Homocysteine as a Predictor of Early Neurological Deterioration in Acute Ischemic Stroke

Abstract

We examined total homocysteine by quartiles of increasing levels to evaluate for possible threshold effects. Baseline and clinical Background and Purpose-Hyperhomocysteinemia is a well-known risk factor for vascular disease. However, its action, mechanism, and role in the acute phase of stroke have not been determined. We tried to determine whether an association existed between elevated serum homocysteine levels and early neurological deterioration (END) in patients with acute ischemic stroke. Methods-We performed a secondary analysis from the Cilostazol in Acute Ischemic Stroke Treatment (CAIST) trial, which was a double-blinded, randomized, multicenter trial, assessing the noninferiority of cilostazol over aspirin within 48 hours of an acute ischemic stroke. END was defined as an increase of ≥1 point in motor power or an increase of ≥2 points in the total National Institute of Health Stroke Scale score within 7 days. Results-The mean (±SD) serum homocysteine level was 11.4±4.7 μmol/L. Of the 396 patients studied, 57 (14.4%) patients worsened during the 7 days after inclusion. Most (68%) of the END cases occurred within the first 24 hours after treatment. High levels (>10.3 μmol/L) of serum homocysteine were independent predictors for END (third quartile odds ratio, 3.45; 95% confidence intervals, 1.25-9.50; P=0.016; fourth quartile odds ratio, 3.36; 95% confidence intervals 1.18-9.52; P=0.023) in multivariate analysis. Conclusions-Patients

A Systematic Review and Meta-Analysis of Molecular Biomarkers Associated with Early Neurological Deterioration Following Acute Stroke

“…Raised total cholesterol, low-density lipoprotein, triglycerides and triglyceride/high-density lipoprotein ratio were predictive of IS-END; however, lower levels of these predicted ICH-END [9,23,25,26,35,[39][40][41][42][43][44][45] [5M, 5S-U]. This concurs with current understanding about cholesterol and the risk of IS/ICH.…”

“…This was mirrored in glycosylated haemoglobin A1c, a marker of chronic raised glucose, also predicting END [9,23,25,26,29,30,35,39] [5K]. One study stratified the effect of glucose by the presence of diabetes mellitus, finding elevated glucose level was associated with END in non-diabetics [38].…”

“…Furthermore, post-hoc analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels trial showed early treatment post-IS with high-dose lipid-lowering agents increased ICH risk [47]. There was no association between high-density lipoprotein and END [9,23,29,35,[40][41][42][43][44] [5L].…”

The Link between Early Biomarker Analysis and the Neurological Outcome in Stroke Patients

“…END being defined as worsening of the neurological status 48-72 h after admission [12]. END can possibly be linked to a worse clinical outcome [20]. The question remained if TNFα is linked to the prognosis or linked to END, which could in turn complicate the patient's outcome.…”

Hyperhomocysteinemia and Ischemic Stroke

“…Как было подтверждено многими исследованиями, даже умеренная гипергомоцистеинемия (ГГЦ) может уве-личить риск развития ИИ, вероятно, из-за плейотропных биохимических свойств ГЦ и его влияния на атероскле-ротические изменения сосудов [41][42][43][44][45]. Фактически ГЦ подавляет продуцирование NO эндотелиальными клетка-ми и тромбоцитами и увеличивает образование активных форм кислорода благодаря высвобождению арахидоно-вой кислоты из тромбоцитов.…”