Mesenquimal stem cell transplantation can reduce induced ventricular arrhythmias in rats with myocardial infarction?

• Grant number: 21/05084-4
• Support Opportunities: Regular Research Grants
• Duration: November 01, 2021 - October 31, 2023
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Andrey Jorge Serra
• Grantee: Andrey Jorge Serra
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
• Associated researchers: Luís Felipe Neves dos Santos

Abstract

Myocardial infarction (MI) causes irreversible loss of cardiomyocytes with replacement by fibrous tissue, resulting in adverse cardiac remodeling and heart failure (HF). This is ideal for the development of complex ventricular arrhythmias and, consequently, ventricular tachycardia (VT) and fibrillation (VF) is routine in clinical practice. In recent years, considering the well-documented effects of mesenchymal stem cells (MSCs) on cardiac remodeling, the hypothesis of using cell therapy as an antiarrhythmic intervention after MI has been suggested. Although some studies have illustrated benefits of MSCs, other researchers have documented pro-arrhythmic effects or no action of the therapy. In addition, it is not yet known whether the possible antiarrhythmic effects of MSCs are present in the acute phase of MI, during congestive heart failure or both. Therefore, the study proposed to FAPESP was designed to examine the arrhythmogenic pattern in the hearts of infarcted rats subjected to transplantation of adipose tissue-derived MSCs (AMSCs). To evaluate the actions of cell therapy in the temporal course of the disease, rats with large infarctions will receive an AMSCs transplant three and thirty days after coronary occlusion, respectively. The electrical events will be recorded by means of a surface electrocardiogram and an octopolar catheter implanted inside the left ventricular. Which makes it possible to induce and register ventricular arrhythmias. To substantiate the results found, we will analyze the myocardial content of different types of collagen, connexins and inflammatory cytokines well-known to be involved in the genesis of post-MI arrhythmia. Moreover, the study of myocardial oxidative stress as a valid analysis in our experiments. (AU)