Stroke severity–dependent prognostic value of the C-reactive protein–triglyceride glucose index after acute ischemic stroke

Abstract

Functional outcomes after acute ischemic stroke vary substantially among patients with similar neurological deficit severity, suggesting that factors beyond acute injury burden contribute to recovery. Metabolic–inflammatory dysregulation represents a chronic host condition that may influence the poststroke recovery processes. Whether such background vulnerability modifies stroke prognosis across different levels of baseline neurological severity remains unclear. We conducted a single-center retrospective cohort study including 1,017 consecutive patients with acute ischemic stroke admitted within 24 h of symptom onset. The C-reactive protein–triglyceride glucose index (CTI), calculated using a previously published logarithmic formula incorporating hs-CRP, triglycerides, and fasting blood glucose, was categorized into quartiles. The primary outcome was poor functional outcome at 90 days (modified Rankin Scale score 3–6). Multivariable logistic regression models with sequential adjustment were applied. Potential interaction between CTI and baseline stroke severity was evaluated using multiplicative interaction terms between CTI and admission National Institutes of Health Stroke Scale (NIHSS). Overall, 423 patients (41.6%) experienced poor functional outcome at 90 days. In unadjusted analyses, rates of poor outcome did not differ significantly across CTI quartiles. After adjustment for baseline NIHSS, higher CTI levels were associated with increased odds of poor functional outcome; however, in the fully adjusted model incorporating treatment modality, this association was attenuated and became borderline significant (OR 1.53, 95% CI 0.99–2.37, P  = 0.055). An interaction between CTI and admission NIHSS was observed ( P  = 0.039). Stratified analyses suggested that elevated CTI was associated with poor functional outcome among patients with moderate-to-severe stroke (NIHSS ≥ 6), whereas no clear association was observed among those with mild stroke. Rates of symptomatic intracranial hemorrhage and early hemorrhagic transformation did not differ across CTI quartiles. The prognostic relevance of CTI after acute ischemic stroke appears to vary according to baseline stroke severity. In exploratory analyses, elevated CTI may help identify patients with moderate-to-severe stroke who are at increased risk of poor functional recovery beyond what is captured by baseline neurological severity. However, given the borderline statistical significance in the fully adjusted model, these findings should be interpreted as hypothesis-generating and suggest that CTI may reflect chronic metabolic–inflammatory vulnerability and may provide prognostic information complementary to admission NIHSS.