Pentoxifylline reduces inflammation and prevents myocardial perfusion derangements in experimental chronic Chagas' cardiomyopathy.

Chronic Chagas cardiomyopathy coronary microcirculation hamsters inflammation ventricular dysfunction

Journal

Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology
ISSN: 1532-6551
Titre abrégé: J Nucl Cardiol
Pays: United States
ID NLM: 9423534

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 09 09 2022
accepted: 14 03 2023
medline: 21 1 2024
pubmed: 21 1 2024
entrez: 20 1 2024
Statut: ppublish

Résumé

Myocardial perfusion defect (MPD) is common in chronic Chagas cardiomyopathy (CCC) and is associated with inflammation and development of left ventricular systolic dysfunction. We tested the hypothesis that pentoxifylline (PTX) could reduce inflammation and prevent the development of MPD in a model of CCC in hamsters. We investigated with echocardiogram and rest myocardial perfusion scintigraphy at baseline (6-months after T. cruzi infection/saline) and post-treatment (after additional 2-months of PTX/saline administration), female Syrian hamsters assigned to 3 groups: T. cruzi-infected animals treated with PTX (CH + PTX) or saline (CH + SLN); and uninfected control animals (CO). At the baseline, all groups showed similar left ventricular ejection fraction (LVEF) and MPD areas. At post-treatment evaluation, there was a significant increase of MPD in CH + SLN group (0.8 ± 1.6 to 9.4 ± 9.7%), but not in CH + PTX (1.9 ± 3.0% to 2.7 ± 2.7%) that exhibited MPD area similar to CO (0.0 ± 0.0% to 0.0 ± 0.0%). The LVEF decreased in both infected groups. Histological analysis showed a reduced inflammatory infiltrate in CH + PTX group (395.7 ± 88.3 cell/mm The prolonged use of PTX is associated with positive effects, including prevention of MPD development and reduction of inflammation in the chronic hamster model of CCC.

Sections du résumé

BACKGROUND BACKGROUND
Myocardial perfusion defect (MPD) is common in chronic Chagas cardiomyopathy (CCC) and is associated with inflammation and development of left ventricular systolic dysfunction. We tested the hypothesis that pentoxifylline (PTX) could reduce inflammation and prevent the development of MPD in a model of CCC in hamsters.
METHODS AND RESULTS RESULTS
We investigated with echocardiogram and rest myocardial perfusion scintigraphy at baseline (6-months after T. cruzi infection/saline) and post-treatment (after additional 2-months of PTX/saline administration), female Syrian hamsters assigned to 3 groups: T. cruzi-infected animals treated with PTX (CH + PTX) or saline (CH + SLN); and uninfected control animals (CO). At the baseline, all groups showed similar left ventricular ejection fraction (LVEF) and MPD areas. At post-treatment evaluation, there was a significant increase of MPD in CH + SLN group (0.8 ± 1.6 to 9.4 ± 9.7%), but not in CH + PTX (1.9 ± 3.0% to 2.7 ± 2.7%) that exhibited MPD area similar to CO (0.0 ± 0.0% to 0.0 ± 0.0%). The LVEF decreased in both infected groups. Histological analysis showed a reduced inflammatory infiltrate in CH + PTX group (395.7 ± 88.3 cell/mm
CONCLUSIONS CONCLUSIONS
The prolonged use of PTX is associated with positive effects, including prevention of MPD development and reduction of inflammation in the chronic hamster model of CCC.

Identifiants

pubmed: 38245038
pii: S1071-3581(24)00173-9
doi: 10.1007/s12350-023-03270-y
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2327-2337

Informations de copyright

Copyright © 2023 American Society of Nuclear Cardiology. Published by ELSEVIER INC. All rights reserved.

Auteurs

Denise Mayumi Tanaka (DM)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Camila Godoy Fabricio (CG)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

José A Marin-Neto (JA)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Antônio Carlos Leite de Barros Filho (ACL)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Luciano Fonseca Lemos de Oliveira (LFL)

Department of Applied Physical Therapy, Institute of Health Sciences, Federal University of Triangulo Mineiro, Uberaba, Brazil.

Jorge Mejia (J)

Hospital Israelita Albert Einstein, Sao Paulo, Brazil.

Rafael Ribeiro Almeida (RR)

Faculty of Medicine, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil.

Raquel de Souza Vieira (R)

Faculty of Medicine, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil.

Carla Duque Lopes (CD)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Sabrina Setembre Batah (SS)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Henrique Turin Moreira (HT)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Maria de Lourdes Higuchi (M)

Faculty of Medicine, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil.

Edecio Cunha Neto (EC)

Faculty of Medicine, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil.

Alexandre Todorovic Fabro (AT)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Stephan G Nekolla (SG)

Department of Nuclear Medicine at Technische Universität, Munich, Germany.

Minna Moreira Dias Romano (MMD)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.

Marcus Vinícius Simões (MV)

Medical School of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil; Cardiology Division, Internal Medicine Department, Hospital das Clínicas, Faculdade de Medicina de Ribeirão Preto, 3900 Bandeirantes Avenue, Ribeirão Preto, 14048900, São Paulo, Brazil. Electronic address: msimoes@fmrp.usp.br.

Classifications MeSH