Heart type fatty acid binding protein (H-FABP) TechNotes
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Heart type fatty acid binding protein (H-FABP) TechNotes.
Fatty acid-binding proteins (FABPs) are a group of relatively small cytoplasmic proteins (12 to 15 kDa), which are abundant in tissues with active fatty acid metabolism, including the heart. All FABPs exhibit rather complicated tertiary structures and their 10 anti-parallel ß-strands are organized into 2 nearly orthogonal ß-sheets, which form a slightly elliptical ß-barrel, with two 8-10 residue helixes linking the first 2 ß-strands together.
Heart-type fatty acid-binding protein (H-FABP or FABP3) consists of 133 amino acid residues with a molecular mass of 14858 Da and theoretical pI 6.29. For almost two decades FABP has been used in clinical practice as an early, highly sensitive marker of myocardial injury. It is widely applied in emergency triage of patients with acute coronary syndromes. Although H-FABP is a small protein abundant in the cytosol, it is readily released into the circulation following myocardial damage. After acute myocardial infarction (AMI), H-FABP is released from damaged myocytes much more rapidly than, for example, troponins, which are the most specific markers of cardiac injury. H-FABP elevation in the patient’s blood could be detected within 1 to 3 hours after symptom onset, reaching its peak within 6 hours, and then returning to a normal level within 12 to 24 hours. On the other hand, H-FABP is evidently more cardiac specific than myoglobin, the other early marker of cardiac injury. H-FABP distribution in the heart (about 0.6 mg/g) is almost 10-fold lower than in skeletal muscle tissue, whereas myoglobin’s distribution in heart (2.7 mg/g) is equal to or even lower than that in skeletal muscle tissue (2.2 - 6.7 mg/g).
This difference in tissue distribution helps to differentiate between myocardial and skeletal muscle injury. Previous studies suggested that H-FABP can be used as a reliable marker for hypertrophic and dilated cardiomyopathy, heart failure, early estimation of infarct size, a reperfusion marker and for the early detection of postoperative myocardial tissue loss in patients undergoing coronary bypass surgery, stroke, and obstructive sleep apnea syndrome. Moreover, H-FABP levels were associated with the risk of death during the long-term follow-up in patients with chronic thromboembolic pulmonary hypertension. In addition, H-FABP appears to be a marker that will enable the successful detection of cardiac injury in the early asymptomatic period in patients with metabolic syndrome.
The imperfection of H-FABP as a diagnostic marker of AMI includes the relatively lower (than for troponins) cardiospecificity, smaller diagnostic window (1-24 hours following the onset of the chest pain) and its elimination from plasma mainly by renal clearance, possibly causing a falsely high value in the case of kidney malfunction.
However, these drawbacks can be overcome through the simultaneous utilization of late and more specific markers, such as cTnI.
A new generation of unique anti-FABP monoclonal antibodies, which was recently produced by HyTest, makes possible the development of highly sensitive and rapid sandwich immunoassays. Our in-house assays have a linear detection range from 0.15 to 500 mg/L (with detection limit of 0.05 mg/L). All recommended MAb combinations were evaluated in small-scale clinical trials with blood samples from AMI patients.
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