Unbound Free Fatty Acids and Heart-Type Fatty Acid–Binding Protein: Diagnostic Assays and Clinical Applications

Abstract

Background: A biomarker that reliably detects myocardial ischemia in the absence of necrosis would be useful for initial identification of unstable angina patients and for differentiating patients with chest pain of an etiology other than coronary ischemia, and could provide clinical utility complementary to that of cardiac troponins, the established markers of necrosis.

The use of biomarkers in detecting subclinical cardiotoxicity in doxorubicin-based treatment for paediatric patients with acute lymphoblastic leukaemia

“…It is a low molecular weight protein, found in the cytosol, and it has been more recently developed as cardiac biomarker [9,10,11]. It can be detected as soon as one hour after onset of ischemia and it can be seen as the earliest plasma marker available [12].…”

Point-of-care test of heart-type fatty acid-binding protein for the diagnosis of early acute myocardial infarction

“…However, it has been noted that H-FABP isoform is produced not only in cardiomyocytes but also, to a lesser extent, in skeletal muscle, distal tubular cells of the kidney, specific parts of the brain, lactating mammary glands and the placenta [16] . In the clinical studies, serum H-FABP level is also elevated under heart failure, hypertension, aortic valve regurgitation, renal dysfunction and muscular exercise [17][18][19][20] .…”

Predictive value of heart-type fatty acid-binding protein for left ventricular remodelling and clinical outcome of hypertensive patients with mild-to-moderate aortic valve diseases

“…There are two possible mechanisms of H-FABP leakage into the circulation; first, irreversible myocardial injury caused by cell necrosis or apoptosis and second reversible disturbances of cell membrane metabolism. 13 Cardiac overload or continuous mechanical stress results in disturbances in cell membrane integrity so that cell membrane become permeable to small size molecule such as H-FABP, 14 since the prevention of membrane leaks is an energy-dependent process in which myocardial plasma membranes become permeable to macromolecule under conditions of energy storage. 13 In comparison with troponin T that is bound to myocyte structure, H-FABP, soluble small-sized protein abundantly expressed in cytosol, is more likely to leak into the blood circulation at minor membrane injury or disintegration.…”