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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
Published on: August 30, 2020
Left ventricular dysfunction and cerebral infarction from vasospasm after subarachnoid hemorrhage
Richard E Temes1, Elena Tessitore, J Michael Schmidt
1Neurological Intensive Care Unit, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Left ventricular dysfunction after subarachnoid hemorrhage (SAH) increases risks for cerebral infarction and other complications. However, with intensive care, it does not impact short-term survival or functional outcomes in SAH patients.
Area of Science:
- Cardiology
- Neurology
- Critical Care Medicine
Background:
- Neurogenic stunned myocardium (NSM) following subarachnoid hemorrhage (SAH) is recognized, but its clinical impact is not fully understood.
- Investigating the relationship between left ventricular (LV) dysfunction, cerebral vasospasm, and patient outcomes after SAH is crucial.
Purpose of the Study:
- To determine the influence of LV dysfunction and cerebral vasospasm on cerebral infarction.
- To assess the impact of LV dysfunction on serious cardiovascular events and functional outcomes post-SAH.
Main Methods:
- Analysis of 119 SAH patients with echocardiograms and transcranial Doppler (TCD) data, excluding those with prior cardiac disease.
- LV dysfunction defined as ejection fraction <40%; infarction from vasospasm adjudicated via clinical and imaging data.
- Functional outcomes measured using the modified Rankin Scale (mRS) at 15 and 90 days.
Main Results:
- 11% of patients exhibited LV dysfunction, associated with younger age, hydrocephalus, and specific ventricular filling patterns.
- Patients with LV dysfunction had higher rates of vasospasm-induced infarction, hypotension, and pulmonary edema.
- No significant association found between LV dysfunction and 14-day outcomes after adjusting for prognostic variables.
Conclusions:
- LV dysfunction post-SAH elevates the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema.
- Aggressive intensive care unit (ICU) support mitigates the effect of LV dysfunction on short-term survival and functional outcomes.
- Antihypertensive medication may offer cardioprotection and reduce catecholamine-mediated injury following SAH.
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