Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage

Parekh, Nilesh, Venkatesh, Bala, Cross, David, Leditschke, Anne, Atherton, John, Miles, William, Winning, Adam, Clague, Alan and Rickard, Claire (2000) Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage. Journal of the American College of Cardiology, 36 4: 1328-1335. doi:10.1016/S0735-1097(00)00857-3


Author Parekh, Nilesh
Venkatesh, Bala
Cross, David
Leditschke, Anne
Atherton, John
Miles, William
Winning, Adam
Clague, Alan
Rickard, Claire
Title Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage
Journal name Journal of the American College of Cardiology   Check publisher's open access policy
ISSN 0735-1097
1558-3597
Publication date 2000-10
Sub-type Article (original research)
DOI 10.1016/S0735-1097(00)00857-3
Volume 36
Issue 4
Start page 1328
End page 1335
Total pages 8
Place of publication San Diego, CA, United States
Publisher Elsevier
Language eng
Formatted abstract
OBJECTIVES We studied the incidence of myocardial injury in aneurysmal subarachnoid hemorrhage (SAH) using the more sensitive cardiac troponin I (cTnI) assay, correlated changes in cTnI with creatine kinase, MB fraction (CK-MB), myoglobin, and catecholamine metabolite assays, and examined the predictive value of changes in cTnI for myocardial dysfunction.
BACKGROUND Myocardial injury in aneurysmal SAH as evidenced by elevated CK-MB fraction has been reported. Little published data exist on the value of cTnI measurements in aneurysmal SAH.
METHODS Thirty-nine patients were studied for seven days. Clinical cardiovascular assessment, electrocardiographic (ECG), echocardiography, cTnI, CK, CK-MB and CK-MB index, myoglobin and 24-h urinary catecholamine assays were performed in all patients. The ECG abnormalities were defined by the presence of ST-T changes, prolonged QT intervals, and arrhythmias. An abnormal echocardiogram was defined by the presence of wall-motion abnormalities and a reduced ejection fraction. The severity of SAH was graded clinically and radiologically.
RESULTS Eight patients demonstrated elevations in cTnI (upper limit of normal is 0.1 μg/liter with the immunoenzymatic assay and 0.4 μg/liter with the sandwich immunoassay), while five had abnormal CK-MB levels (upper limit of normal is 8 μg/liter). Patients with more severe grades of SAH were more likely to develop a cTnI leak (p < 0.05). Patients with cTnI elevations were more likely to demonstrate ECG abnormalities (p < 0.01) and manifest clinical myocardial dysfunction (p < 0.01) as evidenced by the presence of a gallop rhythm on auscultation and clinical or radiological evidence of pulmonary edema as compared to those with CK-MB elevations. The sensitivity and specificity of cTnI to predict myocardial dysfunction were 100% and 91%, respectively, whereas the corresponding figures for CK-MB were 60% and 94%, respectively. Elevations in myoglobin levels (upper limit of normal <70 μg/liter) and urinary catecholamine metabolites (urinary vanilmandelate/creatinine ratio upper limit of normal, 2.6) are a nonspecific finding.
CONCLUSIONS Measurements of cTnI reveal a higher incidence of myocardial injury than predicted by CK-MB in aneurysmal SAH, and elevations of cTnI are associated with a higher incidence of myocardial dysfunction. Thus, cTnI is a highly sensitive and specific indicator of myocardial dysfunction in aneurysmal SAH.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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Created: Wed, 30 May 2012, 12:03:14 EST by Associate Professor John Atherton on behalf of Medical Imaging - RBWH