ArticleInternal and emergency medicine2015
Left ventricular mass and progenitor cells in chronic heart failure patients.
Article in Internal and emergency medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Biomarkers in Heart Failure: A Review and a Wish.International journal of molecular sciences · 2025Review
- Endothelial Progenitor Cells: An Appraisal of Relevant Data from Bench to Bedside.International journal of molecular sciences · 2021Review
- Endothelial Progenitor Cells in Heart Failure: an Authentic Expectation for Potential Future Use and a Lack of Universal Definition.Journal of cardiovascular translational research · 2018Review
- Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the study was to evaluate the association between circulating (CPCs) and endothelial (EPCs) progenitor cells and left ventricular (LV) remodeling in chronic heart failure (HF). 85 HF patients, ranging 29-89 years, 83.5% males, 45.9% ischemic, NYHA functional class II-IV, with a LV ejection fraction ≤40% were studied. LV ejection fraction, LV end-diastolic and end-systolic (LVESV) volumes, LV mass and tricuspid annular plane systolic excursion (TAPSE) were evaluated, and, when indicated, indexed for body surface area (BSA). CPCs and EPCs number was assessed using flow cytometry. CPCs were defined as CD34+, CD133+ and CD34+/CD133+. EPCs, identified through their expression of KDR, were defined as CD34+/KDR+, CD133+/KDR+ and CD34+/CD133+/KDR+. All EPCs were negatively related to LVESV/BSA (r = -0.24, p = 0.02 for all EPC's populations), and to LVmass/BSA (CD34+KDR+; r = -0.30, p = 0.005; CD133+KDR+; r = -0.31, p = 0.004; CD34+CD133+KDR+; r = -0.29, p = 0.007). No differences in EPCs levels in relation to cardiovascular risk factors, medications, etiology, age or gender were observed. CPCs number was higher in women, and lower in ischemic patients. In logistic regression analyses, the low EPCs' number was associated with an increased likelihood of abnormal LVmass/BSA. CPCs proved to be higher and EPCs lower in patients with severely abnormal LVmass/BSA (gr/m(2), ≥122 in women and ≥149 in men). Our results suggest a correlation between LV remodeling and progenitor cells. This is noteworthy considering that it has been suggested that bone marrow-derived EPCs participate in cardiac regeneration and function recovery in the setting of progressive HF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.