Evidence map›Paper›PMID 33298102›Full record

ArticleJournal of translational medicine2020

Prophylactic, single-drug cardioprotection in a comparative, experimental study of doxorubicin-induced cardiomyopathy.

Mária Lódi, Viktor Bánhegyi, Beáta Bódi, Alexandra Gyöngyösi, Árpád Kovács, Anita Árokszállási, Nazha Hamdani, Miklós Fagyas, István Édes, Zoltán Csanádi and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 14 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

17 authors at 2 institutions in 2 countries.

Mária LódiDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Viktor BánhegyiDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Beáta BódiDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Alexandra GyöngyösiDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
Árpád KovácsDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Anita ÁrokszállásiDepartment of Oncology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Nazha HamdaniDepartment of Molecular and Experimental Cardiology, Ruhr University Bochum, Bochum, Germany.
Miklós FagyasDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
István ÉdesDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zoltán CsanádiDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
István CzurigaDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zoltán KisvárdayDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
István LekliDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
Péter BaiMTA-DE Lendület Laboratory of Cellular Metabolism, Debrecen, Hungary.
Attila TóthDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zoltán PappDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Dániel CzurigaDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. dczuriga@med.unideb.hu.ORCID 0000-0002-6972-0781
University of Debrecen · HUSt. Josef-Hospital · DE

Funding

European Union EFOP-3.6.2-16-2017-00006European Union GINOP-2.3.2-15-2016-00043János Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00523/16/5Nemzeti Kutatási, Fejlesztési és Innovaciós Alap NKFIH-1150-6/2019, K123975
6 · The paper itself

Abstract

backgroundCardiomyopathy is a common side effect of doxorubicin (DOX) chemotherapy. Despite intensive research efforts in the field, there is still no evidence available for routine cardioprotective prophylaxis to prevent cardiotoxicity in the majority of oncological patients at low risk of cardiovascular disease. We have recently demonstrated the advantages of a prophylactic, combined heart failure therapy in an experimental model of DOX-induced cardiomyopathy. In the current work, we focus on individually applied prophylactic medications studied in the same translational environment to clarify their distinct roles in the prevention of DOX cardiotoxicity.

methodsTwelve-week-old male Wistar rats were divided into 5 subgroups. Prophylactic β-blocker (BB, bisoprolol), angiotensin-converting enzyme inhibitor (ACEI, perindopril) or aldosterone antagonist (AA, eplerenone) treatments were applied 1 week before DOX administration, then 6 cycles of intravenous DOX chemotherapy were administered. Rats receiving only intravenous DOX or saline served as positive and negative controls. Blood pressure, heart rate, body weight, and echocardiographic parameters were monitored in vivo. Two months after the last DOX administration, the animals were sacrificed, and their heart and serum samples were frozen in liquid nitrogen for histological, mechanical, and biochemical measurements.

resultsAll prophylactic treatments increased the survival of DOX-receiving animals. The lowest mortality rates were seen in the BB and ACEI groups. The left ventricular ejection fraction was only preserved in the BB group. The DOX-induced increase in the isovolumetric relaxation time could not be prevented by any prophylactic treatment. A decreased number of apoptotic nuclei and a preserved myocardial ultrastructure were found in all groups receiving prophylactic cardioprotection, while the DOX-induced fibrotic remodelling and the increase in caspase-3 levels could only be substantially prevented by the BB and ACEI treatments.

conclusionPrimary prophylaxis with cardioprotective agents like BB or ACEI has a key role in the prevention of DOX-induced cardiotoxicity in healthy rats. Future human studies are necessary to implement this finding in the clinical management of oncological patients free of cardiovascular risk factors.

Indexed as

CardiomyopathiesPharmaceutical PreparationsAnimalsDoxorubicinHumansMaleRatsRats, WistarStroke VolumeVentricular Function, LeftDoxorubicinPharmaceutical PreparationsAnimal modelAnthracyclineCardiotoxicityDoxorubicinHeart failure

Identifiers

PMID33298102
PMCPMC7725221
OpenAlexW3111604815

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.