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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 1975167, 9 pages
https://doi.org/10.1155/2018/1975167
Research Article

Apoptosis and Mobilization of Lymphocytes to Cardiac Tissue Is Associated with Myocardial Infarction in a Reperfused Porcine Model and Infarct Size in Post-PCI Patients

1Department of Medicine, Cardiovascular Medicine Unit, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
2Department of Medicine, University of Valencia, Valencia, Spain
3Institute of Health Research INCLIVA, Valencia, Spain
4Department of Cardiology, Hospital Clinico Universitario de Valencia, Valencia, Spain
5Department of Pathology, University of Valencia, Valencia, Spain
6Intensive Care Unit, Hospital Clinico Universitario de Valencia, Valencia, Spain
7Centro de Investigación Biomédica en Red-Cardiovascular (CIBERCV), Madrid, Spain

Correspondence should be addressed to Maria J. Forteza; es.ik@seyer.sol.ed.azetrof.airam and Vicente Bodi; moc.liamtoh@idobtneciv

Received 1 March 2017; Accepted 13 November 2017; Published 18 March 2018

Academic Editor: Nageswara Madamanchi

Copyright © 2018 Maria J. Forteza et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

ST-segment elevation myocardial infarction (STEMI) is the most severe outcome of coronary artery disease. Despite rapid reperfusion of the artery, acute irrigation of the cardiac tissue is associated with increased inflammation. While innate immune response in STEMI is well described, an in-depth characterization of adaptive immune cell dynamics and their potential role remains elusive. We performed a translational study using a controlled porcine reperfusion model of STEMI and the analysis of lymphocyte subsets in 116 STEMI patients undergoing percutaneous coronary intervention (PCI). In the animal model, a sharp drop in circulating T lymphocytes occurred within the first hours after reperfusion. Notably, increased apoptosis of circulating lymphocytes and infiltration of proinflammatory Th1 lymphocytes in the heart were observed 48 h after reperfusion. Similarly, in STEMI patients, a sharp drop in circulating T lymphocyte subsets occurred within the first 24 h post-PCI. A cardiac magnetic resonance (CMR) evaluation of these patients revealed an inverse association between 24 h circulating T lymphocyte numbers and infarction size at 1-week and 6-month post-PCI. Our translational approach revealed striking changes in the circulating and tissue-infiltrating T lymphocyte repertoire in response to ischemia-reperfusion. These findings may help in developing new diagnostic and therapeutic approaches for coronary diseases.