Abstract 17212: T-Cell Compartment Shifts Following Reperfusion After Primary Angioplasty in Patients with Acute Myocardial Infarction
Background: Primary PCI (PPCI) has substantially improved clinical outcomes of patients with acute ST elevation myocardial infarction (STEMI). However, myocardial ischemia-reperfusion (I/R) injury still remains an important clinical problem. CD4+ T-lymphocytes have been shown to promote I/R injury in a mouse model. It is unknown though, whether T-cells play any role in I/R inflammatory response in patients with STEMI. The goal of our study was to identify relevant changes in T-cell subsets in reperfused STEMI by using newly established 13-parameter flow cytometry (FACS) and hierarchical cluster analysis (HCA) of surface expression as a screening tool.
Methods and Results: We analysed 30 patients (pts) with STEMI (12-24h after PCI), 24 stable post-STEMI pts and 18 healthy controls (ctrl) (all male, mean age 60 y). Peripheral blood mononuclear cells were stained for T-cell subset markers (CD3, CD4, CD8, CCR7, CD45RA), co-stimulatory molecules (CD27, CD28) and proliferation-associated markers (CD57, KLRG1, PD1). Following FACS data aquisition, HCA and sequential gating were performed using MATLAB software. While total lymphocyte counts did not differ between STEMI pts, stable post-STEMI pts and ctrl, the analysis of T-cell subsets revealed a significant increase in CD45RA-CCR7+ central memory (CM) populations in both CD4 and CD8 T-cells (see table). HCA revealed strong upregulation of the proliferation marker CD57 on CD4 CM T-cells in STEMI pts. Mean telomere length (mTL) in sorted CD4 T-cells was also reduced in STEMI. A pilot time course study showed a rapid decrease in CD4 T-cells by approx. 30% during the first 60 min following PPCI, possible due to invasion of myocardial tissue by T-cells, which might trigger compensatory proliferation of memory cells.
Conclusion: Our results identify for the first time expansion of memory T-cells following reperfusion after PPCI in STEMI, which could provide novel insight into the mechanism of myocardial reperfusion injury.
- © 2011 by American Heart Association, Inc.