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Myocardial Ischemia and Vasospasm in Aneurysmal SAH

Myocardial Ischemia and Vasospasm in Aneurysmal SAH
动脉瘤性蛛网膜下腔出血的心肌缺血和血管痉挛
批准号:
7033052
负责人:
AMIN B KASSAM
金额:
$56.29万
依托单位国家:
美国
项目类别:
财政年份:
2004
资助国家:
美国
项目状态:
已结题
起止时间:
2004-04-01 至 2009-03-31

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中文摘要
翻译
描述(由申请人提供):动脉瘤性蛛网膜下腔出血(SAH)后5天内的心肌功能障碍包括心律失常、缺血和“神经源性休克心肌”。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、未被发现的或致命的。该应用程序将前瞻性地评估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SAH后主要并发症症状性血管痉挛(SV)的风险。该应用的中心假设是,在SAH后立即出现的儿茶酚胺激增(去甲肾上腺素(NE)肾上腺素(EPI))提供了一种与心肌和脑血管血管痉挛相关的共同机制,增加了继发性心肌和脑缺血和梗死的风险。具体目的是:1)确定儿茶酚胺释放(NE, EPI)的大小与心肌缺血和梗死的发生(通过ECG心律失常(ST段改变和T波反转)、心室功能下降之间的关系;升高的CB-K, CPK和cTnI水平))和2)决定SAH后前5天内心肌缺血和梗死的存在是否增加SAH后14天内SV的风险。将采用前瞻性、纵向、受试者组间重复测量设计,所有受试者将接受连续的血清采样(NE、EPI、心脏酶),同时进行强烈的神经生理监测、每日床边便携式超声心动图筛查和临床检查,以检测心肌梗死、缺血和SV的存在。
英文摘要
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.
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Myocardial Ischemia and Vasospasm in Aneurysmal SAH
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