Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage.
OBJECTIVE
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 microg/liter with the immunoenzymatic assay and 0.4 microg/liter with the sandwich immunoassay), while five had abnormal CK-MB levels (upper limit of normal is 8 microg/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 microg/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.
Parekh
N
N
Royal Brisbane Hospital, Herston, Australia.
Venkatesh
B
B
Cross
D
D
Leditschke
A
A
Atherton
J
J
Miles
W
W
Winning
A
A
Clague
A
A
Rickard
C
C
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000652:urine; D009202:Cardiomyopathies / Q000097:blood* / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism; D002395:Catecholamines / Q000652:urine; D003402:Creatine Kinase / Q000097:blood; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D009211:Myoglobin / Q000097:blood; D011379:Prognosis; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013345:Subarachnoid Hemorrhage / Q000097:blood* / Q000150:complications; D019210:Troponin I / Q000097:blood*
D015415:Biomarkers; D002395:Catecholamines; D009211:Myoglobin; D019210:Troponin I; D003402:Creatine Kinase