ST elevation myocardial infarction.
Methods:
Neutrophil and monocyte activation (by flow cytometric assessment of the surface expression of CD11b and CD62L adhesion molecules) was assessed in 39 patients during the subacute period of a previous ST elevation myocardial infarction initially treated with fibrinolytic agents, before and after diagnostic coronary angiography (coronary angiography control phase) as well as before and after stent implantation (percutaneous coronary intervention phase). Simultaneous evaluation of C-reactive protein (C-reactive protein immonoturbidimetry) and plasma cytokine levels (interleukins-1, -6, -10 and tumor necrosis alpha by immunoassay) was also performed. To track the earliest detectable change in the first few minutes after stent deployment, all measurements were performed before and 60 min after the procedures.
Results:
CD11b expression increased 1 h after stent deployment in neutrophils (P<0.0001) and monocytes (P<0.0001). A comparable increase, however, was also observed after coronary angiography (neutrophils, P=0.03; monocytes, P=0.01), although the increase of CD11b expression was greater after percutaneous coronary intervention on both neutrophils (90 vs. 40%, P=0.014) and monocytes (65 vs. 33%, P=0.04). CD62L expression decreased significantly after percutaneous coronary intervention (neutrophils, P=0.01; monocytes, P=0.006), but remained unchanged after coronary angiography. Plasma cytokine and C-reactive protein concentrations did not change after the procedures.
Conclusion:
CD62L appears to be a specific and reliable early cellular biomarker of leukocyte activation after percutaneous coronary intervention, when this procedure is performed in patients with previous ST elevation myocardial infarction. Whether this marker represents also a potential predictor of future events and/or restenosis in this group of patients remains to be defined.
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