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Effect of carotid endarterectomy on brain damage markers
Author(s) -
Iłżecki M.,
Iłżecka J.,
Przywara S.,
Terlecki P.,
Grabarska A.,
Stepulak A.,
Zubilewicz T.
Publication year - 2017
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/ane.12607
Subject(s) - carotid endarterectomy , medicine , proinflammatory cytokine , endarterectomy , stenosis , stroke (engine) , gastroenterology , brain damage , internal carotid artery , cardiology , pathology , surgery , inflammation , mechanical engineering , engineering
Objectives Carotid endarterectomy (CEA) is a recommended treatment in the prevention of ischemic stroke. However, this procedure may cause neurological complications caused by cerebrovascular damage. While YKL‐40 is a proinflammatory protein, neurofilament light polypeptide (NEFL) and brain lipid‐binding protein (FABP7) are structural components of the brain. The aim of the study was to investigate YKL‐40, NEFL, and FABP7 in the serum of patients undergoing CEA. Materials and methods The study included 25 participants who underwent CEA due to internal carotid artery stenosis. Blood samples were taken from each patient at three different intervals: prior to the surgery, 12 h after the surgery, and 48 h after the surgery. Serum levels of these brain damage markers were measured by enzyme‐linked immunosorbent assay (ELISA). Results The study showed that the serum YKL‐40 level was significantly increased 48 h after CEA when compared to the level prior to surgery and also when compared to levels 12 h after surgery. There were no statistically significant differences in serum NEFL and FABP7 levels between all three recorded measurements. Conclusions Data from our study showed that CEA affects serum YKL‐40 but not NEFL and FABP7 levels. This implicates that YKL‐40 may be a valuable serum marker of brain damage after CEA. However, the observed change in serum YKL‐40 level in patients after CEA does not necessarily warrant a change in recommendations concerning the use of this treatment in patients with high‐grade internal carotid artery stenosis.