Role of Heart-Type Fatty Acid-binding Protein in Early Detection of Acute Myocardial Infarction

Abstract

Biochemical evidence of acute myocardial infarction (AMI) is delayed by the delay of appearance of serum cardiac markers in the blood after myocardial injury. Heart-type fatty acid-binding protein (H-FABP), a small (15 kDa) cytoplasmic protein (1) involved in lipid homeostasis, is abundant in heart muscle (2). H-FABP is ∼10-fold lower in skeletal muscle than in heart muscle, and the amounts in the kidney, liver, and small intestine are even lower (3). After myocardial damage, H-FABP is released into the intercellular space and appears in the bloodstream (4). The magnitude of the increase in plasma H-FABP has also demonstrated a good correlation with the size of the infarction (5). Myoglobin, another small protein (18 kDa), appears in the plasma within 2–3 h after myocardial infarction and is considered a useful marker in the early detection of AMI (6). Myoglobin lacks specificity because myoglobin released from skeletal muscles cannot be distinguished from that released from the heart. Cardiac troponin I (cTnI) and creatine kinase MB isoenzyme (CK-MB) are more specific for myocardial injury but lack early sensitivity because their blood concentrations do not increase appreciably until 6–8 h after the onset of AMI (7). The aim of this multicenter study was to compare H-FABP with myoglobin, cTnI, and CK-MB in the early detection of AMI in patients presenting with …