Decrease of CD4+ T Lymphocytes after myocardial infarction is related with extensive myocardial fibrosis

Purpose: Myocardial fibrosis plays a potential role in left ventricular remodeling and patients' outcome. After myocardial infarction innate immune cells infiltrate infarcted area and replace necrotic tissue by fibrotic tissue. However the role of adaptive immunity, especially T cells, has not yet been investigated in this scenario. Methods: We studied 94 patients with a first STEMI treated with percutaneous revascularization. Leucocyte subsets and a wide variety of lymphocyte subtypes were determined in peripheral blood 24 h after reperfusion by means of flow cytometry. Infarct size and cardiac fibrosis were measured by late enhancement Cardiac Magnetic Resonance (CRM) 1 week and 6 months after infarction. Results: Innate immune cells were significantly increased at 24 h post-reperfusion in patients with extensive infarction, considered as ≥30% of left ventricular mass at first week, with more neutrophils (9440±1980 vs 7910±1570) and monocytes (695±195 vs 549±120) cells/ul (p<0.05 in both cases). However, there were no significantly differences between innate immune cells and extensive cardiac fibrosis, considered as ≥30% of left ventricular mass at 6th month. Lymphocyte subsets did not relate with the extent of infarction (Figure A). But remarkably T cells were significantly decreased at 24 h post-reperfusion in patients with extensive cardiac fibrosis (Figure B). CD4+ cells dropped while CD8 did not change, a reduction of CD4 T cell effector cells occurred (CXCR3 cells and CCR4 cells) and anti-inflammatory CD4 T regulatory cells were also decreased in patients with extensive cardiac fibrosis (p<0.05 in all cases). ![Figure][1] Conclusion: Lymphocyte-mediated immunity during first 24 hours of reperfused STEMI is related with cardiac fibrosis and it could participate in wound healing of the myocardium. [1]: pending:yes