Preservation From Left Ventricular Remodeling by Front-Integrated Revascularization and Stem Cell Liberation in Evolving Acute Myocardial Infarction by Use of Granulocyte-Colony–Stimulating Factor (FIRSTLINE-AMI)
- 15 November 2005
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 112 (20) , 3097-3106
- https://doi.org/10.1161/circulationaha.105.541433
Abstract
Background— Considering experimental evidence that stem cells enhance myocardial regeneration and granulocyte colony–stimulating factor (G-CSF) mediates mobilization of CD34+ mononuclear blood stem cells (MNC CD34+ ), we tested the impact of G-CSF integrated into primary percutaneous coronary intervention (PCI) management of acute myocardial infarction in man. Methods and Results— Fifty consecutive patients with ST-segment elevation myocardial infarction were subjected to primary PCI stenting with abciximab and followed up for 6 months; 89±35 minutes after successful PCI, 25 patients were randomly assigned in this pilot study (PROBE design) to receive subcutaneous G-CSF at 10 μg/kg body weight for 6 days in addition to standard care, including aspirin, clopidogrel, an ACE inhibitor, β-blocking agents, and statins. By use of CellQuest software on peripheral blood samples incubated with CD45 and CD34, mobilized MNC CD34+ were quantified on a daily basis. With homogeneous demographics and clinical and infarct-related characteristics, G-CSF stimulation led to mobilization of MNC CD34+ to between 3.17±2.93 MNC CD34+ /μL at baseline and 64.55±37.11 MNC CD34+ /μL on day 6 ( P CD34+ liberation led to enhanced resting wall thickening in the infarct zone of between 0.29±0.22 and 0.99±0.32 mm versus 0.49±0.29 mm in control subjects ( P −1 · min −1 ), wall motion score index showed improvement from 1.66±0.23 to 1.41±0.21 ( P P P P P P 18 F-deoxyglucose uptake in the infarct zone ( P Conclusions— G-CSF and mobilization of MNC CD34+ after reperfusion of infarcted myocardium may offer a pragmatic strategy for preservation of myocardium and prevention of remodeling without evidence of aggravated restenosis.Keywords
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