Are atherogenic index of plasma and triglyceride-glucose index associated with early neurological deterioration in patients with acute large artery atherosclerotic ischemic stroke?
Higher atherogenic index of plasma and triglyceride-glucose index are associated with an increased risk of early neurological deterioration in patients with acute large artery atherosclerotic ischemic stroke.
BACKGROUND: Stroke due to large artery atherosclerosis (LAA-stroke) has a poor early prognosis despite appropriate medical treatment. Recently, various parameters reflecting pathological conditions such as insulin resistance or atherogenic dyslipidemia have been proposed using triglyceride (TG) and other biomarkers. In this study, we evaluated the association between TG andTG-related parameters and early neurological deterioration (END) in patients with acute LAA stroke. METHODS: (TG level/high-density lipoprotein level) and TG-glucose (TyG) index = Ln (TG level x glucose level/2). END was defined as an increase of ≥ 2 in the total National Institutes of Health Stroke Scale (NIHSS) score or ≥ 1 in the motor NIHSS score within the first 72 h of admission. RESULTS: Six hundred and forty patients with acute LAA-stroke were evaluated. In multivariable analyses, AIP (adjusted odds ratio aOR: 1.93, 95% confidence interval: 1.32-2.82) was closely associated with END after adjustment for confounders. The TyG index (aOR: 2.22, 95% confidence interval: 1.51-3.27) also showed close association with END. The AIP and TyG index showed significant differences between the END and no END groups only in patients with LAA-stroke caused by intracranial atherosclerosis. In addition, AIP and TyG index were closely related to END only in patients with LAA-stroke caused by artery-to-artery embolism and branch atheromatous disease mechanisms. CONCLUSIONS: We found that TG and TG-related parameters were associated with the occurrence of END in patients with acute LAA-stroke. This association appeared differently depending on the location or mechanism of the relevant vessel that caused LAA-stroke.
Nam et al. (Wed,) studied this question.