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 …
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