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Myocardial injury and left ventricular performance after subarachnoid hemorrhage
1Department of Neurology, Columbia-Presbyterian Medical Center, New York, NY, USA. sam14@columbia.edu
Insights
Subarachnoid hemorrhage can cause cardiac injury, leading to impaired left ventricular performance. This cardiac dysfunction may increase the risk of cerebral ischemia and vasospasm in affected patients.
Area of Science:
- Cardiology
- Neurology
- Critical Care Medicine
Background:
- Subarachnoid hemorrhage (SAH) frequently causes electrocardiographic abnormalities and elevated cardiac enzymes (CK-MB).
- Neurogenic left ventricular dysfunction is observed in some SAH patients via echocardiography.
- The impact of this cardiac injury on cardiovascular hemodynamics remains unclear.
Purpose of the Study:
- To investigate the association between cardiac injury severity and hemodynamic performance after aneurysmal subarachnoid hemorrhage.
- To determine if cardiac dysfunction following SAH affects cardiovascular hemodynamics.
Main Methods:
- Retrospective study of 72 patients with aneurysmal SAH.
- Inclusion criteria: CK-MB levels, pulmonary artery catheter, echocardiogram, no prior cardiac disease.
- Hemodynamic profiles assessed, and cardiac injury classified by peak CK-MB levels and left ventricular wall motion abnormalities.
Main Results:
- Abnormal left ventricular wall motion correlated with higher CK-MB levels, poor neurological grade, and female sex.
- Left ventricular stroke volume and stroke work indices decreased with increasing cardiac injury severity.
- Reduced cardiac index was an independent predictor of symptomatic vasospasm.
Conclusions:
- Myocardial enzyme release and wall motion abnormalities indicate impaired left ventricular performance post-SAH.
- Severe cardiac injury can lead to reduced cardiac output, potentially increasing cerebral ischemia risk.
- This highlights a link between cardiac dysfunction and neurological outcomes in SAH patients.
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 <1%, n=36), mild (peak CK-MB 1% to 2%, n=21), moderate (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.