Plasma growth differentiation factor − 8 / Myostatin level as prognostic biomarker of patients with ischemic stroke and acute revascularization therapy. PARADISE study

医学 四分位间距 改良兰金量表 内科学 血运重建 GDF15型 临床终点 溶栓 生物标志物 逻辑回归 冲程(发动机) 心脏病学 缺血性中风 缺血 临床试验 机械工程 生物化学 化学 心肌梗塞 工程类
作者
Pauline Jakubina,Alexandre Méloux,Gauthier Duloquin,Serge Aho,Catherine Vergely,Yannick Béjot
出处
期刊:Journal of the Neurological Sciences [Elsevier BV]
卷期号:448: 120611-120611 被引量:1
标识
DOI:10.1016/j.jns.2023.120611
摘要

Identifying biological markers of ischemic stroke (IS) is an important research approach to develop innovative therapeutic strategies. This study aimed to assess the association between plasma Growth Differentiation Factor-8 (GDF-8)/Myostatin levels and outcome of IS patients.Consecutive patients with acute IS treated with either intravenous thrombolysis and/or mechanical thrombectomy at Dijon University Hospital, France were prospectively included. Clinical variables were recorded, and plasma GDF-8 was collected just after the revascularization procedure. Primary endpoint was functional outcome at 3 months assessed by the modified Rankin Scale (mRS) score. Secondary endpoints included mRS scores at 6 and 12 months, and overall mortality over 1-year of follow-up.Among the 173 included patients (median age: 76 years, Interquartile range (IQR): 66-85; 49% women), median plasma GDF-8 levels at admission were significantly lower in those with a poor outcome at 3 months defined as a mRS score > 2 (2073 (IQR: 1564-2757) pg/mL versus 1471 (1192-2241) pg/mL, p < 0.001). Lower GDF-8 levels at admission were associated with higher 3-months mRS score in multivariable ordinal logistic regression analysis (OR = 0.9995; 95% CI: 0.9991-0.9999, p = 0.011). The association was also observed with 6- and 12-month mRS scores. Although mortality was higher in patients with lower GDF-8 levels, the association was not significant in multivariable Cox analysis.Lower plasma GDF-8 levels were associated with a poorer functional outcome in IS patients treated with acute revascularization therapy. Underlying pathophysiological mechanisms involving GDF-8 in post-stroke outcome remain to be elucidated.
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