Evidence map›Paper›PMID 22733365›Full record

ReviewWiener medizinische Wochenschrift (1946)2012

Arrhythmia-associated cardiac Ca²(+) cycling proteins and gene mutations.

Simon Kochhäuser, Eric Schulze-Bahr, Uwe Kirchhefer

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Wiener medizinische Wochenschrift (1946), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Simon KochhäuserDivision of Experimental and Clinical Electrophysiology,Department of Cardiology and Angiology,University Hospital Münster,Albert-Schweitzer-Campus 1 (Gebäude A1),48149 Muenster, Germany. simon.kochhaeuser@ukmuenster.de
Eric Schulze-Bahr
Uwe Kirchhefer
University Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium is an important mediator in cardiac excitation and disorders in cardiac Ca(2+) homeostasis have great influence on the cardiac action potential. Therefore dysfunction in regulatory proteins that are involved in Ca(2+) handling can lead to the occurrence of severe arrhythmia. Although mutations in Ca(2+) regulating proteins are quite rare, they can offer general insights into arrhythmogenesis. Here, we briefly review some important aspects of arrhythmia-associated mutations in Ca(2+) regulating proteins with special emphasis to its associated pathophysiology.

Indexed as

MutationArrhythmias, CardiacAutistic DisorderBrugada SyndromeCalciumCalcium-Binding ProteinsCalcium Channels, L-TypeCalsequestrinCytosolDiastoleElectrocardiographyFemaleHomeostasisHumansLong QT SyndromeMaleCalciumCalcium-Binding ProteinsCalcium Channels, L-TypeCalsequestrinCASQ2 protein, humanRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum Calcium-Transporting ATPasesSodium-Calcium Exchanger

Identifiers

PMID22733365
OpenAlexW1824934807

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.