Evidence map›Paper›PMID 25973058›Full record

ArticleInternational journal of clinical and experimental pathology2015

Structural changes in the progression of atrial fibrillation: potential role of glycogen and fibrosis as perpetuating factors.

Ling Zhang, Bing Huang, Benjamin J Scherlag, Jerry W Ritchey, Abraham A Embi, Jialu Hu, Yuemei Hou, Sunny S Po

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Enhancing Fatty Acids OxidationFrontiers in pharmacology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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

8 authors at 7 institutions in 2 countries.

Ling ZhangArrhythmia Research Lab, First Affiliated Hospital of Xinjiang Medical University Urumqi, China.
Bing HuangDepartment of Cardiology, Renmin Hospital of Wuhan University Wuhan, China.
Benjamin J ScherlagHeart Rhythm Institute, University of Oklahoma Health Sciences Center Oklahoma City, Oklahoma, USA.
Jerry W RitcheyCenter for Veterinary Health Sciences, Oklahoma State University Stillwater, Oklahoma, USA.
Abraham A Embi13442 SW 102 Lane Miami, Florida, USA.
Jialu HuDepartment of Cardiovascular Diseases, Zhongshan Hospital Fudan University Shanghai, China.
Yuemei HouDepartment of Cardiovascular Diseases, The 6th People's Hospital affiliated to Shanghai Jiaotong University Shanghai, China.
Sunny S PoHeart Rhythm Institute, University of Oklahoma Health Sciences Center Oklahoma City, Oklahoma, USA.
University of Oklahoma Health Sciences Center · USCollege of Business and Technology · USFudan University · CNOklahoma State University · USShanghai Jiao Tong University · CNWuhan University · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies of the goat heart subjected to prolonged atrial pacing induced sustained atrial fibrillation (AF). Structural changes included marked accumulation of glycogen in atrial myocytes.

aimsIn the present study, we hypothesized that glycogen deposition in canine atrial myocytes promotes paroxysmal forms of AF and is involved in fibrosis development in the later stages of AF. MATERIAL &

methodsIn dogs under pentobarbital anesthesia, tissues were obtained from the right and left atrial appendages (LAA/RAA). Periodic acid Schiff (PAS) and Masson's trichrome staining of the LAA/RAA from normal dogs, and those subjected to atrial pacing induced AF for 48 h or 8 weeks determined glycogen and collagen concentrations, respectively, using morphometric analysis.

resultsAt baseline, there was a significant greater concentration of glycogen in the LAA than the RAA (P ≤ 0.05). Compared to the RAA, the LAA glycogen, was dense and locked against the intercalated discs. After pacing induced AF for 48 hours and 8 weeks there was a marked increase in glycogen deposition, significantly greater than in the baseline state (P ≤ 0.05). There was a similar and progressive increase in collagen concentrations in each group (P ≤ 0.05).

conclusionsThe differential in glycogen concentration, in conjunction with other factors, neural and electrophysiological, provide a basis for the greater propensity of the left atrium for paroxysmal AF, at baseline and 48 hours of pacing induced AF. The marked increase in collagen at 8 weeks of pacing provides a substrate for sustained AF. Evidence is presented linking glycogen accumulation and fibrosis as factors in the persistent forms of AF.

Indexed as

AnimalsAtrial AppendageAtrial FibrillationDisease ProgressionDogsFemaleFibrosisGlycogenHeart AtriaImage Processing, Computer-AssistedMaleGlycogenAtrial fibrillationfibrosisglycogen

Identifiers

PMID25973058
PMCPMC4396299
OpenAlexW2419105949

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.