6533b7d8fe1ef96bd126a3bb

RESEARCH PRODUCT

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

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Simple Summary Ischemic heart disease is one of the leading causes of death. A series of processes occur during acute myocardial infarction that contribute to the development of ventricular dysfunction, with subsequent heart failure and ventricular arrhythmias, which account for most episodes of sudden cardiac death in these patients. These complications are associated with the adverse cardiac remodeling that occurs during the healing process following an acute episode. The remodeling causes the appearance of a substrate that can trigger life-threatening arrhythmias, such as tachycardia and/or ventricular fibrillation. The development of experimental models for analyzing the basic mechanisms involved in the pathophysiology of myocardial infarction enables the study of different therapeutic approaches aimed at improving the patient´s prognosis. The present study describes the methodology and the results obtained in a 5-week chronic infarction (one hour followed by reperfusion) in a rabbit model. The viability of the model, the care provided, the characteristics and extent of the lesions, the inducibility of arrhythmias, and the reproducibility of the methods and results have been analyzed. 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.