Abstract 17014: Pericardial Fluid Levels of Granulocyte Colony-Stimulating Factor are Closely Correlated with Left Ventricular Remodeling in Post-Myocardial Infarction Patients Undergoing Coronary Artery Bypass Grafting Surgery

Abstract

Purpose: Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to play an important role in the progression of left ventricular (LV) remodeling following myocardial damage by regulating the enzymatic systems of proteolysis and antiproteolysis. The purpose of this study was to investigate whether G-CSF acts as autocrine/paracrine factors and is accumulated in pericardial fluids, and to evaluate whether LV dysfunction or myocardial ischemia is related to the production and release of G-CSF. Methods and Results: We measured the concentrations of G-CSF and N-terminal pro-brain natriuretic peptide (NT-proBNP) in both plasma and pericardial fluid in 22 post-myocardial infarction (MI) patients undergoing coronary artery bypass grafting surgery for unstable angina (n=8) or stable angina (n=14). The G-CSF level was significantly higher in pericardial fluid than in plasma (89±93 vs. 15±8 pg/ml, p<0.001). Interestingly, pericardial fluid levels of G-CSF were significantly higher in patients with impaired LV function (less than 55% in LV ejection fraction) than in those with normal LV function (145±95 vs. 21±7 pg/ml, p<0.001). Pericardial fluid G-CSF levels were correlated with LVEDVI (r=0.746, p<0.0001) and LVESVI (r=0.843, p<0.0001) than did plasma G-CSF level (LVEDVI: r=0.233, p=NS; LVESVI: r=0.259, p=NS). G-CSF levels in pericardial fluid but not in plasma were inversely correlated with LV ejection fraction (r=-0.824, p<0.0001). In addition, pericardial fluid G-CSF levels were correlated with pericardial fluid NT-proBNP levels indicating LV remodeling following MI (r=0.427, p<0.05). However, pericardial fluid G-CSF levels in patients with unstable angina were not significantly elevated compared to those with stable angina (117±102 pg/ml vs. 73±88 pg/ml, p=NS). Conclusions: G-CSF accumulated in pericardial fluid may play an important role in the LV remodeling process by promoting proteolysis, and G-CSF may be secreted from the heart into the pericardial space in response to not myocardial ischemia but LV dysfunction.