CARDIAC AUTONOMIC CONSEQUENCES OF HEMISPHERE STROKE

中风的受害者大多死于心脏原因。 虽然他们 缺血性心脏病的发病率很高，尸检和实验 对急性中风的研究表明，心肌缺血不是中风的原因， 死亡 相反，交感神经张力增加导致心脏损伤， 心律失常也有牵连。 根据以往的研究结果，建议 左侧大脑中动脉（MCA）中风涉及大脑中动脉或右侧大脑中动脉 MCA卒中使心脏自主神经平衡向 交感神经优势，可导致心律失常。 没有 前瞻性临床研究已经比较了中风位置和心脏 结果。 我们的总体目标是 减少中风相关的主要原因 通过确定急性卒中后的心脏结局是否不同 根据：卒中位置（AIM 1）;与心脏自主神经相关 张力（AIM 2）;以及患者是否存在不良心脏事件的长期风险 结果可以通过临床神经，心脏和自主神经来预测 多变量分析（AIM 3）。 总体研究设计 包括选择大脑半球或脑干1周内的患者 中风 每日进行心脏和神经系统检查， 再过一周 既存冠心病（CAD）将 通过检查、病史、ECG、铊扫描和 超声心动图; CAD对心脏结局的贡献将通过以下方式治疗 多变量分析 心脏结局包括：新发ECG变化， 心律失常和心脏收缩力和心脏功能的变化 心肌梗死、心绞痛和心源性猝死。 这些 将在入选研究后的第一周内进行评估， 此后定期1年。 心脏事件的发生率为 与中风位置和心脏自主神经张力相关，并与 TIA患者作为对照组。 心血管自主 将通过心率和血压的频谱分析来评估音调 使用专门设计的心脏自主平台， 尿儿茶酚胺排泄 用于比较的对照组 包括TIA患者和年龄匹配正常个体。 完成 这些目标应指明针对最常见原因的预防战略 中风后死亡

Victims of stroke most commonly die from cardiac causes. Although they have a high incidence of ischemic heart disease, autopsy and experimental studies in acute stroke indicate that cardiac ischemia is not the cause of death. Instead, increased sympathetic tone causing cardiac damage and arrhythmias is implicated. As a result of previous studies it is suggested that left middle cerebral artery (MCA) stroke involving the insula or right MCA stroke sparing the insula shifts cardiac autonomic balance towards sympathetic predominance which can cause cardiac arrhythmias. No prospective clinical studies have yet compared stroke location and cardiac outcome. Our overall goal is to reduce the prime cause of stroke-related mortality by determining whether cardiac outcomes after acute stroke differ according to: stroke location (AIM 1); in relation to cardiac autonomic tone (AIM 2); and whether patients at longterm risk for adverse cardiac outcome can be predicted by clinical neurological, cardiac and autonomic status using multivariate analysis (AIM3). The overall study design involves selection of patients within 1 week of hemisphere or brainstem stroke. Daily cardiac and neurological examinations will be performed for a further week. Pre-existing coronary artery disease (CAD) will be ascertained by examination, history, ECG, thallium scan and echocardiography; contribution of CAD to cardiac outcome will be treated by multivariate analysis. Cardiac outcomes include: new onset ECG changes, cardiac arrhythmias and changes in cardiac contractility and cardiac enzymes; myocardial infarction, angina and sudden cardiac death. These will be assessed during the first week after inclusion in the study and regularly for 1 year thereafter. Incidence of cardiac events will be related to stroke location and cardiac autonomic tone, and compared to the incidence in TIA patients as a control group. Cardiovascular autonomic tone will be assessed by spectral analysis of heart rate and blood pressure variability using a specially designed cardiac autonomic platform and by urinary catecholamine excretion. Control groups for comparison will include TIA patients and age-matched normal individuals. Accomplishment of these aims should indicate prevention strategies for the most common cause of post-stroke death.