Regional CXCR4 Upregulation in Patients Early after Reperfused Myocardial Infarction is Associated with Systemic Inflammation and Left Ventricular Dysfunction

Objectives: The chemokine receptor CXCR4 plays a pivotal role in the recruitment of immune cells to injured and inflamed tissue. It has emerged as a therapeutic target to support tissue repair. PET/CT using the specific CXCR4 ligand, 68Ga-Pentixafor, has recently been successfully employed to identify myocardial inflammation early after acute myocardial infarction (AMI). We speculated that myocardial CXCR4 upregulation is associated with left ventricular dysfunction, and sought to evaluate systemic inflammatory interactions. Methods: 65 patients underwent 68Ga-Pentixafor PET/CT of the chest at a median of 4 days after stent-based reperfusion for acute myocardial infarction. Maximum standardized uptake values (SUVs) in infarcted myocardium were determined, and correlated with uptake in systemic organs, left ventricular ejection fraction (LVEF) as determined by cardiac magnetic resonance imaging and with clinical parameters at the time of PET. Results: CXCR4 upregulation in infarcted myocardium showed considerable variability among patients (SUVmax, 2.8±0.5; range, 1.4 to 4.3). Postinfarct myocardial inflammation was significantly higher in patients with left ventricular dysfunction compared to those with normal LVEF (2.9±0.5 vs. 2.5±0.6, p=0.03). LVEF demonstrated a statistically significant inverse correlation with the maximum intensity (SUVmax) of postinfarction myocardial inflammation (r=-0.32, p=0.02), and other markers of inflammation/cell damage such as CRP (r=-0.49, p=0.0002) and CKmax (r=-0.64, p