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Circulating endothelial progenitor cells and coronary collaterals in patients with non-ST segment elevation
Eli I Lev1, Neal S Kleiman, Yochai Birnbaum
1The Methodist DeBakey Heart Center and Baylor College of Medicine, Houston, TX 77030, USA.
Insights
Circulating endothelial progenitor cells (EPCs) are linked to better collateral artery formation after non-ST segment elevation myocardial infarction (NSTEMI). Higher EPC levels before treatment indicate improved collateralization in heart attack patients.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Cell Biology
Background:
- Endothelial progenitor cells (EPCs) are crucial for neovascularization, responding to ischemic conditions.
- Their role in collateral artery formation following myocardial infarction requires further elucidation.
Purpose of the Study:
- To investigate the association between circulating EPC levels and collateral formation in patients with non-ST segment elevation myocardial infarction (NSTEMI).
Main Methods:
- Twenty NSTEMI patients undergoing percutaneous coronary intervention (PCI) were classified into groups with (coll+) or without (coll-) significant collaterals.
- Peripheral blood mononuclear cells were isolated to culture and quantify EPC colonies.
- Flow cytometry assessed co-expression of vascular endothelial growth factor receptor-2 and CD133 on cells.
Main Results:
- The collateral-positive group exhibited higher culprit vessel stenosis and lower initial flow grade.
- Pre-PCI circulating EPC levels were significantly higher in patients with collaterals compared to those without (1.49% vs. 0.77%, p=0.045).
- EPC colony numbers increased post-PCI in the no-collateral group (p=0.01).
Conclusions:
- Circulating EPC levels are associated with collateral artery formation in NSTEMI patients.
- This suggests a potential role for EPCs in the adaptive response to coronary artery disease.
Background:
Endothelial progenitor cells (EPCs) are bone marrow-derived cells that are augmented in response to ischemia and incorporated into neovascularization sites. We sought to determine whether circulating EPCs are related to collateral formation following non-ST segment elevation myocardial infarction (NSTEMI).
Methods:
Twenty patients who underwent percutaneous coronary intervention (PCI) within a week of NSTEMI were divided into two groups: patients without collaterals (coll-, n=10) and patients with Rentrop grade 3--4 collaterals (coll+, n=10). Blood samples were drawn before PCI and 24+/- 2 h after PCI. EPC colonies were grown from peripheral blood mononuclear cells, characterized, and counted. Using flow cytometry the percentage of cells co expressing vascular endothelial growth factor receptor-2 and CD 133 was determined.
Results:
The coll+ group had higher degree of culprit vessel stenosis and lower initial thrombolysis in myocardial infarction flow grade. The relative number of EPCs before PCI was significantly higher in the coll+ group than in the coll- group (1.49 +/- 0.9% vs. 0.77+/- 0.4%, p= 0.045). There were no significant intergroup differences in the number of EPC colony-forming cells. The number of EPC colonies increased in the coll- group after PCI (9.5 +/- 4.8 to 14.0 +/- 5.9/10(6) cells, p=0.01).
Conclusions:
This study supports an association between circulating EPC levels and collateral formation in patients with an NSTEMI.
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