Myocardial Ischemia and Vasospasm in Aneurysmal SAH

描述(由申请人提供)：动脉瘤性蛛网膜下腔出血(SAH)后前五天内的心肌功能障碍包括心律失常、缺血和“神经源性顿抑心肌”。一部分患者肌钙蛋白I水平升高，表明心肌缺血和梗死。然而，在这一人群中，心肌缺血的真实发生率是未知的，因为缺血发作是短暂的、未被检测到的或致命的。这项应用将前瞻性地评估SAH人群中心肌缺血和梗死的发生率，并确定心肌缺血的存在是否显著增加了症状性血管痉挛(SV)的风险，SV是SAH后的一个主要并发症。这一应用的中心假设是，SAH后立即出现儿茶酚胺激增(去甲肾上腺素(NE)、肾上腺素(EPI))，提供了与心肌和脑血管痉挛相关的共同机制，从而增加了继发性心肌和脑缺血和梗塞的风险。其具体目的是：1)确定儿茶酚胺释放的大小(NE、EPI)与心肌缺血和梗塞的发生(如心电图心律失常(ST段改变和T波倒置)、心功能下降；CB-K、CPK和cTnI水平升高)之间的关系；以及2)确定SAH后前5天内存在心肌缺血和梗塞是否增加了SAH后14天内SV的风险。所有受试者将采用前瞻性、纵向、组内重复测量设计，在进行密集的神经生理监测、每日床边便携式超声心动图筛查和临床检查的同时，对血清(NE、EPI、心肌酶)进行连续采样，以检测是否存在心肌梗死、缺血和SV的结果。

DESCRIPTION (provided by applicant): Myocardial dysfunction within the first five days following aneurysmal subarachnoid hemorrhage (SAH) includes dysrhythmia, ischemia and "neurogenic stunned myocardium." A subset of patients has elevated troponin I levels indicative of myocardial ischemia and infarct. However, the true incidence of myocardial ischemia in this population is unknown in that ischemic episodes are short-lived, undetected, or deadly. This application will prospectively evaluate the incidence of myocardial ischemia and infarct in the SAH population and determine whether the presence of myocardial ischemia significantly increases the risk of symptomatic vasospasm (SV), a major complication following SAH. The central hypothesis of this application is that a catecholamine surge (norepinephrine (NE) epinephrine (EPI)) immediately after SAH provides a common mechanism associated with both vasospasm of the myocardial and cerebral vessels that increases the risk for secondary myocardial and cerebral ischemia and infarct. The specific aims are to: 1) determine the association between the magnitude of the catecholamine release (NE, EPI) the occurrence of myocardial ischemia and infarct (as detected by ECG arrythmias (ST changes and T wave inversion), decreased ventricular function; elevated CB-K, CPK, and cTnI levels)) and 2) determine whether the presence of myocardial ischemia and infarct within the first 5 days after SAH increases the risk of SV within 14 days following an SAH. A prospective, longitudinal, within-subject between-group repeated measure design will be used in that all subjects will undergo serial sampling of serum (NE, EPI, cardiac enzymes) concurrent with intense neurophysiologic monitoring, daily bedside portable echocardiography screening and clinical examinations in order to detect the presence of the outcomes of myocardial infarct and ischemia and SV.