Abstract 16161: Bone Marrow Characteristics are Associated With Changes in Infarct Size Following STEMI: A Biorepository Evaluation From the CCTRN TIME Trial
OBJECTIVE: Despite significant interest in bone marrow cell mononuclear cell (BMC) therapy for ischemic heart disease, current techniques have shown only modest benefit. However, select patients show improvements after autologous BMC therapy for unknown reasons. The purpose of this study was to identify BMC characteristics associated with infarct size reduction following STEMI.
METHODS: This study evaluated prospectively the cohort of patients enrolled in the CCTRN TIME trial who agreed to their BMCs being stored and used for further analyses at the CCTRN Biorepository. Analyses were pre-specified and the core laboratories were blinded to clinical data and treatment assignments. The changes in infarct size between baseline (three days after PCI) and 6 months was measured by cMRI. BMC product underwent phenotype analysis using FACS identifying cells expressing CD45, CD34, CD31, CD133, CXCR4, CD3, CD11, CD14, and CD19 and functional analysis with the CFU-Hill, ECFC and CFU-F assays.
RESULTS: Quantification of BMC characteristics and infarct size was available in 101 patients. The patients’ mean age was 56.5 years, with a mean screening ejection fraction of 37% and mean baseline cMRI ejection fraction of 45%. At 6 months, 75 (74.3%) patients had reductions in infarct size (mean -21.0% ± 17.6%). Multiple regression analysis revealed that, regardless of treatment allocation, an increased percentage of BMC that expressed CD31 (p=0.046) was associated with greater reductions in infarct size. Greater reductions in infarct size also were associated with more rapid growth rates for BMC functional assays (CFU-Hill, ECFC) (p=0.033, p=0.032, respectively).
CONCLUSIONS: This study demonstrates a correlation between characteristics of BMCs in the acute STEMI phase and subsequent changes in infarct size. These data suggest that resident BMCs (specifically, endothelial precursors) play an important role in regenerating infarcted myocardium irrespective of treatment with autologous BMC transplantation.
Author Disclosures: R.C. Schutt: None. B.H. Trachtenberg: None. J.P. Cooke: None. J.H. Traverse: Research Grant; Modest; NHLBI. Research Grant; Significant; modest. T.D. Henry: None. C.J. Pepine: None. J.T. Willerson: None. E.C. Perin: None. S.G. Ellis: None. D.X. Zhao: None. A. Bhatnagar: None. B.H. Johnstone: None. D. Lai: None. M. Resende: None. R.F. Ebert: None. J.C. Wu: None. S.L. Sayre: None. R.D. Simari: None. L. Moye': None. C.R. Cogle: None. D.A. Taylor: None.
- © 2014 by American Heart Association, Inc.