Inflammatory and metabolic markers and short-time outcome in patients with acute ischemic stroke in relation to TOAST subtypes

Abstract

The aim of this study was to evaluate the association between inflammatory and metabolic markers and short-time outcome with acute ischemic stroke subtypes. A total of 121 patients was classified according to TOAST criteria, such as large artery atherosclerosis (LAAS), lacunar infarct (LAC), cardioembolic infarct (CEI), other determined etiology (ODE), and undetermined etiology (UDE). The functional impairment was evaluated within the first eight hours of stroke and the outcome after three-month follow-up using the modified Rankin Scale. Blood samples were obtained up to 24 h of stroke. Compared with 96 controls, patients with LAAS, CEI, and LAC subtypes showed higher levels of white blood cells, high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6), metalloproteinase 9 (MMP-9), glucose, and iron (p < 0.05); and lower high-density lipoprotein cholesterol (HDL-C) (p < 0.0001); platelets, insulin, insulin resistance, and homocysteine were higher in LAC (p < 0.0001); ferritin was higher in LAAS (p < 0.0001); and total cholesterol (TC) was lower in LAAS and CEI (p < 0.01). When stroke subtypes were compared, insulin was higher in LAAS vs. LAC and in LAC vs. CEI (p < 0.05); and TC was lower in LAAS vs. LAC (p < 0.05). Outcome and rate of mortality after three-month were higher in LAAS vs. LAC (p < 0.001 and p = 0.0391 respectively). The results underscored the important role of the inflammatory response and metabolic changes in the pathogenesis of ischemic stroke subtypes that might be considered on the initial evaluation of stroke patients to identify those that could benefit with individualized therapeutic strategies that taken into account these markers after acute ischemic event.

Severe Blood–Brain Barrier Disruption in Cardioembolic Stroke

“…This can be another evidence that links BBB disruption and CE. Moreover, previous studies revealed that C-reactive protein (CRP) was higher in patients with CE ( 28 , 29 ). It has been proved that CRP could cause endothelial cells contraction, which went along with disruption of tight junction molecules and finally resulting in BBB disruption ( 30 ).…”

The Diagnostic Value of Stweak in Acute Ischemic Stroke

“…Several studies have been conducted to investigate the rapid diagnosis of AIS and the prediction of neurological deficit or mortality. Some of the markers whose value in diagnosis and predicting mortality and prognosis that have recently been investigated are glucose, iron, ferritin, homocysteine, insulin, P-selectin, matrix metalloproteinase-9, high-density lipoprotein cholesterol, platelets, C-reactive protein, glial fibrillary acidic protein, TNF-α, interleukin-6, and proenkephalin-A ( 14 , 15 , 16 , 17 , 18 , 19 ). Recently, sTWEAK has become a highly investigated protein, mainly due to its effect on apoptosis stimulation and inflammatory cytokine release ( 6 , 7 , 8 , 9 , 10 , 11 ).…”

<p>The Role of Selected Pro-Inflammatory Cytokines in Pathogenesis of Ischemic Stroke</p>

“…The highest concentration of IL-6 in plasma and other immune-inflammatory and thromboembolic/fibrinolytic agents (PAI-1, TPA) was found in patients with cardiogenic stroke caused by a cardiac embolism. 48,67 This group of patients was observed with not only an increased immune-inflammatory activity but also with a greater degree of neurological deficit as assessed according to the Scandinavian Stroke Scale (SSS). 48 In a lacunar stroke, which is caused by cerebral microangiopathy, lower levels of pro-inflammatory cytokines (IL-6 and TNF-α) in plasma and lower P-selectin and ICAM-1 (intercellular adhesion molecule-1) were observed.…”