Changes in the spatial distribution of the Purkinje network after acute myocardial infarction in the pig

Autores de INCLIVA

• Maria Teresa Izquierdo De Francisco

  Autor

• César Rios Navarro

  Autor

• 

  Vicent Bodí Peris

  Autor

• 

  Francisco Javier Chorro Gascó

  Autor

• 

  Amparo Ruiz Sauri

  Autor

Participantes ajenos a INCLIVA

• Garcia-Bustos, V
• Sebastian, R

Grupos y Plataformas de I+D+i

• Grupo de Investigación en Electrofisiología cardiaca experimental

  

  Leading Researcher

  Antonio M. Alberola Aguilar

• Grupo de Investigación en Histopatología e Ingeniería Tisular

  

  Leading Researcher

  Manuel Mata Roig

• Grupo de Investigación Traslacional en Cardiopatía Isquémica

  

  Leading Researcher

  Vicent Bodí Peris

Abstract

Purkinje cells (PCs) are more resistant to ischemia than myocardial cells, and are suspected to participate in ventricular arrhythmias following myocardial infarction (MI). Histological studies afford little evidence on the behavior and adaptation of PCs in the different stages of MI, especially in the chronic stage, and no quantitative data have been reported to date beyond subjective qualitative depictions. The present study uses a porcine model to present the first quantitative analysis of the distal cardiac conduction system and the first reported change in the spatial distribution of PCs in three representative stages of MI: an acute model both with and without reperfusion; a subacute model one week after reperfusion; and a chronic model one month after reperfusion. Purkinje cells are able to survive after 90 minutes of ischemia and subsequent reperfusion to a greater extent than cardiomyocytes. A decrease is observed in the number of PCs, which suffer reversible subcellular alterations such as cytoplasm vacuolization, together with redistribution from the mesocardium-the main localization of PCs in the heart of ungulate species-towards the endocardium and perivascular epicardial areas. However, these changes mainly occur during the first week after ischemia and reperfusion, and are maintained in the chronic stages. This anatomical substrate can explain the effectiveness of endo-epicardial catheter ablation of monomorphic ventricular tachycardias in the chronic scar after infarction, and sets a basis for further electrophysiological and molecular studies, and future therapeutic strategies.

© 2019 Garcia-Bustos et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited