Evidence map›Paper›PMID 25445234›Full record

ReviewClinical biochemistry2015

Use of biomarkers for the assessment of chemotherapy-induced cardiac toxicity.

Eric S Christenson, Theodore James, Vineet Agrawal, Ben H Park

Open access · greenAbstract readReview
In one paragraph

Review in Clinical biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 125 citations in OpenAlex.

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  14. Global longitudinal strain: an early marker for cardiotoxicity in patients treated for breast cancer.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2023
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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

4 authors at 1 institution in 1 country.

Eric S ChristensonJohns Hopkins University, Department of Medicine, Baltimore, MD 21287, USA. Electronic address: echris14@jhmi.edu.
Theodore JamesJohns Hopkins University, Department of Medicine, Baltimore, MD 21287, USA.
Vineet AgrawalJohns Hopkins University, Department of Medicine, Baltimore, MD 21287, USA.
Ben H ParkJohns Hopkins University, Department of Oncology, Baltimore, MD 21287, USA.
Johns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

objectivesTo review the evidence for the use of various biomarkers in the detection of chemotherapy associated cardiac damage. DESIGN AND

methodsPubmed.gov was queried using the search words chemotherapy and cardiac biomarkers with the filters of past 10years, humans, and English language. An emphasis was placed on obtaining primary research articles looking at the utility of biomarkers for the detection of chemotherapy-mediated cardiac injury.

resultsBiomarkers may help identify patients undergoing treatment who are at high risk for cardiotoxicity and may assist in identification of a low risk cohort that does not necessitate continued intensive screening. cTn assays are the best studied biomarkers in this context and may represent a promising and potentially valuable modality for detecting cardiac toxicity in patients undergoing chemotherapy. Monitoring cTnI levels may provide information regarding the development of cardiac toxicity before left ventricular dysfunction becomes apparent on echocardiography or via clinical symptoms. A host of other biomarkers have been evaluated for their utility in the field of chemotherapy related cardiac toxicity with intermittent success; further trials are necessary to determine what role they may end up playing for prediction and prognostication in this setting.

conclusionsBiomarkers represent an exciting potential complement or replacement for echocardiographic monitoring of chemotherapy related cardiac toxicity which may allow for earlier realization of the degree of cardiac damage occurring during treatment, creating the opportunity for more timely modulation of therapy.

Indexed as

AnimalsAntineoplastic AgentsBiomarkersCardiotoxicityHeart DiseasesHumansNatriuretic Peptide, BrainTroponin ITroponin TAntineoplastic AgentsBiomarkersNatriuretic Peptide, BrainTroponin ITroponin TAnthracyclinesCardiac toxicityChemotherapyNatriuretic peptidesTroponin

Identifiers

PMID25445234
PMCPMC4363159
OpenAlexW2017624575

What OpenQuestion holds

Textmetadata
LicenceTDM
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.