H-FABP is a low molecular-weight (15kD) cytoplasmic protein that is involved in the intracellular uptake and buffering of free fatty acids in the myocardium1. The combination of its low molecular weight and cytoplasmic location enables H-FABP to be a highly sensitive early rise marker of acute coronary syndrome (ACS), detectable as early as 30 minutes following the onset of an ischemic episode2. H-FABP concentrations peak at approx. 6-8 hours and return to normal within approx. 24-30 hours3. Although H-FABP has similar release kinetics to Myoglobin, it is approx 15-20 times more cardiac specific, hence making it a more effective marker of myocardial injury4.
Using a combination of H-FABP and Troponin has been shown to significantly improve the diagnostic sensitivity for MI/ACS during the early hours after symptom onset (at presentation5, <4 hours6 or <6 hours7), compared to using Troponin alone. Prognostically, a number of large trials have illustrated the value of H-FABP in stratifying long-term ACS risk in both Troponin positive and Troponin negative patients8, 9, 10. H-FABP has also be shown to be incrementally additive to Troponin, diagnostically and prognostically, even when a highly sensitive Troponin assay is used11, 12.
In addition to ACS, H-FABP has been found to be clinically useful in a range of other applications, such as pulmonary embolism (PE)13, coronary artery bypass surgery (CABG)14 and cerebrovascular disease15.