CD133+ Stem Cell Therapy Effects on Myocardial Regeneration Through Increased Vascular Endothelial Growth Factor Correlate with Cardiac Magnetic Resonance Imaging Results in Coronary Artery Bypass Graft Surgery Patients with Low Ejection Fraction

Background: Stem cell implantation has become a promising therapy for heart failure due to coronary heart disease (CHD). CD133+ stem cell therapy, together with increases of vascular endothelial growth factor (VEGF) and other growth hormones, can induce myocardial repair. Objective: To prove that VEGF plays a role in cardiac regeneration. Methods: Twenty-six patients with CHD and ejection fractions <35% from Harapan Kita Heart and Vascular Center, Jakarta, Indonesia, from 2016 to 2018 were randomized into 2 groups. The treatment group underwent coronary artery bypass graft (CABG) + CD133+ implantation, and the control group underwent CABG only. Six months later, perfusion and myocardial function were assessed by ejection fraction, wall motion score index (WMSI), ventricular dimensions, and scar size using cardiovascular magnetic resonance imaging. VEGF was assessed with enzyme-linked immunosorbent assay. Results: There was significant improvement in ejection fraction (8.69% ± 9.49% versus 1.43% ± 7.87%, P = .04), WMSI (0.51 ± 0.48 versus –0.01 ± 0.21, P = .003), and scar size (25.46 ± 12.91 versus 27.32 ± 12.92 mm, P = .047) and a significant increase in blood VEGF levels (61.05 ± 63.01 versus 19.88 ± 33.78 pg/mL, P = .01). Improvements in perfusion defects (13.69 ± 5.03 versus 11.53 ± 5.81 P = .32) and ventricular dimensions (–27.59 ± 84.48 versus –19.08 ± 36.79 mm, P = .06) were not statistically significant. Conclusion: CD133+ stem cell implantation improves myocardial function. The increase in VEGF levels is expected to continue improving restoration of myocardial function when myocardial perfusion improvement is still not optimal.

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Intense remodeling of extracellular matrix within the varicose vein: the role of gelatinases and vascular endothelial growth factor

Irish Journal of Medical Science (1971 -) ◽

10.1007/s11845-020-02289-1 ◽

2020 ◽

Author(s):

Anna Horecka ◽

Anna Hordyjewska ◽

Jadwiga Biernacka ◽

Wojciech Dąbrowski ◽

Tomasz Zubilewicz ◽

...

Keyword(s):

Extracellular Matrix ◽

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Varicose Veins ◽

Artery Bypass ◽

Bypass Graft ◽

Clinical State ◽

Vascular Endothelial ◽

Altered Expression ◽

Endothelial Growth Factor

Abstract Background Increased blood pressure in the varicose veins (VV) can contribute to the overexpression of matrix metalloproteinases (MMPs), affecting the endothelium, smooth muscle, and extracellular matrix of the vein wall. Gelatinases (MMP-2 and MMP-9), hypoxia, and inflammation occurring in the VV wall contribute to the increased expression of vascular endothelial growth factor (VEGF). Aims Our objective was to analyze the concentration of gelatinases and VEGF in the great saphenous VV wall and plasma of patients. Methods In total, 65 patients (2nd degree according to clinical state classification, etiology, anatomy, and pathophysiology—CEAP classification) aged 22 to 70 were enrolled. Control veins (n = 10) were collected from the patients who underwent coronary artery bypass graft surgery. Control plasma (n = 20) was obtained from healthy individuals. Gelatinases and VEGF levels were measured with the usage of ELISA method. Results A significant increase in MMP-9 (11.2 vs. 9.98 ng/mg of protein) and VEGF (41.06 vs. 26 ng/g of protein) concentration in VV wall compared with control veins was observed. A positive correlation between VEGF versus MMP-2 (p = 0.03, r = 0.27) was found in the VV wall. However, no correlation was found between the concentration of VEGF and MMP-9 (p = 0.4, r = 0.11) in the VV wall. In addition, no statistical differences between MMP-9, MMP-2, and VEGF levels in plasma of VV patients compared with controls were noticed. Conclusions The results of the present study confirm that VV’s patients have altered expression of MMPs and VEGF. Overexpression of MMP-9 and VEGF in the VV wall may contribute to the spreading of inflammatory process and suggests the intense remodeling of extracellular tissue within the VV wall.

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