Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits.

Patricia Genovés,Irene Del Canto,Carlos Soler,Francisco J Chorro,Luis Such-Miquel,Eva Blanch,Antonio Alberola,Luis Such,Germán Parra,Óscar J Arias-Mutis,Manuel Zarzoso,Ana Díaz

doi:10.3390/ani10091576

Abstract

A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.

Highlights

Cardiovascular disease, especially ischemic heart disease, is the leading cause of death nowadays [1,2,3,4,5], and global medium-term projections still consider ischemic heart disease as the most frequent [6]
It is of interest to investigate the mechanisms implicated in its occurrence, which, in most cases, are related to the induction of malignant ventricular arrhythmias, such as ventricular tachycardia (VT) or fibrillation (VF)
The intergroup comparisons showed that the troponin T (TnT) levels were significantly higher in the acute myocardial infarction (AMI) group than in the sham group at 60 min of reperfusion (p = 0.003, r = 0.692)

Summary

Introduction

Cardiovascular disease, especially ischemic heart disease, is the leading cause of death nowadays [1,2,3,4,5], and global medium-term projections still consider ischemic heart disease as the most frequent [6]. The use of animal models to study ischemic heart disease and, the phenomena that characterize the processes of myocardial ischemia and reperfusion has provided a wide range of information This information covers the molecular mechanisms and signaling pathways involved in the development of myocardial damage to the local and general regulatory mechanisms that can be modified to protect and limit the adverse consequences of the disease, including remodeling, ventricular dysfunction, cardiac arrhythmias, and sudden death [7,8,10,15,16,17,18,19,20,21,22,23,24]. Experimental models have provided valid information on the meaning, usefulness, and applications of various diagnostic and therapeutic techniques, including those based on cardiac imaging, recording of electrophysiological activity, and coronary intervention [13,15,26], which are all techniques that can improve patient care when used in clinical practice

Objectives

Methods

Results

Discussion

Conclusion