Charité-Universitätsmedizin Berlin, Center for Stroke Research Berlin, Berlin, Germany.
Charité-Universitätsmedizin Berlin, Department of Neurology, Berlin, Germany.
Ann Neurol. 2017 Apr;81(4):502-511. doi: 10.1002/ana.24906. Epub 2017 Apr 3.
Elevated levels of cardiac troponin, and especially their relative changes over time, indicate acute myocardial injury. They are also frequently observed after acute ischemic stroke (AIS), indicating poor functional outcome and increased mortality. However, recent evidence showed that, in most AIS patients, myocardial injury is not caused by coronary ischemia. Instead, stroke lesion location has been suggested to precipitate myocardial injury.
Voxel-based lesion-symptom mapping (VLSM) was used in 299 patients who had a magnetic resonance imaging-confirmed acute ischemic stroke within the anterior circulation and a high-sensitivity cardiac troponin T (hs-cTnT) acquired on the day of admission. Of these, 228 had a second troponin measurement during the acute phase. The absolute hs-cTnT levels above the 99th percentile of a healthy reference population (≥14ng/l) as well as their relative temporal changes were used as continuous variables of interest in the VLSM model, including a multiple regression analysis adjusted for confounding variables.
The anterior insular cortex of the right hemisphere, in particular its dorsal subregion, was significantly associated with the relative temporal changes of hs-cTnT (p < 0.01, corrected for multiple comparisons). In contrast, the baseline hs-cTnT levels on admission were not related to lesion location anywhere within the anterior circulation.
Our results amplify recent evidence from functional neuroimaging, which suggests a prominent role of dorsal anterior insular cortex in the parasympathetic control of cardiac and autonomic function. Acute vascular damage of this insular subregion might lead to autonomic dysbalance and an upregulation of sympathetic function, thereby resulting in myocardial injury. Ann Neurol 2017;81:502-511.
心肌肌钙蛋白水平升高，尤其是其相对时间变化，提示急性心肌损伤。这些变化在急性缺血性脑卒中（AIS）后也经常观察到，表明预后不良和死亡率增加。然而，最近的证据表明，在大多数 AIS 患者中，心肌损伤不是由冠状动脉缺血引起的。相反，卒中病灶位置被认为可引发心肌损伤。
对 299 例前循环磁共振成像证实的急性缺血性脑卒中患者进行基于体素的病灶-症状映射（VLSM）分析，这些患者在入院当天检测到高敏心肌肌钙蛋白 T（hs-cTnT）。其中 228 例在急性期进行了第二次肌钙蛋白检测。绝对 hs-cTnT 水平高于健康参考人群第 99 百分位数（≥14ng/l）以及其相对时间变化被用作 VLSM 模型中的连续变量，包括调整混杂变量的多元回归分析。
右半球前岛叶皮质，特别是其背侧亚区，与 hs-cTnT 的相对时间变化显著相关（p<0.01，经多重比较校正）。相比之下，入院时的 hs-cTnT 基线水平与前循环内任何部位的病灶位置均无相关性。
我们的研究结果放大了来自功能神经影像学的最新证据，该证据表明背侧前岛叶皮质在心脏和自主神经功能的副交感神经控制中起重要作用。该岛叶亚区的急性血管损伤可能导致自主神经失衡和交感神经功能上调，从而导致心肌损伤。Ann Neurol 2017;81:502-511.
