Relation of Elevation in Cardiac Troponin I to Clinical Severity, Cardiac Dysfunction, and Pulmonary Congestion in Patients With Subarachnoid Hemorrhage

An increase in cardiac troponin I (cTnI) occurs often after aneurysmal subarachnoid hemorrhage (SAH), but its significance is not well understood. One hundred three patients with SAH were prospectively evaluated in the SAHMII Study to determine the relations of cTnI to clinical severity, systolic and diastolic cardiac function, pulmonary congestion, and length of intensive care unit stay. Echocardiographic ejection fraction, wall motion score, mitral inflow early diastolic (E) and mitral annular early (E′) velocities were assessed. Thirty patients (29%) had mildly positive cTnI (0.1 to 1.0 ng/ml), 24 (23%) had highly positive cTnI (>1.0 ng/ml), and 49 (48%) had negative cTnI (<0.1 ng/ml). Highly positive cTnI was associated with worse neurologic disease, longer intensive care unit stay, and slight depression of ejection fraction (51 ± 11% [p <0.05] vs 59 ± 8% and 63 ± 6% in mildly positive or negative cTnI groups, respectively). Highly positive cTnI was also associated with abnormal wall motion acutely (>1.31 ng/ml; 76% sensitivity, 91% specificity), which typically resolved within 5 to 10 days. Both mildly or highly positive cTnI were associated with acute diastolic dysfunction, with E/E′ of 17 ± 6 and 16 ± 6 (both p <0.05) vs 13 ± 4 in patients with negative cTnI. Prevalences of pulmonary congestion were 79% (p <0.05) in patients with highly positive cTnI, 53% (p <0.05) in patients with mildly positive cTnI, and 29% in cTnI-negative patients. In conclusion, highly positive cTnI with SAH was associated with clinical neurologic severity, systolic and diastolic cardiac dysfunction, pulmonary congestion, and longer intensive care unit stay. Even mild increases in cTnI were associated with diastolic dysfunction and pulmonary congestion.