Endothelial progenitor cells as markers of severity in hypertrophic cardiomyopathy
Athanasia Kalyva1, Maria E Marketou2, Fragiskos I Parthenakis2
1Molecular Cardiology Laboratory, School of Medicine, University of Crete, Greece.
Insights
Endothelial progenitor cells (EPCs) are elevated in hypertrophic cardiomyopathy (HCM) patients, correlating with diastolic dysfunction. This finding offers new insights into HCM pathophysiology and treatment strategies.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Regenerative Medicine
Background:
- Endothelial progenitor cells (EPCs) are crucial for neovascularization.
- EPCs are bone marrow-derived cells that differentiate into mature endothelial cells.
- Their role in hypertrophic cardiomyopathy (HCM) is not fully understood.
Purpose of the Study:
- To evaluate circulating EPC levels in HCM patients.
- To investigate the association between EPCs and clinical parameters in HCM.
- To explore the potential of EPCs as biomarkers for HCM.
Main Methods:
- Flow cytometry was used to quantify EPC subpopulations (CD45-/CD34+/VEGFR2+ and CD45-/CD34+/CD133+) in 40 HCM patients and 23 healthy controls.
- Correlation analysis was performed with clinical parameters like LV mass index and E/e' ratio.
Main Results:
- Circulating CD45-/CD34+/VEGFR2+ EPCs were significantly increased in HCM patients compared to controls (P=0.002).
- No significant difference was observed in CD45-/CD34+/CD133+ EPCs between groups (P=0.153).
- The CD45-/CD34+/VEGFR2+ subpopulation correlated with LV mass index (r=0.35, P=0.026), and both EPC subpopulations correlated strongly with the E/e' ratio (P<0.001 for CD45-/CD34+/CD133+).
Conclusions:
- HCM patients exhibit increased mobilization of EPCs, particularly the CD45-/CD34+/VEGFR2+ subtype.
- Elevated EPC levels correlate with diastolic dysfunction in HCM.
- These findings suggest a potential role for EPCs in HCM pathophysiology and may inform future diagnostic and therapeutic approaches.
Aims:
Endothelial progenitor cells (EPCs) are bone marrow-derived cells that are mobilized into the circulation to migrate and differentiate into mature endothelial cells contributing to post-natal physiological and pathological neovascularization. In this study, we evaluated circulating EPCs in patients with hypertrophic cardiomyopathy (HCM) and examined a potential association with clinical parameters of the disease.
Methods And Results:
We included 40 HCM patients and 23 healthy individuals. Using flow cytometry we measured EPCs in peripheral blood as two subpopulations of CD45-/CD34+/VEGFR2+ and CD45-/CD34+/CD133+ cells. Circulating CD45-/CD34+/VEGFR2+ cells were significantly increased in HCM patients in comparison with the controls (0.000238 ± 0.0003136 vs. 0.000057 ± 0.0001316, respectively, P = 0.002). However, there was no significant difference in the number of circulating CD45-/CD34+/CD133+ cells (0.003079 ± 0.0033288 vs. 0.002065 ± 0.0022173, respectively, P = 0.153). The CD45-/CD34+/VEGFR2+ subpopulation revealed a moderate correlation with LV mass index (r = 0.35, P = 0.026), while both EPC subpopulation levels showed strong positive correlations with th E/e' ratio (r = 0.423, P = 0.007 for CD45-/CD34+/VEGFR2+ and r = 0.572, P < 0.001 for CD45-/CD34+/CD133+).
Conclusion:
HCM patients showed an increased mobilization of EPCs compared with healthy individuals that correlated with diastolic dysfunction. Our findings may open up new dimensions in the pathophysiology, prognostication, and treatment of HCM.
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