Abstract 13537: Early Increase in Serum Fatty Acid Binding Protein 4 Levels in Patients with Acute Myocardial Infarction: Lipolysis as a Novel Marker for Myocardial Ischemia
Introduction: Emerging evidence indicates that circulating fatty acid binding protein 4 (FABP4), predominantly expressed in adipocytes, are released from the cells through undefined mechanisms and are associated with obesity, insulin resistance and cardiovascular events. We investigated the time course of circulating FABP4 levels as well as cardiac troponin T (TnT) and heart-type FABP (H-FABP), established makers for myocardial necrosis, in patients with acute myocardial infarction (AMI).
Methods and Results: Serial blood samples were analyzed in 67 consecutive AMI patients (48 men, aged 68 ± 13 years). FABP4 concentrations were significantly increased on admission in AMI patients compared with patients with stable exertional angina [median (interquatile range); 25.1 (17.0 to 45.4) vs 11.2 (8.8 to 18.3) ng/ml] and declined over the time course of 7 days thereafter while TnT and H-FABP levels increased after admission and peaked after PCI. A FABP4 level > 15.9 ng/ml on admission can discriminate AMI from stable angina with 86% and 70% of sensitivity and specificity, respectively (p<0.001). Simple linear regression analysis revealed that age and glomerular filtration rate were independent contributors to peak FABP4 levels. Neither peak nor on-admission FABP4 concentrations correlated with TnT and H-FABP concentrations, strongly suggesting that FABP4 levels are not associated with myocardial necrosis. In vitro studies using 3T3-L1 adipocytes showed that norepinephrine (NE) induced lipolysis with a rapid and marked increase in FABP4 efflux into culture medium through β3-adrenergic receptor in the absence of cell death as shown by no increase in adiponectin level. Consistent with this, serum levels of adioponectin were not elevated on admission in AMI patients, implying that an acute increase in circulating FABP4 does not result from adipocyte necrosis.
Conclusions: Given that myocardial ischemia causes robust NE release from cardiac sympathetic nerve terminals and that there is no fascia between cardiac myocytes and epicardial adipocytes unlike skeletal muscle, our data may represent the NE-induced lipolysis occurred prior to myocardial necrosis, and imply that FABP4 is a potential biomarker that can be used to improve the early diagnosis of AMI.
Author Disclosures: H. Sunaga: None. Y. Ohyama: None. M. Obokata: None. T. Iso: None. T. Kawaguchi: None. N. Koitabashi: None. R. Funada: None. N. Takama: None. M.A. Syamsunarno: None. H. Matsui: None. T. Yokoyama: None. M. Kurabayashi: None.
- © 2014 by American Heart Association, Inc.