Evidence map›Paper›PMID 40409406›Full record

ArticleJournal of molecular and cellular cardiology2025

Colitis induced ventricular alternans increases the risk for ventricular arrhythmia.

Carlos H Pereira, Hiroki Kittaka, Edward J Ouille V, Jonathas F Q Almeida, Andrès F Pélaez, Ali Keshavarzian, Lothar A Blatter, Kathrin Banach

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular and cellular cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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.

Carlos H PereiraDepartment of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA. Electronic address: h85.carlos@gmail.com.
Hiroki KittakaDepartment of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA. Electronic address: Hiroki_Kittaka@rush.edu.
Edward J Ouille VDepartment of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA. Electronic address: Edward_J_OuilleV@rush.edu.
Jonathas F Q AlmeidaDepartment of Pharmacology & Toxicology, Virginia Commonwealth University, 1220 E. Broad St, Richmond, VA 23298, USA. Electronic address: jonathas.almeida@vcuhealth.org.
Andrès F PélaezDepartment of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA. Electronic address: Andres_F_Pelaez@rush.edu.
Ali KeshavarzianRush Center for Integrated Microbiome and Chronobiology Research and Dept. of Internal Medicine/Gastroenterology, Rush University Medical Center, 1725 W. Harrison St., Chicago, IL 60612, USA. Electronic address: Ali_Keshavarzian@rush.edu.
Lothar A BlatterDept. of Physiology & Biophysics, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA. Electronic address: Lothar_Blatter@rush.edu.
Kathrin BanachDepartment of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA. Electronic address: Kathrin_Banach@rush.edu.

Funding

Atrial Excitation-Contraction Coupling, Calcium Signaling and Electro-Mechanical AlternansR01HL164453 · RUSH UNIVERSITY MEDICAL CENTER · 2025 to 2025
$707k
IP3 receptor, NOX2 and calcium signaling domains in atrial physiology and pathophysiologyR01HL155762 · RUSH UNIVERSITY MEDICAL CENTER · 2025 to 2025
$674k
NHLBI NIH HHS R01 HL132871NHLBI NIH HHS R01 HL155762NHLBI NIH HHS R01 HL164453
6 · The paper itself

Abstract

Inflammatory bowel disease was linked to an increased risk for conduction defects and ventricular arrhythmia. It coincides with dysregulation of gut microbiota, increased inflammation, and deregulation of the renin-angiotensin system. In this study, we aimed to determine the mechanism of colitis-induced electrophysiological remodeling that increases the risk for ventricular arrhythmia. In a mouse model of dextran sulfate sodium induced active colitis (3.5 %, 7 days) cardiac electrophysiological properties were quantified during active inflammation. Electrocardiographic recordings exhibited a prolonged QT duration in mice with active colitis compared to control. Field potential (FP) recordings of Langendorff perfused colitis-hearts exhibited increased FP dispersion, a reduced threshold for ventricular alternans, and an increased propensity for spatially discordant alternans. The increased propensity for alternans was also reflected in isolated ventricular myocytes where Ca

Indexed as

Arrhythmias, CardiacColitisHeart VentriclesAction PotentialsAngiotensin IIAnimalsCalciumDextran SulfateDisease Models, AnimalElectrocardiographyMaleMiceMice, Inbred C57BLMyocytes, CardiacSarcoplasmic Reticulum Calcium-Transporting ATPasesAngiotensin IICalciumDextran SulfateSarcoplasmic Reticulum Calcium-Transporting ATPasesCalcium transient alternansExcitation-contraction couplingInflammatory bowel diseaseRenin-angiotensin systemVentricular alternans

Identifiers

PMID40409406
PMCPMC12355935

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.