The Structure-function remodeling in rabbit hearts of myocardial infarction.

Haotian Wu,Fengshun Zhang,Pei Niu,Yunlong Huo,Xu Huang,Wenchang Tan,Li Li,Wenzeng Shen,Yiling Wu,Jinyi Liu

doi:10.14814/phy2.13311

Haotian Wu, Fengshun Zhang + Show 8 more

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https://doi.org/10.14814/phy2.13311

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Abstract

Animal models are of importance to investigate basic mechanisms for ischemic heart failure (HF). The objective of the study was to create a rabbit model through multiple coronary artery ligations to investigate the postoperative structure‐function remodeling of the left ventricle (LV) and coronary arterial trees. Here, we hypothesize that the interplay of the degenerated coronary vasculature and increased ventricle wall stress relevant to cardiac fibrosis in vicinity of myocardial infarction (MI) precipitates the incidence and progression of ischemic HF. Echocardiographic measurements showed an approximately monotonic drop of fractional shortening and ejection fraction from 40% and 73% down to 28% and 58% as well as persistent enlargement of LV cavity and slight mitral regurgitation at postoperative 12 weeks. Micro‐CT and histological measurements showed that coronary vascular rarefaction and cardiac fibrosis relevant to inflammation occurred concurrently in vicinity of MI at postoperative 12 weeks albeit there was compensatory vascular growth at postoperative 6 weeks. These findings validate the proposed rabbit model and prove the hypothesis. The post‐MI rabbit model can serve as a reference to test various drugs for treatment of ischemic HF.

Highlights

Heart failure (HF) is caused by cardiovascular diseases, for example, myocardial ischemia and infarction, hypertension, valvular heart diseases, etc (Hunt et al 2005)
Since rabbit models are less expensive than large animal models, show similarities to the human heart, and allow the sequential evaluation of hemodynamic parameters and organ function (Ezzaher et al 1992; Muders and Elsner 2000), myocardial infarction induced by a distal ligation of left circumflex artery (LCx) in rabbits has become the gold standard in the study of ischemic HF (Mahaffey et al 1995; White et al 2000; Edwards et al 2002; Ziv et al 2012)
The postmyocardial infarction rabbit model develops a region of complete akinesis only near the apical region of left ventricle (LV) and limits the study of HF resulting from myocardial infarction on the anterior and lateral walls of the LV

Summary

Introduction

Heart failure (HF) is caused by cardiovascular diseases, for example, myocardial ischemia and infarction, hypertension, valvular heart diseases, etc (Hunt et al 2005). Since rabbit models are less expensive than large animal models, show similarities to the human heart, and allow the sequential evaluation of hemodynamic parameters and organ function (Ezzaher et al 1992; Muders and Elsner 2000), myocardial infarction induced by a distal ligation of left circumflex artery (LCx) in rabbits has become the gold standard in the study of ischemic HF (Mahaffey et al 1995; White et al 2000; Edwards et al 2002; Ziv et al 2012). The postmyocardial infarction (post-MI) rabbit model develops a region of complete akinesis only near the apical region of LV and limits the study of HF resulting from myocardial infarction on the anterior and lateral walls of the LV

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