Depressed cardiac index following subarachnoid hemorrhage was an independent predictor of symptomatic vasospasm (OR 2.1; 95% CI 1.0-4.1; P=0.04).
Cohort (n=72)
No
Myocardial injury after subarachnoid hemorrhage is associated with impaired left ventricular performance, and the resulting reduction in cardiac output may increase the risk of cerebral ischemia from vasospasm.
Odds Ratio: 2.1 (95% CI 1–4.1)
p-value: p=0.04
BACKGROUND AND PURPOSE: Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. METHODS: We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (n=67) or on the day of echocardiography (n=5) if surgery was not performed (mean, 3. 3+/-1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB 2%, n=6), or severe (abnormal left ventricular wall motion, n=9). RESULTS: Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels >2% (P<0.0001), poor neurological grade (P=0.002), and female sex (P=0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels <1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both P<0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (P<0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval 95% CI, 1.0 to 3.4; P=0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; P=0.04) were independent predictors of symptomatic vasospasm. CONCLUSIONS: Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm.
Mayer et al. (1999) conducted a cohort in Aneurysmal subarachnoid hemorrhage (n=72). Depressed cardiac index vs. Normal or elevated cardiac index was evaluated on Symptomatic vasospasm (OR 2.1, 95% CI 1.0-4.1, p=0.04). Depressed cardiac index following subarachnoid hemorrhage was an independent predictor of symptomatic vasospasm (OR 2.1; 95% CI 1.0-4.1; P=0.04).