Abstract 12875: Cardiovascular Event Rates During the Four-Year Follow-Up Were Lower in ST-Elevation Myocardial Infarction Patients With Early Increases in Mobilization of Oct-4highNanoghigh Stem Cells Into the Peripheral Circulation
Backgroud: Embryonic stem cell markers such as Oct-4 and Nanog are expressed in various types of stem cells; however, their clinical implication has not been investigated. The aim of this study was to investigate the effects of early peripheral mobilization of stem cells with pluripotency gene expression on cardiovascular events in patients with ST-elevation myocardial infarction (STEMI) during the 4-year follow-up.
Methods: Peripheral blood mononuclear cells (PBMCs) were isolated on days 0, 1 and 7 from patients with STEMI (n=40) and healthy controls (n=20). The numbers of CD34+, CD117+, CD133+ and c-met+ stem cells were measured by flow-cytometry, and PBMCs were analyzed by real-time PCR for Oct-4 and Nanog gene expressions. The plasma concentrations of CRP, IL-6, SCF, SDF-1 and VEGF were measured with ELISA kits. Major adverse cardiovascular events (MACEs) such as non-fatal MI, death, stroke, target lesion revascularization were observed during the 4-year follow-up.
Results: MACEs were significantly lower in patients with Oct-4 gene expression ≥ 1.13 and Nanog gene expression ≥ 1.20 on admission (Table 1). The numbers of CD34+, CD117+, CD133+ and c-met+ cells within 7 days after AMI did not show significant differences in patients with or without MACE. Anti-inflammatory marker such as IL-10 was significantly higher within 7 days after AMI in patients without MACE. Inflammatory and angiogenic markers such as CRP, IL-6, SCF, SDF-1, and VEGF did not show significant differences in patients with or without MACE.
Conclusions: mRNA levels of pluripotent embryonic stem markers such as Oct-4 and Nanog were significantly higher in AMI patients without MACE during the 4-year follow-up. Baseline Oct-4 and Nanog gene expression levels could be used as predictors of MACE in STEMI patients.
- © 2011 by American Heart Association, Inc.