Evidence map›Paper›PMID 33614751›Full record

ReviewFrontiers in cardiovascular medicine2021

Arrhythmogenic Mechanisms in Hypokalaemia: Insights From Pre-clinical Models.

Gary Tse, Ka Hou Christien Li, Chloe Kwong Yee Cheung, Konstantinos P Letsas, Aishwarya Bhardwaj, Abhishek C Sawant, Tong Liu, Gan-Xin Yan, Henggui Zhang, Kamalan Jeevaratnam and 3 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 24 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

13 authors at 12 institutions in 5 countries.

Gary TseTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China.
Ka Hou Christien LiFaculty of Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Chloe Kwong Yee CheungLi Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Konstantinos P LetsasSecond Department of Cardiology, Laboratory of Cardiac Electrophysiology, Evangelismos General Hospital of Athens, Athens, Greece.
Aishwarya BhardwajDivision of Cardiology, Department of Internal Medicine, State University of New York at Buffalo, Buffalo, NY, United States.
Abhishek C SawantDivision of Cardiology, Department of Internal Medicine, State University of New York at Buffalo, Buffalo, NY, United States.
Tong LiuTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China.
Gan-Xin YanLankenau Institute for Medical Research and Lankenau Medical Center, Wynnewood, PA, United States.
Henggui ZhangSchool of Physics and Astronomy, The University of Manchester, Manchester, United Kingdom.
Kamalan JeevaratnamFaculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom.
Nazish SayedStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, United States.
Shuk Han ChengDepartment of Biomedical Sciences, College of Veterinary Medicine and Life Science, City University of Hong Kong, Hong Kong, China.
Wing Tak WongSchool of Life Sciences, Chinese University of Hong Kong, Hong Kong, China.
University at Buffalo, State University of New York · USCardiovascular Institute of the South · USChinese University of Hong Kong · CNCity University of Hong Kong · HKEvangelismos Hospital · GRLankenau Medical Center · USNewcastle University · GBSecond Hospital of Tianjin Medical University · CNTianjin Medical University · CNUniversity of Hong Kong · HKUniversity of Manchester · GBUniversity of Surrey · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Potassium is the predominant intracellular cation, with its extracellular concentrations maintained between 3. 5 and 5 mM. Among the different potassium disorders, hypokalaemia is a common clinical condition that increases the risk of life-threatening ventricular arrhythmias. This review aims to consolidate pre-clinical findings on the electrophysiological mechanisms underlying hypokalaemia-induced arrhythmogenicity. Both triggers and substrates are required for the induction and maintenance of ventricular arrhythmias. Triggered activity can arise from either early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs). Action potential duration (APD) prolongation can predispose to EADs, whereas intracellular Ca

Indexed as

cardiac arrhythmiaconductionhypokalaemiapotassiumrepolarization

Identifiers

PMID33614751
PMCPMC7887296
OpenAlexW3126349158

What Socratic 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 Socratic graph.