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Updated: Jul 10, 2026
Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Circulating endothelial cell count, plasma vWF and soluble ICAM-1 levels following primary or elective percutaneous
K Vargová1, E Toth-Zsamboki, B J Beres
1Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University, 44 Robert Karoly str., 1134 Budapest, Hungary. katuskav78@yahoo.com
Insights
Percutaneous coronary intervention (PCI) causes mild endothelial injury in stable angina. However, ST-elevation myocardial infarction (STEMI) patients experience more pronounced damage due to the procedure, ischemia, and atherothrombosis.
Area of Science:
- Cardiology
- Vascular Biology
- Interventional Cardiology
Background:
- Percutaneous coronary intervention (PCI) is a key treatment for ischemic heart disease.
- Assessing endothelial injury from PCI in stable angina (SA) and acute ST-elevation myocardial infarction (STEMI) is crucial.
Purpose of the Study:
- To evaluate the extent of endothelial injury induced by PCI in SA and STEMI patients.
- To compare endothelial damage between SA and STEMI following PCI and angiography.
Main Methods:
- Measured circulating endothelial cell (CEC) count, von Willebrand factor (vWF), and soluble intercellular adhesion molecule-1 (sICAM-1) pre- and post-PCI.
- Included SA patients undergoing PCI (n=23) and coronarography only (n=23), and STEMI patients undergoing PCI (n=28).
Main Results:
- PCI and coronarography in SA showed non-significant increases in CEC and vWF.
- STEMI patients had higher baseline CEC and vWF, with a significant CEC increase post-PCI (peak at 24h).
- A positive correlation was observed between baseline CKMB and 24h CEC count in STEMI patients.
Conclusions:
- Both coronary angiography and elective PCI result in mild endothelial injury.
- In STEMI, endothelial damage is exacerbated by myocardial ischemia and the atherothrombotic process, not solely the procedure.
Background:
Percutaneous coronary intervention (PCI) is an important therapeutic strategy in patients with ischaemic heart disease. Our aim was to clarify the extent of endothelial injury induced by PCI in stable angina (SA) or in acute ST-elevation myocardial infarction (STEMI).
Methods:
Circulating endothelial cell (CEC) count, von Willebrand factor (vWF) and soluble intercellular adhesion molecule-1 (sICAM-1) levels were determined pre-, post-, 24 and 96h after PCI in patients with SA (n=23) and with STEMI (n=28). To provide control data regarding the effect of angiography itself stable angina patients with coronarography only (n=23) were enrolled.
Results:
PCI and coronarography in stable angina patients caused measurable, but only non-significant elevation of CEC count and plasma vWF (p=NS). In STEMI, significantly higher baseline CEC count (p=0.019) and vWF plasma levels (p=0.046) were found compared to SA with PCI/or coronarography. After PCI, explicit increase in CEC count was observed (significant peak at 24h) (p=0.036). Positive correlation was found between baseline CKMB and CEC count at 24h (r=0.51, p<0.05).
Conclusion:
Both coronary angiography and elective PCI cause only mild endothelial injury. However, in patients with STEMI, not only the procedure itself but myocardial ischemia and the ongoing atherothrombotic process might be responsible for the prolonged and more pronounced endothelial damage.
