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Online ISSN 1827-1847
Odero Jr. A., Baldassarre E., Montanelli A., Poletto G., Franciosi E., Popovich A., Casabianca E., Busoni C., Valaperta S., Rognone E., Giorgetti P. L.
1 Service of Vascular Surgery I, IRCCS Humanitas, Rozzano, Milan, Italy
2 Clinical Laboratory, IRCCS Humanitas, Rozzano, Milan, Italy
3 Service of Neuroradiology, IRCCS Humanitas, Rozzano, Milan, Italy
Aim. Real silent brain ischemia incidence due carotid endarterectomy (CEA) is still unknown. No biological marker is available for the diagnosis of silent brain ischemia yet. Brain fatty acid binding protein (BFABP) could be used as a valid diagnostic biomarker for silent brain ischemia.
Methods. Local ethical committee approved this monocentric primary observational study involving 71 patients with carotid stenosis who were managed with CEA. Patients underwent diffusion-weighed imaging magnetic resonance imaging (DWI MRI) and blood collection one day preoperatively and 24/48 hours postoperatively. BFABP measurements where performed with an in-house indirect Enzyme Linked Immunosorbent Assay (ELISA). Five negative controls and 4 patients underwent neurosurgical ceerebral hemorrage drainage (positive controls).
Results. Our in-home test is based on policlonal brain fatty-acid-binding proteins (BFABP) antibodies and allows only a semiquantitative evaluation of the circulating BFABP (AU/mL: arbitrary unit): negative controls demonstrate an average 0.04 AU/mL, positive one 2.1 AU/mL (P<0.001). Patients with carotid stenosis present preoperatively value higher than negative controls (P<0.001). Uncomplicated surgical procedure does not modify this biochemical marker. Patients underwent intraoperative shunting; those with positive MRI and the only patient with postoperative ischemic stroke demonstrate average value similar to positive controls.
Conclusion. BFABP is a novel biochemical neuromarker of ischemia in patients with neurological deficits and in patients with asymptomatic silent ischemia. Uncomplicated CEA does not increase BFABP serum levels. Carotid stenosis alone seems to be responsible of a basal increasing of BFABP levels, suggesting a chronic ischemia due to microembolization from carotid plaque: further study are necessary to assess the role of BFABP in carotid plaque instability.