Effect of carotid endarterectomy on brain damage markers

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Ischemic strokes are important causes of morbidity. Various therapeutic strategies may improve the clinical state of patients 1.
Carotid endarterectomy (CEA) is the recommended treatment in the prevention of ischemic stroke 2. However, this surgical procedure may cause neurological complications during the perioperative period. These complications include micro‐ and macroembolisms resulting in ischemic brain damage. Moreover, clamping and declamping of the internal carotid artery during CEA produces acute ischemia and reperfusion injury that leads to cerebrovascular autoregulation impairment, post‐ischemic hyperperfusion, and brain edema 5.
YKL‐40, also named chitinase 3‐like 1 (CHI3L1), is a proinflammatory glycoprotein mainly produced by fetal and embryonic stem cells, neutrophils, macrophages, reactive astrocytes, and cancer cells. This protein plays a role in angiogenesis, inflammation, and cellular proliferation and differentiation 9. YKL‐40 is also a biomarker of brain damage in different neurological diseases, including Alzheimer's disease, meningitis, traumatic brain injury, and brain gliomas. Elevated YKL‐40 levels in cerebrospinal fluid (CSF) has been proposed as a candidate biomarker to diagnose, predict, and monitor Alzheimer's disease 10. In addition, patients who have succumbed to purulent meningitis had significantly higher CSF levels of YKL‐40 than patients who survived 12. It was also reported that after traumatic brain injury, YKL‐40 may be a useful biomarker for understanding secondary injury and ultimately a useful measurement for patient prognosis 13. Moreover, plasma YKL‐40 was found to demonstrate significant differences between patients with glioblastoma multiforme and non‐glial brain tumors 14.
Neurofilaments are highly specific structural proteins and a major component of neurons. They consist predominantly of four subunits: neurofilament light, medium, and heavy chains, and alpha‐internexin. As studies demonstrate that neurofilaments are obligate heteropolymers and are required for proper radial growth of axons, these neurofilaments are released following axonal damage or neuronal degeneration 15. Data from the literature showed that neurofilament light polypeptide (NEFL) may be a brain damage marker in neurological disorders, including multiple sclerosis and other neurodegenerative diseases, such as amyotrophic lateral sclerosis. CSF concentrations of NEFL can be used as a prognostic marker for accumulating disability, therefore suggesting it as a good prognostic tool for treatment and monitoring the progression of multiple sclerosis, as well as amyotrophic lateral sclerosis 18. Moreover, neurofilaments in CSF have a high relevance for the differential diagnosis of motor neuron diseases and should be included in the diagnostic workup of patients 21.
Long‐chain polyunsaturated fatty acids (PUFAs) are critical structural components of the brain. The cellular transportation and physiological actions of PUFAs are mediated by fatty acid‐binding proteins (FABPs) which are also expressed in the brain 22. FABPs bind to fatty acids and transfer these lipid ligands within the cytoplasm. Brain lipid‐binding protein, FABP7, is specifically localized in neural stem/progenitor cells, neurons, and glia. It functions in a cell‐type‐specific manner and plays an important role in neurogenesis 23. FABP7 expressed by astrocytes in developing and mature brains is involved in uptake and transportation of fatty acids, signal transduction, and gene transcription 24. With these characteristics, research has shown that FABP7 has a clinical relevance. Impaired FABP7 signaling might be a major characteristic for the failure of remyelination and clinical progression of multiple sclerosis leading to disability 25. Moreover, FABP7 may be also a marker of glioma cells. It is known that FABP7 is highly expressed in the majority of glioblastomas and could have possible significance for glioma diagnosis and treatment 26.
There are no specific data in the literature in regard to the biomarkers evaluated in this study following CEA.
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