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Published on: August 13, 2015
Intracoronary platelet and monocyte activation status within platelet-monocyte complexes are determinants of
B Majumder1, S Koganti1, M W Lowdell2
1Department of Cardiology, Royal Free Hospital, London, UK.
Insights
Platelet monocyte complexes (PMCs) are linked to inflammation in ST-elevation myocardial infarction (STEMI). Activated platelets and monocytes within these complexes, specifically P-selectin and tissue factor expression, drive local inflammation in STEMI patients.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Hematology
Background:
- Platelet monocyte complexes (PMCs) are associated with coronary artery disease, but their role in ST-elevation myocardial infarction (STEMI) requires further elucidation.
- This study investigates the pathological significance of locally activated PMCs and their correlation with intracoronary inflammation in STEMI and stable angina.
Purpose of the Study:
- To evaluate the relationship between locally activated Platelet Monocyte Complexes (PMCs) and intracoronary inflammation in ST-elevation myocardial infarction (STEMI).
- To assess the role of P-selectin and tissue factor expression on PMCs in determining local inflammatory burden within the coronary artery.
Main Methods:
- Blood samples were collected from the coronary artery, aorta, and right atrium of STEMI and stable angina patients.
- Flow cytometry was used to identify PMCs (CD14+CD61+ cells) and assess P-selectin (CD62P) and tissue factor (CD142) expression.
- Plasma levels of TNF-alpha, IL-6, and CRP were measured using ELISA and immunoassay.
Main Results:
- Overall PMC expression did not differ significantly between STEMI and stable angina patients or across sampling sites.
- Intracoronary P-selectin expression on PMCs was significantly higher in STEMI patients compared to aorta or right atrium samples (p=0.003).
- Intracoronary PMC activation markers, P-selectin and tissue factor, correlated significantly with intracoronary TNF-alpha and IL-6 levels in STEMI patients.
Conclusions:
- PMC formation itself is not the sole driver of inflammation in STEMI.
- Increased intracoronary P-selectin and tissue factor expression on activated platelets and monocytes within PMCs are key determinants of local inflammatory burden in STEMI.
Introduction:
Platelet Monocyte Complexes (PMCs) are commonly expressed in coronary artery disease but their pathologic significance in ST elevation myocardial infarction (STEMI) is unclear. This study evaluates the relationship between locally activated PMCs and intracoronary inflammation in stable and unstable coronary disease.
Material And Methods:
Micro catheter aspirated blood samples of 15 STEMI and 7 stable angina patients are collected from the coronary artery (CA), aorta (AO) and right atrium (RA). Samples are labelled with monoclonal antibodies and prepared for flow cytometry. CD 14 and CD 61 double positive cells are identified as PMC. P-selectin expression is identified by additional CD62P positivity and TF expression by additional CD142 positivity. Plasma TNF-alpha and IL-6 are measured using ELISA and CRP is measured in plasma using a high sensitivity automated microparticle enhanced latex turbidimetric immunoassay.
Results:
No site-specific difference is seen in overall PMC expression in STEMI or stable angina. Surface P-selectin expression in STEMI [median (IQR)] is significantly higher in CA [35.01 (23.15-56.99)] compared with AO [15.99 (10.3-18.85)] or RA [14.02 (10.42-26.08)] (p = 0.003). Intracoronary PMC correlates significantly with intracoronary TNF-alpha (r = 0.87, p = 0.001) and intracoronary IL-6 (r = 0.76, p = 0.03). Bound monocytes within P-selectin positive and tissue factor positive complexes correlate positively with intracoronary TNF-alpha (r = 0.81, p = 0.008 & r = 0.80, p = 0.009 respectively) and IL-6 (r = 0.54, p = 0.16 & r = 0.71, p = 0.05 respectively). No such correlation is observed in the peripheral circulation of STEMI and stable angina patients.
Conclusion:
Inflammation is not attributable to PMC formation per se. However, increased intracoronary P-selectin expression by activated platelets and tissue factor expression by activated monocytes within the complexes are determinants of local intracoronary inflammatory burden in STEMI.
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