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Vol 29, No 3 (2023)
Research paper
Published online: 2023-09-25

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Serum level of αII-spectrin breakdown products (SBDPs) as a potential marker of brain ischemia-reperfusion injury after carotid endarterectomy

Jędrzej Tkaczyk1, Stanisław Przywara2, Tomasz Zubilewicz3, Bożena Kiczorowska4, Marek Iłżecki5
DOI: 10.5603/aa.96787
Acta Angiologica 2023;29(3):76-84.

Abstract

Introduction: Stroke remains one of the main causes of morbidity and mortality worldwide. Carotid endarterectomy (CEA) reduces the incidence of ischemic stroke or death in patients with symptomatic carotid artery stenosis more effectively than pharmacological therapy alone. SBDPs (spectrin breakdown products): SBDP 120, SBDP145, and SBDP150 are the product of proteolysis of αII-spectrin (280 kDa) — an important structural component of the neuronal cytoskeleton, particularly present in axons. Increased serum level of SBDPs was previously observed in traumatic brain injury, subarachnoid hemorrhage (SAH), or brain ischemia.

Material and methods: The aim of our study was to investigate changes in serum levels of SBDP120 and SBDP145 in patients undergoing uncomplicated CEA. The study included 22 patients with severe carotid artery stenosis, qualified for CEA. Blood samples were taken from the antecubital vein at three different intervals (24 h before CEA, 12 and 48 h after surgery). SBDP’s serum levels were measured by a commercially available enzyme-linked immunosorbent assay (ELISA).

Results: The study showed that serum SBDP120 levels were significantly decreased 48 h after CEA when compared to the level before the surgery. SBDP145 levels were significantly decreased 12h after the procedure and then remained at a similar level 48h after CEA.

Conclusions: In patients with high-grade carotid artery stenosis SBDP120 and SBDP145 serum level decreases after an uncomplicated CEA, therefore alterations from this curve may be a marker of neurological complications after the procedure. Higher SBDP levels before the procedure may represent brain damage caused by chronic ischemia.

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