title: Sustained myocardial production of stromal cell-derived factor-1α was associated with left ventricular adverse remodeling in patients with myocardial infarction.
abstract: The role of stromal cell-derived factor-1α (SDF-1α) expressed in infarcted myocardium is unknown in humans. We examined whether SDF-1α produced in an infarcted myocardial lesion may play a role in left ventricle (LV) remodeling and dysfunction in patients with acute myocardial infarction (AMI). We measured SDF-1α levels in plasma obtained from aortic root (AO) and anterior interventricular vein (AIV) in the early phase (2 wk after MI) and the chronic phase (6 mo after MI) in 80 patients with anterior MI. An increment in SDF-1α level from AO to AIV, reflecting SDF-1α release from infarcted myocardium, was more frequent in patients with MI in the early phase of MI [n = 52 (65%), P = 0.03] but not in the chronic phase of MI [n = 46 (58%), P = 0.11] compared with that in control patients [n = 6/17 (35%)]. On linear regression analysis, the transmyocardial gradient in SDF-1α level in the chronic phase of MI was correlated with percentage changes in LV end-diastolic volume index (r = 0.39, P < 0.001), LV end-systolic volume index (r = 0.38, P < 0.001), and LV ejection fraction (r = -0.26, P = 0.01) 6 mo after AMI. By contrast, the transmyocardial gradient of SDF-1α in the early phase of MI had no significant correlations. In conclusion, the production of SDF-1α in infarcted myocardium in the chronic phase of MI was associated with LV adverse remodeling and progressive dysfunction in AMI survivors.
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Manabu
authors.initials: M
authors.lastname: Uematsu
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Yoshizaki
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Takuya
authors.initials: T
authors.lastname: Shimizu
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Jun-ei
authors.initials: JE
authors.lastname: Obata
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Takamitsu
authors.initials: T
authors.lastname: Nakamura
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Fujioka
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Watanabe
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan.
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Watanabe
authors.affiliation: Department of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Chuo, Yamanashi, Japan kugiyama@yamanashi.ac.jp.
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Kugiyama
mesh_terms: D000368:Aged; D001011:Aorta; D016022:Case-Control Studies; D054377:Chemokine CXCL12 / Q000378:metabolism*; D003331:Coronary Vessels; D018450:Disease Progression; D005260:Female; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000378:metabolism* / Q000503:physiopathology; D020257:Ventricular Remodeling
chemical_list: C515255:CXCL12 protein, human; D054377:Chemokine CXCL12
keywords: acute myocardial infarction; inflammation; stromal cell-derived factor-1α; ventricular dysfunction; ventricular remodeling