Evidence map›Paper›PMID 29422093›Full record

ReviewCardiovascular diabetology2018

Reduced coronary collateralization in type 2 diabetic patients with chronic total occlusion.

Ying Shen, Feng Hua Ding, Yang Dai, Xiao Qun Wang, Rui Yan Zhang, Lin Lu, Wei Feng Shen

Open access · goldAbstract readReview
In one paragraph

Review in Cardiovascular diabetology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
12.5field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 91 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ying ShenDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.
Feng Hua DingDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.
Yang DaiInstitute of Cardiovascular Disease, Shanghai Jiao Tong University School of Medicine, 197 Rui Jin Road II, Shanghai, 200025, People's Republic of China.
Xiao Qun WangDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.
Rui Yan ZhangDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.
Lin LuDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.
Wei Feng ShenDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China. rjshenweifeng@126.com.
Shanghai Jiao Tong University · CNRuijin Hospital · CN

Funding

Medico-engineering Project Shanghai ScienceMedico-engineering Project Technology CommitteeNational Natural Science Foundation of China 81400327Shanghai Science and Technology Committee 14ZR1425800Talent Young Investigators of Shanghai Jiao Tong University School of Medicine 17XJ11009
6 · The paper itself

Abstract

backgroundThe extent of coronary collateral formation is a primary determinant of the severity of myocardial damage and mortality after coronary artery occlusion. Type 2 diabetes mellitus (T2DM) represents an important risk factor for impaired collateral vessel growth. However, the mechanism of reduced coronary collateralization in type 2 diabetic patients remains unclear.

methodsWith the reference to the recent researches, this review article describes the pathogenic effects of T2DM on collateral development and outlines possible clinical and biochemical markers associated with reduced coronary collateralization in type 2 diabetic patients with chronic total occlusion (CTO).

resultsDiffuse coronary atherosclerosis in T2DM reduces pressure gradient between collateral donor artery and collateral recipient one, limiting collateral vessel growth and function. An interaction between advanced glycation end-products and their receptor activates several intracellular signaling pathways, enhances oxidative stress and aggravates inflammatory process. Diabetic condition decreases pro-angiogenic factors especially vascular endothelial growth factor and other collateral vessel growth related parameters. Numerous clinical and biochemical factors that could possibly attenuate the development of coronary collaterals have been reported. Increased serum levels of glycated albumin, cystatin C, and adipokine C1q tumor necrosis factor related protein 1 were associated with poor coronary collateralization in type 2 diabetic patients with stable coronary artery disease and CTO. Diastolic blood pressure and stenosis severity of the predominant collateral donor artery also play a role in coronary collateral formation.

conclusionsT2DM impairs collateral vessel growth through multiple mechanisms involving arteriogenesis and angiogenesis, and coronary collateral formation in patients with T2DM and CTO is influenced by various clinical, biochemical and angiographic factors. This information provides insights into the understanding of coronary pathophysiology and searching for potential new therapeutic targets in T2DM.

Indexed as

Collateral CirculationCoronary CirculationNeovascularization, PathologicAnimalsCoronary Artery DiseaseCoronary OcclusionCoronary VesselsDiabetes Mellitus, Type 2Diabetic AngiopathiesGlycation End Products, AdvancedHumansInflammation MediatorsOxidative StressPrognosisReceptor for Advanced Glycation End ProductsRisk FactorsAGER protein, humanGlycation End Products, AdvancedInflammation MediatorsReceptor for Advanced Glycation End ProductsVascular Endothelial Growth Factor AVEGFA protein, humanChronic total occlusionCoronary artery diseaseCoronary collateral circulationType 2 diabetes mellitus

Identifiers

PMID29422093
PMCPMC5804044
OpenAlexW2803397956

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.