Clinical significance of elevated troponin I levels in patients with nontraumatic subarachnoid hemorrhage.
OBJECTIVE
Aneurysmal subarachnoid hemorrhage (SAH) is associated with electrocardiographic abnormalities, regional or focal wall-motion abnormalities on echocardiograms, and/or increased creatine kinase MB isoenzyme (CK-MB) or cardiac troponin I (cTnI). The goal of this prospective study was to compare the sensitivity and specificity of cTnI with those of CK-MB in the prediction of left ventricular dysfunction on echocardiograms in patients with nontraumatic SAH. In addition, those patients with abnormal findings on their echocardiograms and elevated cTnI levels were further evaluated for the presence of coronary artery disease (CAD) by a cardiologist and to determine whether any left ventricular dysfunction that had been detected was reversible.


METHODS
The authors obtained electrocardiograms and echocardiograms, and measured serial levels of cardiac enzymes (CK-MB and cTnI) in 43 patients with nontraumatic SAH. Patients with known CAD were excluded. Those patients found to have elevated enzyme levels and abnormal findings on their echocardiograms underwent additional evaluation for CAD. The sensitivity and specificity of both cTnI and CK-MB for detecting left ventricular function were determined. Twenty-eight percent of patients with SAH in the study had elevated cTnI levels within the first 24 hours after hemorrhage. Seven of the 12 patients had evidence of left ventricular dysfunction on echocardiograms. In all these patients a return to baseline function was found during follow-up examinations. The authors found that cTnI is much more sensitive than CK-MB (100% compared with 29%) in the detection of left ventricular dysfunction in patients with SAH.


CONCLUSIONS
An elevated level of cTnI is a good indicator of left ventricular dysfunction in patients with SAH. In this study cardiac dysfunction was reversible and should not necessarily preclude these patients from undergoing operative interventions or becoming heart donors. Clinical management may require more aggressive hemodynamic monitoring until cardiac function returns to normal.
Deibert
Ellen
E
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63108, USA. deiberte@neuro.wustl.edu
Barzilai
Benico
B
Braverman
Alan C
AC
Edwards
Dorothy Farrar
DF
Aiyagari
Venkatesh
V
Dacey
Ralph
R
Diringer
Michael
M
D000328:Adult; D000368:Aged; D015415:Biomarkers; D002395:Catecholamines / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications; D009211:Myoglobin / Q000097:blood; D011654:Pulmonary Edema / Q000175:diagnosis / Q000209:etiology; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013345:Subarachnoid Hemorrhage / Q000097:blood* / Q000000981:diagnostic imaging; D014057:Tomography, X-Ray Computed; D014335:Tropomyosin / Q000097:blood; D019210:Troponin I / Q000097:blood*
D015415:Biomarkers; D002395:Catecholamines; D009211:Myoglobin; D014335:Tropomyosin; D019210:Troponin I; D003402:Creatine Kinase