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Updated: Aug 18, 2026

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
SSRI and statin use increases the risk for vasospasm after subarachnoid hemorrhage
A B Singhal1, M A Topcuoglu, D J Dorer
1Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. asinghal@partners.org
Insights
Selective serotonin reuptake inhibitors (SSRIs) and statin use are linked to increased vasospasm risk after subarachnoid hemorrhage (SAH). Further research is needed to understand the exact cause of this association.
Area of Science:
- Neurology
- Pharmacology
- Critical Care Medicine
Background:
- Medications affecting blood vessel tone may influence vasospasm risk post-aneurysmal subarachnoid hemorrhage (SAH).
- Understanding these medication effects is crucial for managing SAH patients.
Purpose of the Study:
- To investigate the association between pre-hemorrhagic medication use and the risk of vasospasm after aneurysmal SAH.
- To determine if specific drug classes predict vasospasm, symptomatic vasospasm, or poor outcomes.
Main Methods:
- Retrospective review of 514 SAH patients (1995-2003) using ICD-9 codes and medical records.
- Analysis of pre-hemorrhagic use of calcium channel blockers, beta-blockers, ACE inhibitors, aspirin, SSRIs, non-SSRI antidepressants, and statins.
- Evaluation of vasospasm and symptomatic vasospasm risk, and clinical outcomes.
Main Results:
- 62% of patients developed vasospasm; 29% had symptomatic vasospasm.
- SSRI use was associated with increased risk of symptomatic vasospasm (OR 1.42).
- Statin use increased the risk for vasospasm (OR 2.75), potentially due to withdrawal.
Conclusions:
- Patients using SSRIs or statins before SAH have a higher risk of developing vasospasm.
- The underlying reasons (indication, direct effects, withdrawal) for this increased risk require further investigation.
Background:
Use of medications with vasoconstrictive or vasodilatory effects can potentially affect the risk for vasospasm after aneurysmal subarachnoid hemorrhage (SAH).
Methods:
Using International Classification of Diseases-9 diagnostic codes followed by medical record review, the authors identified 514 patients with SAH admitted between 1995 and 2003 who were evaluated for vasospasm between days 4 and 14. The authors determined risks for vasospasm, symptomatic vasospasm, and poor clinical outcomes in patients with documented pre-hemorrhagic use of calcium channel blockers, beta-receptor blockers, ACE inhibitors, aspirin, selective serotonin reuptake inhibitors (SSRIs), non-SSRI vasoactive antidepressants, or statins.
Results:
Vasospasm developed in 62%, and symptomatic vasospasm in 29% of the cohort. On univariate analysis, the risk for all vasospasm tended to increase in patients taking SSRIs (p = 0.09) and statins (p = 0.05); SSRI use increased the risk for symptomatic vasospasm (p = 0.028). The Cochran-Armitage trend test showed that the proportion of patients taking SSRIs and statins increased significantly across three worsening categories (none, asymptomatic, symptomatic) of vasospasm. Logistic regression analysis showed that SSRI use tended to predict all vasospasm (O.R. 2.01 [0.91 to 4.45]), and predicted symptomatic vasospasm (O.R. 1.42 [1.06 to 4.33]). Statin exposure increased the risk for vasospasm (O.R. 2.75 [1.16 to 6.50]), perhaps from abrupt statin withdrawal (O.R. 2.54 [0.78 to 8.28]). Age < 50 years, Hunt-Hess grade 4 or 5, and Fisher Group 3 independently predicted all vasospasm, symptomatic vasospasm, poor discharge clinical status, and death.
Conclusion:
Selective serotonin reuptake inhibitor and statin users have a higher risk for subarachnoid hemorrhage-related vasospasm. Whether the underlying disease indication, direct actions, or rebound effects from abrupt drug withdrawal account for the associated risk warrants further investigation.
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