Evidence map›Paper›PMID 32116766›Full record

ReviewFrontiers in physiology2020

Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?

Xuan Shi, Jie Gao, Qiushi Lv, Haodi Cai, Fang Wang, Ruidong Ye, Xinfeng Liu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 4 pooled it
12.0field-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

112 citing papers in PubMed, 4 syntheses or guidelines pooled it, 170 citations in OpenAlex.

  1. Pooled it
  2. Vascular medicine (London, England) · 2025
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  19. The international journal of cardiovascular imaging · 2025
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52 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Xuan ShiDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, China.
Jie GaoDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, China.
Qiushi LvDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, China.
Haodi CaiDepartment of Neurology, Jinling Hospital, Southeast University, Nanjing, China.
Fang WangDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Ruidong YeDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, China.
Xinfeng LiuDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNNanjing General Hospital of Nanjing Military Command · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcification is a clinical marker of atherosclerosis. This review focuses on recent findings on the association between calcification and plaque vulnerability. Calcified plaques have traditionally been regarded as stable atheromas, those causing stenosis may be more stable than non-calcified plaques. With the advances in intravascular imaging technology, the detection of the calcification and its surrounding plaque components have evolved. Microcalcifications and spotty calcifications represent an active stage of vascular calcification correlated with inflammation, whereas the degree of plaque calcification is strongly inversely related to macrophage infiltration. Asymptomatic patients have a higher content of plaque calcification than that in symptomatic patients. The effect of calcification might be biphasic. Plaque rupture has been shown to correlate positively with the number of spotty calcifications, and inversely with the number of large calcifications. There may be certain stages of calcium deposition that may be more atherogenic. Moreover, superficial calcifications are independently associated with plaque rupture and intraplaque hemorrhage, which may be due to the concentrated and asymmetrical distribution of biological stress in plaques. Conclusively, calcification of differential amounts, sizes, shapes, and positions may play differential roles in plaque homeostasis. The surrounding environments around the calcification within plaques also have impacts on plaque homeostasis. The interactive effects of these important factors of calcifications and plaques still await further study.

Indexed as

atherosclerosiscalcificationinflammationoptical coherence tomographypathologyplaque

Identifiers

PMID32116766
PMCPMC7013039
OpenAlexW3004961890

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.