Evidence map›Paper›PMID 32948843›Full record

ArticleLeukemia2021

IDH1/2 mutations in acute myeloid leukemia patients and risk of coronary artery disease and cardiac dysfunction-a retrospective propensity score analysis.

Badder Kattih, Amir Shirvani, Piroska Klement, Abel Martin Garrido, Razif Gabdoulline, Alessandro Liebich, Maximilian Brandes, Anuhar Chaturvedi, Timon Seeger, Felicitas Thol and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 53 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

19 authors at 4 institutions in 1 country.

Badder KattihDepartment of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.ORCID http://orcid.org/0000-0003-1324-5536
Amir ShirvaniDepartment of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Piroska KlementDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Abel Martin GarridoDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, Ludolf-Krehl-Strasse 7-11, 68167, Mannheim, Germany.
Razif GabdoullineDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Alessandro LiebichDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Maximilian BrandesDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Anuhar ChaturvediDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.ORCID http://orcid.org/0000-0002-9597-3010
Timon SeegerDepartment of Medicine III, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Felicitas TholDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Gudrun GöhringDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.
Brigitte SchlegelbergerDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.
Robert GeffersGenome Analytics, Helmholtz Center for Infection Research, Braunschweig, Germany.ORCID http://orcid.org/0000-0003-4409-016X
David JohnInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Udo BavendiekDepartment of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Johann BauersachsDepartment of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.ORCID http://orcid.org/0000-0002-9341-117X
Arnold GanserDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany.
Joerg Heineke *Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany. Joerg.Heineke@medma.uni-heidelberg.de.ORCID http://orcid.org/0000-0002-1541-3030
Michael Heuser *Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Carl-Neuberg Strasse 1, 30625, Hannover, Germany. heuser.michael@mh-hannover.de.ORCID http://orcid.org/0000-0001-5318-9044
Medizinische Hochschule Hannover · DEHeidelberg University · DEGoethe University Frankfurt · DEHelmholtz Centre for Infection Research · DE

Funding

European Research Council 638035
6 · The paper itself

Abstract

Clonal hematopoiesis of indeterminate potential (CHIP) is linked to leukemia gene mutations and associates with an increased risk for coronary artery disease and poor prognosis in ischemic cardiomyopathy. Two recurrently mutated genes in CHIP and adult acute myeloid leukemia (AML) encode for isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2). Global expression of mutant IDH2 in transgenic mice-induced dilated cardiomyopathy and muscular dystrophy. In this retrospective observational study, we investigated whether mutant IDH1/2 predisposes to cardiovascular disease in AML patients. Among 363 AML patients, IDH1 and IDH2 mutations were detected in 26 (7.2%) and 39 patients (10.7%), respectively. Mutant IDH1 patients exhibited a significantly higher prevalence of coronary artery disease (26.1% vs. 6.4%, p = 0.002). Applying inverse probability-weighting analysis, patients with IDH1/2 mutations had a higher risk for a declining cardiac function during AML treatment compared to IDH1/2 wild type patients [left ventricular ejection fraction pretreatment compared to 10 months after diagnosis: 59.2% to 41.9% (p < 0.001) vs 58.5% to 55.4% (p = 0.27), respectively]. Mechanistically, RNA sequencing and immunostaining in hiPS-derived cardiomyocytes indicated that the oncometabolite R-2HG exacerbated doxorubicin mediated cardiotoxicity. Evaluation of IDH1/2 mutation status may therefore help identifying AML patients at risk for cardiovascular complications during cytotoxic treatment.

Indexed as

AdolescentAdultAgedAged, 80 and overBiomarkers, TumorCoronary Artery DiseaseFemaleGenotypeHumansIsocitrate DehydrogenaseLeukemia, Myeloid, AcuteMaleMiddle AgedMutationPrognosisPropensity ScoreBiomarkers, TumorIDH1 protein, humanIDH2 protein, humanIsocitrate Dehydrogenase

Identifiers

PMID32948843
PMCPMC8102189
OpenAlexW3087584220

What OpenQuestion holds

Textmetadata
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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.