Admission serum tropomyosin 4 levels predict 1-year functional outcomes in acute ischemic stroke

入院时血清原肌球蛋白4水平可预测急性缺血性卒中患者1年后的功能预后。

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Abstract

BACKGROUND: Tropomyosin 4 (TPM4) regulates neurite outgrowth and vascular pathology but its role as a biomarker for predicting outcomes in stroke patients is unclear. This study investigated the association between serum TPM4 levels and 1-year functional outcomes in acute ischemic stroke (AIS) patients. METHODS: AIS patients admitted within 24 h post-onset from the Chengdu Stroke Registry were included. Serum TPM4 levels were measured by enzyme-linked immunosorbent assay (ELISA). Poor functional outcomes were defined as a modified Rankin Scale (mRS) score >2 at 1 year after stroke onset. Multivariate logistic regression assessed TPM4's association with outcomes, with its predictive incremental value evaluated by discrimination, reclassification, and overall performance metrics. RESULTS: Among 181 patients (median age 66 years, 64.1% male), 59 (32.6%) experienced poor outcomes at 1 year, including 16 deaths (8.8%). Serum TPM4 levels on admission were negatively correlated with the National Institutes of Health Stroke Scale (NIHSS) score (r = -0.185, p = 0.013). Adjusted for confounders, lower serum TPM4 levels were independently associated with 1-year poor functional outcomes (adjusted OR 0.045, 95% CI [0.005-0.393], p = 0.005). Serum TPM4 levels had acceptable discriminative ability for predicting poor outcomes (AUROC 0.706, 95% CI [0.621-0.791], p < 0.0001). Incorporating TPM4 into the basic model significantly improved the predictive power for poor functional outcomes (net reclassification index: 31.87%, p = 0.041; integrated discrimination improvement: 5.01%, p = 0.008; Brier score decreased from 0.16 to 0.15, p = 0.012). CONCLUSIONS: Lower serum TPM4 levels on admission were independently associated with poor functional outcomes at 1 year in AIS patients, suggesting that TPM4 may serve as a potential biomarker for long-term outcomes and offer insights into its potential role in stroke pathophysiology. These findings need to be further verified in external cohorts.

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