CD34
            <sup>+</sup>
            and Endothelial Progenitor Cells in Patients With Various Degrees of Congestive Heart Failure

Valgimigli, Marco; Rigolin, Gian Matteo; Fucili, Alessandro; Porta, Matteo Della; Soukhomovskaia, Olga; Malagutti, Patrizia; Bugli, Anna Maria; Bragotti, Letizia Zenone; Francolini, Gloria; Echavarría‐Pinto, Mauro; Castoldi, Gianluigi; Ferrari, Roberto

doi:10.1161/01.cir.0000136813.89036.21

Cited by 356 publications

(281 citation statements)

References 16 publications

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“…55 EPC (CD133 ϩ /Flk-1 ϩ ) was also reported to be inversely related to the severity of congestive heart failure. 55,56 Reduced number of EPCs was also seen in cardiac transplantation patients with vasculopathy 57 and in patients with in-stent restenosis. 58 In contrast, elevated EPC levels were reported in patients with unstable angina 59 and in patients with acute myocardial infarction 60 in association with elevation in plasma C-reactive protein levels.…”

Section: Epc and Cardiovascular Diseasesmentioning

confidence: 91%

Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases

et al. 2005

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Abstract-Endothelial dysfunction and cell loss are prominent features in cardiovascular disease. Endothelial progenitor cells (EPCs) originating from the bone marrow play a significant role in neovascularization of ischemic tissues and in re-endothelialization of injured blood vessels. Several studies have shown the therapeutic potential of EPC transplantation in rescue of tissue ischemia and in repair of blood vessels and bioengineering of prosthetic grafts. Recent small-scale trials have provided preliminary evidence of feasibility, safety, and efficacy in patients with myocardial and critical limb ischemia. However, several studies have shown that age and cardiovascular disease risk factors reduce the availability of circulating EPCs (CEPCs) and impair their function to varying degrees. In addition, the relative scarcity of CEPCs limits the ability to expand these cells in sufficient numbers for some therapeutic applications. Priority must be given to the development of strategies to enhance the number and improve the function of CEPCs. Furthermore, alternative sources of EPC such as chord blood need to be explored. Strategies for improvement of cell adhesion, survival, and prevention of cell senescence are also essential to ensure therapeutic viability. Genetic engineering of EPCs may be a useful approach to developing these cells into efficient therapeutic tools. In the clinical arena there is pressing need to standardize the protocols for isolation, culture, and therapeutic application of EPC. Large-scale multi-center randomized trials are required to evaluate the long-term safety and efficacy of EPC therapy. Despite these hurdles, the outlook for EPC-based therapy for cardiovascular disease is promising. (Hypertension. 2005;46:7-18.)

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Section: Epc and Cardiovascular Diseasesmentioning

confidence: 91%

Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases

et al. 2005

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“…Statistical analysis revealed that not only was CFU-EC concentration altered, but that the CFU-EC concentration reflected vascular health, since brachial artery reactivity increased with increasing CFU-EC concentration. Later studies demonstrated that the concentration of CFU-ECs was decreased in patients with type I diabetes, 48 chronic obstructive pulmonary disease, 49 congestive heart failure, 50 and rheumatoid arthritis. 51 However, some studies have contradicted the trend of lower numbers in disease susceptibility; CFU-EC concentration has been shown to be significantly increased in patients with unstable angina, 52 at the time of myocardial infarction (MI), 53 and within 7 days of an acute MI.…”

Section: Spotlightmentioning

confidence: 99%

Working hypothesis to redefine endothelial progenitor cells

et al. 2007

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“…8,9 Recently, advanced stages of heart failure were shown to be associated with reduced levels of cEPCs. 10 One study showed ICM was associated with selective impairment of progenitor cell function in the bone marrow and in the peripheral blood. 11 Endothelial cells can release microparticles after inflammatory stimulation, and the presence of increased levels of circulating endothelial-derived microparticles (cEMPs) has been documented in various pathologic conditions including coronary syndromes, in which they reflect endothelial dysfunction and are associated with a poor clinical outcome.…”

Section: Introductionmentioning

confidence: 99%

Effect of 40 mg Versus 10 mg of Atorvastatin on Oxidized Low‐Density Lipoprotein, High‐Sensitivity C‐Reactive Protein, Circulating Endothelial‐Derived Microparticles, and Endothelial Progenitor Cells in Patients With Ischemic Cardiomyopathy

Huang

Cheng

Xie

et al. 2012

Clinical Cardiology

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Background: There are few recent data to delineate the beyond lipids-decreased effect of statins and the effect of different doses of statins on endothelial-derived microparticles (EMPs) and circulating endothelial progenitor cells (EPCs) in patients with ischemic cardiomyopathy (ICM). Hypothesis: Statins might have the beyond lipids-decreased effect and there were different effects between different doses of statins on EMPs and circulating EPCs in patients with ICM. Methods: One hundred patients with ICM and 100 healthy examined people, who served as the normal control group, were recruited to this study. Patients were randomly divided into 2 groups: 10-mg atorvastatin group (n = 50) and 40-mg atorvastatin group (n = 50). All subjects were followed for 1 year. The levels of serum lipids, oxidized low-density lipoprotein (oxLDL), high-sensitivity C-reactive protein (hsCRP), circulating EPCs, and EMPs were examined in all subjects. The incidences of adverse reactions in the 2 study groups were determined. Results: At the beginning of this study, there were no significant differences in baseline characteristics between the 2 study groups. At the end of this study, the levels of total cholesterol, low-density lipoprotein, serum hsCRP, oxLDL, and circulating EMPs were significantly decreased; circulating EPCs were significantly increased in the 40-mg atorvastatin group compared to the 10-mg atorvastatin group, P < 0.05. The multivariate linear regression analysis indicated that receiving only 40 mg of atorvastatin had a significant effect on the levels of circulating EPCs (β = 0.252, P = 0.014). There were no significant differences in the adverse reactions between the 2 groups. Conclusions: Use of 40 mg of atorvastatin might decrease the levels of circulating EMPs and increase the number of circulating EPCs in patients with ICM in comparison with 10 mg of atorvastatin, and the effect might be independent of the decrease of lipids, oxLDL, and hsCRP. IntroductionStatins, serving as antiatherosclerosis drugs, can significantly decrease the rates of cardiovascular events in patients with coronary heart disease (CHD) and have been extensively administered in secondary prevention of CHD.

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CD34 ⁺ and Endothelial Progenitor Cells in Patients With Various Degrees of Congestive Heart Failure

Cited by 356 publications

References 16 publications

Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases

Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases

Working hypothesis to redefine endothelial progenitor cells

Effect of 40 mg Versus 10 mg of Atorvastatin on Oxidized Low‐Density Lipoprotein, High‐Sensitivity C‐Reactive Protein, Circulating Endothelial‐Derived Microparticles, and Endothelial Progenitor Cells in Patients With Ischemic Cardiomyopathy

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CD34 + and Endothelial Progenitor Cells in Patients With Various Degrees of Congestive Heart Failure

Cited by 356 publications

References 16 publications

Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases

Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases

Working hypothesis to redefine endothelial progenitor cells

Effect of 40 mg Versus 10 mg of Atorvastatin on Oxidized Low‐Density Lipoprotein, High‐Sensitivity C‐Reactive Protein, Circulating Endothelial‐Derived Microparticles, and Endothelial Progenitor Cells in Patients With Ischemic Cardiomyopathy

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CD34 ⁺ and Endothelial Progenitor Cells in Patients With Various Degrees of Congestive Heart Failure