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Updated: Jun 5, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Soluble levels of cell adhesion molecules (CAMs) in coronary artery disease
Manoj R Mashru1, Vinod K Shah, Surendra L Soneji
1Sir H. N. Hospital and Research Centre, Mumbai, Maharashtra, India.
Insights
Soluble cell adhesion molecules (sCAMs) like E-selectin and VCAM-1 are elevated in acute myocardial infarction, indicating plaque destabilization. Levels vary with coronary artery disease severity, suggesting diagnostic potential.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biochemistry
Background:
- Coronary artery disease (CAD) involves complex inflammatory processes.
- Cell adhesion molecules (CAMs) play a role in endothelial dysfunction and atherosclerosis.
- Soluble forms of CAMs (sCAMs) may serve as biomarkers for cardiovascular events.
Purpose of the Study:
- To quantify soluble CAM levels in patients with varying CAD severity.
- To correlate sCAM levels with the degree of coronary artery disease.
- To investigate the role of sCAMs in acute coronary syndromes and stable angina.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure sCAM levels.
- Study included patients with acute myocardial infarction (AMI), unstable angina, and stable angina.
- Levels were compared between patient groups and with healthy controls.
Main Results:
- AMI patients showed significant increases in soluble E-selectin, VCAM-1, PECAM-1, P-selectin, and ICAM-1 compared to controls.
- Unstable angina patients had decreased levels of sE-selectin, sPECAM-1, and sVCAM-1 compared to AMI.
- Elevated sE-selectin, sVCAM-1, and sPECAM-1 suggest their role in plaque destabilization.
Conclusions:
- Soluble E-selectin, VCAM-1, and PECAM-1 are potential biomarkers for plaque destabilization in acute coronary events.
- sCAM levels differ across CAD severity, highlighting their dynamic role in the disease process.
- Elevated sP-selectin in stable angina indicates ongoing platelet activation.
Aims:
To analyze soluble levels ofcell adhesion molecules (CAM) such as Intercellular CAM (ICAM), vascular CAM (VCAM-1), platelet endothelial CAM (PECAM-1), Endothelial (E)-selectin, and Platelet (P)-selectin in coronary artery disease patients and correlate with degree of severity of the disease.
Methods:
Study population included patients who suffered myocardial infarction at presentation (N=49) and those with unstable angina (N=79) and stable angina (N=14). Soluble levels of CAMs were measured by ELISA.
Results:
At acute event in AMI patients, there was significant rise of soluble (s) E-selectin (4.5 fold, P = 0.001), sVCAM-1 (65.6%, p = 0.001), sPECAM-1 (46.2%, p = 0.02), sP-selectin (42.7%, p = 0.001) and sICAM-1 (20.1%, p = 0.003) as compared to controls. In unstable angina group as compared to AMI there was significant decrease in the levels observed in, sE-selectin (62.7%, p = 0.001), sPECAM-1 (47.5%, p = 0.001) as well as sVCAM-1 (17.9%, p = 0.04) and insignificant decrease with respect to sICAM-1 and no change with respect to sP-selectin levels. Stable angina group as compared to unstable angina group demonstrated no significant difference in sCAMs and the trend with AMI group was similar to that seen between unstable angina and AMI group. Significantly elevated levels of sE-selectin, sVCAM-1 and sPECAM-1 at acute event suggest them to be causal molecules as well as markers of plaque destabilization. Levels of sP-selectin in stable angina were similar to that observed in AMI and unstable angina groups suggesting elevated platelet activation in stable angina as well.
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