OBJECTIVES We studied the incidence of myocardial injury in aneurysmal suba
rachnoid hemorrhage (SAH) using the more sensitive cardiac troponin I (cTnI
) assay, correlated changes in cTnI with creatine kinase, MB fraction (CK-M
B), myoglobin, and catecholamine metabolite assays, and examined the predic
tive 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 cardiova
scular 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 prese
nce of ST-T changes, prolonged QT intervals, and arrhythmias. An abnormal e
chocardiogram 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 norm
al is 0.1 mu g/liter with the immunoenzymatic assay and 0.4 mu g/liter with
the sandwich immunoassay), while five had abnormal CK-MB levels (upper lim
it of normal is 8 mu g/liter). Patients with more severe grades of SAH were
more Likely to develop a cTnI leak (p < 0.05). Patients with cTnI elevatio
ns were more likely to demonstrate ECG abnormalities (p < 0.01) and manifes
t clinical myocardial dysfunction (p < 0.01) as evidenced by the presence o
f 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 9
4%, respectively. Elevations in myoglobin levels (upper limit of normal <70
mu g/iiter) 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 in
jury 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 ane
urysmal SAH. (J Am Coll Cardiol 2000;36:1328-35) (C) 2000 by the American C
ollege of Cardiology.