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Research paper
Published online: 2019-05-13
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Pretreatment with antiplatelet drugs improves the cardiac function after myocardial infarction without reperfusion in a mouse model

Kandi Zhang, Wenlong Yang, Mingliang Zhang, Yaping Sun, Tiantian Zhang, Junling Liu, Junfeng Zhang
DOI: 10.5603/CJ.a2019.0051
·
Pubmed: 31106840

open access

Ahead of print
Original articles
Published online: 2019-05-13

Abstract

Background: Reperfusion therapy is known to improve prognosis and limit myocardial damage after myocardial infarction (MI). The administration of antiplatelet drugs prior to percutaneous coronary intervention also proves beneficial to patients with acute MI (AMI). However, a good number of AMI patients do not receive reperfusion therapy, and it is not clear if they would benefit from antiplatelet pre-treatment.

Methods: Experimental C57BL/6 mice were randomly allocated to five groups: the sham group, control, post-treatment, pre-treatment, and pre- and post-treatment groups. Aspirin (15 mg/kg), clopidogrel (11 mg/kg), ticagrelor (27 mg/kg), and prasugrel (1.5 mg/kg) were intragastrically administered in the treatment groups. On day 7 post MI, cardiac function and cardiac fibrosis were evaluated using echocardiography and Masson’s Trichrome staining respectively. Histopathological examinations were performed on tissue sections to grade inflammatory cell infiltration. Platelet inhibition was monitored by measuring thrombin-induced platelet aggregation.

Results: Left ventricular ejection fraction and fractional shortening improved significantly (p < 0.01) in the pre-treatment groups when compared to the post-treatment and control groups. A significant (p < 0.01) decrease in cardiac fibrosis was observed in the pre-treatment group, compared with the post-treatment and control groups. Inflammatory cell infiltration significantly decreased in the pre-treatment group compared with the control group (p < 0.05). Thrombin-induced platelet aggregation was significantly inhibited by antiplatelet drugs, but increased with the exposure to H2O2.

Conclusions: In the absence of reperfusion therapy, pre-treatment with antiplatelet drugs successfully improved cardiac function, reduced cardiac fibrosis and inflammatory cell infiltration, and inhibited oxidative stress-induced platelet aggregation after MI in the mouse model.

Abstract

Background: Reperfusion therapy is known to improve prognosis and limit myocardial damage after myocardial infarction (MI). The administration of antiplatelet drugs prior to percutaneous coronary intervention also proves beneficial to patients with acute MI (AMI). However, a good number of AMI patients do not receive reperfusion therapy, and it is not clear if they would benefit from antiplatelet pre-treatment.

Methods: Experimental C57BL/6 mice were randomly allocated to five groups: the sham group, control, post-treatment, pre-treatment, and pre- and post-treatment groups. Aspirin (15 mg/kg), clopidogrel (11 mg/kg), ticagrelor (27 mg/kg), and prasugrel (1.5 mg/kg) were intragastrically administered in the treatment groups. On day 7 post MI, cardiac function and cardiac fibrosis were evaluated using echocardiography and Masson’s Trichrome staining respectively. Histopathological examinations were performed on tissue sections to grade inflammatory cell infiltration. Platelet inhibition was monitored by measuring thrombin-induced platelet aggregation.

Results: Left ventricular ejection fraction and fractional shortening improved significantly (p < 0.01) in the pre-treatment groups when compared to the post-treatment and control groups. A significant (p < 0.01) decrease in cardiac fibrosis was observed in the pre-treatment group, compared with the post-treatment and control groups. Inflammatory cell infiltration significantly decreased in the pre-treatment group compared with the control group (p < 0.05). Thrombin-induced platelet aggregation was significantly inhibited by antiplatelet drugs, but increased with the exposure to H2O2.

Conclusions: In the absence of reperfusion therapy, pre-treatment with antiplatelet drugs successfully improved cardiac function, reduced cardiac fibrosis and inflammatory cell infiltration, and inhibited oxidative stress-induced platelet aggregation after MI in the mouse model.

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Keywords

antiplatelet drugs, pre-treatment, myocardial infarction, cardiac function, reperfusion therapy

About this article
Title

Pretreatment with antiplatelet drugs improves the cardiac function after myocardial infarction without reperfusion in a mouse model

Journal

Cardiology Journal

Issue

Ahead of print

Article type

Research paper

Published online

2019-05-13

DOI

10.5603/CJ.a2019.0051

Pubmed

31106840

Keywords

antiplatelet drugs
pre-treatment
myocardial infarction
cardiac function
reperfusion therapy

Authors

Kandi Zhang
Wenlong Yang
Mingliang Zhang
Yaping Sun
Tiantian Zhang
Junling Liu
Junfeng Zhang

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