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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