OBJECTIVE: Cardiac dysfunction after aneurysmal subarachnoid hemorrhage (SAH) is associated with elevation of serum cardiac troponin I (cTnI) levels. Elevation of cTnI predicts cardiopulmonary and neurological complications, and poor outcome. METHODS: We retrospectively reviewed the medical and radiologic records of 114 (male : 30, female : 84) patients who developed aneurysmal SAH between January 2006 and June 2007 and had no history of previous cardiac problems. We evaluated their electrocardiography and cTnI level, which had been measured at admission. A cTnI level above 0.5 microg/L was defined as an indicator of cardiac injury following SAH. We examined various clinical factors for their association with cTnI elevation and analyzed data using chi-square test, t-test and logistic regression test with SPSS version 12.0. The results were considered significant at p < 0.05. RESULTS: THE FOLLOWING PARAMETERS SHOWS A CORRELATION WITH CTNI ELEVATION : higher Hunt-Hess (H-H) grade (p = 0.000), poor Glasgow Outcome Scale (GOS) score (p = 0.000), profound pulmonary complication (p = 0.043), higher heart rate during initial three days following SAH (p = 0.029), ruptured aneurysm on communicating segment of internal carotid artery (p = 0.025), incidence of vasospasm (p = 0.421), and duration of hyperdynamic therapy for vasospasm (p = 0.292). A significant determinants for outcome were cTnI elevation (p = 0.046) and H-H grade (p = 0.000) in a multivariate study. CONCLUSION: A cTnI is a good indicator for cardiopulmonary and neurologic complications and outcome following SAH. Consideration of variable clinical factors that related with cTnI elevation may be useful tactics for treatment of SAH and concomitant complications.
OBJECTIVE:Cardiac dysfunction after aneurysmal subarachnoid hemorrhage (SAH) is associated with elevation of serum cardiac troponin I (cTnI) levels. Elevation of cTnI predicts cardiopulmonary and neurological complications, and poor outcome. METHODS: We retrospectively reviewed the medical and radiologic records of 114 (male : 30, female : 84) patients who developed aneurysmalSAH between January 2006 and June 2007 and had no history of previous cardiac problems. We evaluated their electrocardiography and cTnI level, which had been measured at admission. A cTnI level above 0.5 microg/L was defined as an indicator of cardiac injury following SAH. We examined various clinical factors for their association with cTnI elevation and analyzed data using chi-square test, t-test and logistic regression test with SPSS version 12.0. The results were considered significant at p < 0.05. RESULTS: THE FOLLOWING PARAMETERS SHOWS A CORRELATION WITH CTNI ELEVATION : higher Hunt-Hess (H-H) grade (p = 0.000), poor Glasgow Outcome Scale (GOS) score (p = 0.000), profound pulmonary complication (p = 0.043), higher heart rate during initial three days following SAH (p = 0.029), ruptured aneurysm on communicating segment of internal carotid artery (p = 0.025), incidence of vasospasm (p = 0.421), and duration of hyperdynamic therapy for vasospasm (p = 0.292). A significant determinants for outcome were cTnI elevation (p = 0.046) and H-H grade (p = 0.000) in a multivariate study. CONCLUSION: A cTnI is a good indicator for cardiopulmonary and neurologic complications and outcome following SAH. Consideration of variable clinical factors that related with cTnI elevation may be useful tactics for treatment of SAH and concomitant complications.
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