Clinical and Translational Neuroscience Unit, Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY
Department of Neurology, Weill Cornell Medicine, New York, NY.
J Am Heart Assoc. 2017 Sep 22;6(9):e005905. doi: 10.1161/JAHA.117.005905.
Our aim was to determine whether patients with embolic strokes of undetermined source (ESUS) have higher rates of elevated troponin than patients with noncardioembolic strokes.
CAESAR (The Cornell Acute Stroke Academic Registry) prospectively enrolled all adults with acute stroke from 2011 to 2014. Two neurologists used standard definitions to retrospectively ascertain the etiology of stroke, with a third resolving disagreements. In this analysis we included patients with ESUS and, as controls, patients with small- and large-artery strokes; only patients with a troponin measured within 24 hours of stroke onset were included. A troponin elevation was defined as a value exceeding our laboratory's upper limit (0.04 ng/mL) without a clinically recognized acute ST-segment elevation myocardial infarction. Multiple logistic regression was used to evaluate the association between troponin elevation and ESUS after adjustment for demographics, stroke severity, insular infarction, and vascular risk factors. In a sensitivity analysis we excluded patients diagnosed with atrial fibrillation after discharge. Among 512 patients, 243 (47.5%) had ESUS, and 269 (52.5%) had small- or large-artery stroke. In multivariable analysis an elevated troponin was independently associated with ESUS (odds ratio 3.3; 95% confidence interval 1.2, 8.8). This result was unchanged after excluding patients diagnosed with atrial fibrillation after discharge (odds ratio 3.4; 95% confidence interval 1.3, 9.1), and the association remained significant when troponin was considered a continuous variable (odds ratio for log[troponin], 1.4; 95% confidence interval 1.1, 1.7).
Elevations in cardiac troponin are more common in patients with ESUS than in those with noncardioembolic strokes.
我们的目的是确定隐源性脑栓塞(ESUS)患者的肌钙蛋白升高率是否高于非心源性脑梗死患者。
CAESAR(康奈尔急性脑卒中学术登记处)前瞻性纳入 2011 年至 2014 年所有急性脑卒中患者。两名神经科医生使用标准定义回顾性确定卒中病因,第三位医生解决分歧。在本分析中,我们纳入了 ESUS 患者,并将小动脉和大动脉梗死患者作为对照;仅纳入了在卒中发病后 24 小时内测量肌钙蛋白的患者。肌钙蛋白升高定义为超过我们实验室上限(0.04ng/ml)而无临床认可的急性 ST 段抬高型心肌梗死。采用多变量逻辑回归评估校正人口统计学、卒中严重程度、岛叶梗死和血管危险因素后,肌钙蛋白升高与 ESUS 之间的关联。在敏感性分析中,我们排除了出院后诊断为心房颤动的患者。在 512 例患者中,243 例(47.5%)为 ESUS,269 例(52.5%)为小动脉或大动脉梗死。多变量分析显示,肌钙蛋白升高与 ESUS 独立相关(比值比 3.3;95%置信区间 1.2,8.8)。在排除出院后诊断为心房颤动的患者后,这一结果保持不变(比值比 3.4;95%置信区间 1.3,9.1),并且当肌钙蛋白被视为连续变量时,这种关联仍然显著(肌钙蛋白对数的比值比,1.4;95%置信区间 1.1,1.7)。
与非心源性脑梗死患者相比,ESUS 患者的心肌肌钙蛋白升高更为常见。