PDF(Pubmed)
Abstract：
Magnesium (Mg) is a neuroprotectant in preclinical models. Lower serum Mg levels have been associated with symptomatic hemorrhagic transformation (HT) in patients with ischemic stroke. Early treatment of acute ischemic stroke with Mg may reduce rates of symptomatic HT.
In this post hoc study of the Field Administration of Stroke Therapy Magnesium (FAST-MAG) trial, 1,245 participants with a diagnosis of cerebral ischemia received 20 g of Mg or placebo initiated in the prehospital setting. Posttreatment serum Mg level was measured for 809 participants. Cases of clinical deterioration, defined as worsening by ≥4 points on the National Institute of Health Stroke Scale (NIHSS), were imaged and evaluated for etiology. Symptomatic HT was defined as deterioration with imaging showing new hemorrhage.
Clinical deterioration occurred in 187 and symptomatic HT in 46 of 1,245 cases of cerebral ischemia. Rates of deterioration and symptomatic HT were not significantly lower in those who received Mg (15.7% vs. 14.4%, p = 0.591; 2.8% vs. 4.6%, p = 0.281). In cases where serum Mg level was obtained posttreatment, lower serum Mg level (<1.7 mg/dL) was associated with significantly higher rates of deterioration and symptomatic HT (27.5% vs. 15.5%, p = 0.0261; 11.6% vs. 3.65%, p = 0.00819).
Treatment with Mg did not significantly reduce rates of clinical deterioration or symptomatic HT. Future analysis should address whether treatment with Mg could have influenced the subgroup with low serum Mg at baseline.
In this post hoc study of the Field Administration of Stroke Therapy Magnesium (FAST-MAG) trial, 1,245 participants with a diagnosis of cerebral ischemia received 20 g of Mg or placebo initiated in the prehospital setting. Posttreatment serum Mg level was measured for 809 participants. Cases of clinical deterioration, defined as worsening by ≥4 points on the National Institute of Health Stroke Scale (NIHSS), were imaged and evaluated for etiology. Symptomatic HT was defined as deterioration with imaging showing new hemorrhage.
Clinical deterioration occurred in 187 and symptomatic HT in 46 of 1,245 cases of cerebral ischemia. Rates of deterioration and symptomatic HT were not significantly lower in those who received Mg (15.7% vs. 14.4%, p = 0.591; 2.8% vs. 4.6%, p = 0.281). In cases where serum Mg level was obtained posttreatment, lower serum Mg level (<1.7 mg/dL) was associated with significantly higher rates of deterioration and symptomatic HT (27.5% vs. 15.5%, p = 0.0261; 11.6% vs. 3.65%, p = 0.00819).
Treatment with Mg did not significantly reduce rates of clinical deterioration or symptomatic HT. Future analysis should address whether treatment with Mg could have influenced the subgroup with low serum Mg at baseline.
摘要：
背景：镁（Mg）是临床前模型中的神经保护剂。较低的血清Mg水平与缺血性中风患者的症状性出血性转化（HT）有关。早期用Mg治疗急性缺血性卒中可降低有症状HT的发生率。
方法：在这项卒中治疗镁的现场管理（FAST-MAG）试验的事后研究中，1,245名诊断为脑缺血的参与者在院前环境中接受了20gMg或安慰剂。测量809名参与者的治疗后血清Mg水平。临床恶化的病例，定义为在美国国立卫生研究院卒中量表（NIHSS）上恶化≥4分，进行成像和病因评估。症状性HT定义为影像学表现为新出血的恶化。
结果：在1,245例脑缺血中，187例发生临床恶化，46例发生症状性HT。接受Mg治疗的患者的恶化率和有症状的HT并未显着降低（15.7％vs.14.4%,p=0.591;2.8%vs.4.6%,p=0.281）。在治疗后获得血清Mg水平的情况下，较低的血清Mg水平（<1.7mg/dL）与明显较高的恶化率和有症状的HT（27.5％vs.15.5%,p=0.0261；11.6%vs.3.65%,p=0.00819)。
结论：用Mg治疗并没有显著降低临床恶化或有症状的HT的发生率。未来的分析应解决Mg治疗是否可能影响基线血清Mg含量低的亚组。
方法：在这项卒中治疗镁的现场管理（FAST-MAG）试验的事后研究中，1,245名诊断为脑缺血的参与者在院前环境中接受了20gMg或安慰剂。测量809名参与者的治疗后血清Mg水平。临床恶化的病例，定义为在美国国立卫生研究院卒中量表（NIHSS）上恶化≥4分，进行成像和病因评估。症状性HT定义为影像学表现为新出血的恶化。
结果：在1,245例脑缺血中，187例发生临床恶化，46例发生症状性HT。接受Mg治疗的患者的恶化率和有症状的HT并未显着降低（15.7％vs.14.4%,p=0.591;2.8%vs.4.6%,p=0.281）。在治疗后获得血清Mg水平的情况下，较低的血清Mg水平（<1.7mg/dL）与明显较高的恶化率和有症状的HT（27.5％vs.15.5%,p=0.0261；11.6%vs.3.65%,p=0.00819)。
结论：用Mg治疗并没有显著降低临床恶化或有症状的HT的发生率。未来的分析应解决Mg治疗是否可能影响基线血清Mg含量低的亚组。
