Background and Purpose Cardiac injury persistence after aneurysmal subarachnoid hemorrhage (aSAH) is not well described. We hypothesized that post-aSAH cardiac injury, detected by elevated cardiac troponin I (cTnI), is related to aSAH severity and associated with electrocardiographic and structural echocardiographic abnormalities that are persistent. Methods Prospective longitudinal study was conducted of patients with aSAH with Fisher grade ≥2 and/or Hunt/Hess grade ≥3. Serum cTnI was collected on Days 1 to 5; cohort dichotomized into peak cTnI ≥0.3 ng/mL (elevated) or cTnI ≥0.3 ng/mL. Relationships among cTnI and aSAH severity, 12-lead electrocardiography early (≤4 days) and late (≥7 days), Holter monitoring on Days 1 to 5, and transthoracic echocardiogram (left ventricular ejection fraction and regional wall motion abnormalities) early (Days 0 to 5) and late (Days 5 to 12) were evaluated. Results Of 204 subjects, 31% had cTnI ≥0.3 ng/mL. cTnI ≥0.3 ng/mL was incrementally related to aSAH severity by admission symptoms (Hunt/Hess P=0.001) and blood load (Fisher P=0.028). More patients with cTnI ≥0.3 ng/mL had prolonged QTc on early (63% versus 30%, P<0.0001) and late electrocardiography (24% versus 7%, P=0.024). On Holter monitoring, more patients with cTnI ≥0.3 ng/mL had ventricular tachycardia/fibrillation (22% versus 9%, P=0.018) but not atrial fibrillation/flutter (P=0.241). Cardiac troponin I ≥0.3 ng/mL was associated with both early ejection fraction <50% (44% versus 5%, P<0.0001) and regional wall motion abnormalities (44% versus 4%, P<0.0001). Regional wall motion abnormalities predominated in basal and midventricular segments and persisted to some degree in 73% of patients affected, whereas ejection fraction <50% persisted in 59% of patients affected. Conclusions Cardiac injury is incrementally worse with increasing aSAH severity and associated with persistent QTc prolongation and ventricular arrhythmias. Regional wall motion abnormalities and depressed ejection fraction persist to some degree in the majority of those affected.

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.

From these results and those in the published literature, in-stent complication rates are low in carefully selected patients. The use of dual antiplatelet therapy, sensitivity assays, and glycoprotein IIb/IIIa inhibitors may decrease the rate of acute and chronic in-stent complications.