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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Platelet-monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by
M J Ray1, D L Walters, J N H Bett
1Department of Haematology, The Prince Charles Hospital, Brisbane, Australia.
Insights
Elevated platelet-monocyte aggregates before percutaneous coronary intervention (PCI) predict cardiac troponin I elevation post-PCI. Abciximab therapy reduces these aggregates, suggesting it benefits high-risk patients.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Interventional Cardiology
Background:
- Patients undergoing percutaneous coronary intervention (PCI) exhibit elevated platelet activation markers.
- Platelet-monocyte aggregates are increased in patients with coronary artery disease compared to healthy controls.
Purpose of the Study:
- To investigate platelet activation markers before and after PCI with abciximab therapy.
- To assess the correlation between platelet-monocyte aggregation and cardiac troponin I (cTnI) elevation post-PCI.
Main Methods:
- Blood samples from 40 patients were analyzed for platelet activation markers (platelet-monocyte aggregates, P-selectin, PAC-1) via flow cytometry before and after abciximab administration.
- Cardiac troponin I levels were measured at baseline and 24 hours post-PCI.
Main Results:
- Pre-PCI, patients showed higher platelet-monocyte aggregates, P-selectin, and PAC-1 compared to controls.
- Abciximab reduced platelet-monocyte aggregates and PAC-1 but not P-selectin expression.
- Higher pre-PCI platelet-monocyte aggregates correlated with increased cTnI levels 24 hours post-PCI.
Conclusions:
- Elevated platelet-monocyte aggregates may predict patients at risk of troponin elevation after PCI.
- Platelet-monocyte aggregate levels could identify patients who would benefit from abciximab therapy.
Background:
Platelet-monocyte aggregates and other markers of platelet activation were investigated before and after percutaneous coronary intervention (PCI) with abciximab therapy. The study sought to assess the relationship between the level of platelet-monocyte aggregation and increases in cardiac troponin I post coronary intervention.
Methods:
Blood samples were collected from 40 patients before PCI and 10 min after abciximab administration. These were tested for platelet activation markers by flow cytometry. Cardiac troponin I levels were assayed at baseline and at 24 h post PCI.
Results:
Compared to healthy controls, patients with coronary artery disease had elevated markers of platelet activation including platelet-monocyte aggregates, P-selectin and PAC-1 (a marker specific for activated glycoprotein IIb/IIIa) prior to PCI. Increased levels of platelet-monocyte aggregates before PCI were associated with increased expression of P-selectin on the platelet surface. Abciximab therapy reduced platelet-monocyte aggregate levels but had no effect on P-selectin expression. The high levels of expression of activated glycoprotein IIb/IIIa (PAC-1) on platelets prior to PCI was reduced with abciximab therapy. Patients with higher levels of platelet-monocyte aggregates prior to PCI were more likely to develop an elevation of cardiac troponin I during the 24 h after PCI.
Conclusions:
Increased levels of platelet-monocyte aggregates may predict patients at risk for troponin elevation following PCI and identify those most likely to benefit from abciximab.
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