The Structure‐function remodeling in rabbit hearts of myocardial infarction. Issue 12 (22nd June 2017)

• Record Type: Journal Article
• Authors: Wu, Haotian; Li, Li; Niu, Pei; Huang, Xu; Liu, Jinyi; Zhang, Fengshun; Shen, Wenzeng; Tan, Wenchang; Wu, Yiling; Huo, Yunlong
• Is Part Of: Physiological reports. Volume 5:Issue 12(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-06-22
• Subjects: Coronary arterial trees -- ischemic heart failure -- myocardial infarction -- rabbit model -- structure‐function remodeling; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.13311
• Languages: English
• ISSNs: 2051-817X

Abstract

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. Abstract : A novel rabbit model through multiple ligations of coronary arteries shows that vascular rarefaction and cardiac fibrosis relevant to inflammation occur simultaneously in vicinity of myocardial infarction, which is a risk factor for the vicious cycle of ischemia and heart failure.