Evidence map›Paper›PMID 17488770›Full record

ArticleHeart (British Cardiac Society)2007

Vascular endothelial function and circulating endothelial progenitor cells in patients with cardiac syndrome X.

Po-Hsun Huang, Yung-Hsiang Chen, Yuh-Lien Chen, Tao-Cheng Wu, Jaw-Wen Chen, Shing-Jong Lin

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Heart (British Cardiac Society), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Definitions and incidence of cardiac syndrome X: review and analysis of clinical data.Clinical research in cardiology : official journal of the German Cardiac Society · 2010
    Pooled it
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  6. Circulating endothelial progenitor cell dysfunction in patients with bipolar disorder.European archives of psychiatry and clinical neuroscience · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Po-Hsun HuangInstitute of Clinicial Medicine and [corrected] Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan.
Yung-Hsiang Chen
Yuh-Lien Chen
Tao-Cheng Wu
Jaw-Wen Chen
Shing-Jong Lin
National Yang Ming Chiao Tung University · TWNational Yang Ming University Hospital · TWInstitute of Pharmacology · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial dysfunction and microvascular abnormalities have been reported in patients with cardiac syndrome X (CSX), but the underlying mechanisms are unclear. Recent insights suggest that the injured endothelial monolayer is regenerated by circulating bone marrow-derived endothelial progenitor cells (EPCs).

aimTo test the hypothesis that the biology of altered EPCs might contribute to the pathophysiology of CSX.

methods34 subjects (mean (SD) age: 62 (7) years) were enrolled in the study, including 12 patients with CSX, 12 stable subjects with coronary artery disease (CAD) and 10 healthy controls. The number and adhesive function of EPCs were measured in peripheral-blood samples from these study participants.

resultsThe baseline characteristics in patients with CSX and CAD were enhanced Framingham risk scores, more hypertension and lower high-density lipoproteins than the controls. Patients with CSX and CAD had significantly decreased endothelium-dependent flow-mediated vasodilation (FMD) compared with normal controls (normal controls vs CSX vs CAD: 10.6% (3.5%) vs 6.1% (1.8%) vs 4.1% (1.9%), p<0.001), but the difference was not found in endothelium-independent nitroglycerine-mediated vasodilation (p = 0.159). Reduced numbers of colony-forming units (CFU) of EPCs were noted in patients with CSX and CAD (normal vs CSX vs CAD: 41 (9) vs 30 (7) vs 14 (7) CFU/well, p<0.001). Levels of EPCs were shown to be associated with FMD (r = 0.557, p = 0.001) and high-density lipoprotein (r = 0.339, p = 0.049). Also, attenuated fibronectin adhesion function of EPCs was found in patients with CSX and CaD compared with normal subjects (104 (12) vs 80 (20) vs 65 (13)/well, p<0.001).

conclusionsThis study clearly showed for the first time that compared with normal subjects, patients with CSX have decreased levels and adhesive function of circulating EPCs. These findings may explain the underlying mechanisms which contribute to the endothelial dysfunction and microvascular abnormalities observed in patients with CSX.

Indexed as

AgedCell AdhesionCells, CulturedColony-Forming Units AssayCoronary DiseaseC-Reactive ProteinDose-Response Relationship, DrugEndothelial CellsEndothelium, VascularExerciseFemaleHumansMaleMicrovascular AnginaMiddle AgedStem CellsC-Reactive ProteinTumor Necrosis Factor-alpha

Identifiers

PMID17488770
PMCPMC1954999
OpenAlexW2142220820

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.