Eicosapentaenoic Acid Cerebral Vasospasm Therapy Study
Eicosapentaenoic Acid Cerebral Vasospasm Therapy Study (EVAS): Effect of Eicosapentaenoic Acid on Cerebral Vasospasm Following Subarachnoid Hemorrhage
  • Phase

    Phase 4
  • Study Type

  • Status

    Completed No Results Posted
  • Intervention/Treatment

    icosapent ethyl ...
  • Study Participants

Cerebral vasospasm following subarachnoid hemorrhage (SAH) is the most common cause of morbidity and mortality. Recent studies indicate that Rho-kinase play an important role in the occurrence of such cerebral vasospasm. Eicosapentaenoic acid (EPA) inhibits sphingosylphosphorylcholine (SPC)-induced Rho-kinase activation in vitro. So this study examines whether EPA prevents cerebral vasospasm occurrence after SAH in patients.
Cerebral vasospasm occasionally seen after subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm is the most common cause of morbidity and mortality in these cases. Recent studies indicate that Rho-kinase plays an important role in such cerebral vasospasm and that numerous agents, such as thromboxane A2 (TXA2), sphingosylphosphorylcholine (SPC) and arachidonic acid (AA), can activate Rho-kinase directly or through receptors in the cell membrane; among these agents, SPC has been described as a novel messenger for Rho-kinase-mediated Ca2+ sensitization of vascular smooth muscle contraction. Eicosapentaenoic acid (EPA) has recently been reported to inhibit SPC-induced Rho-kinase activation in vitro, and thereby vascular smooth muscle contraction, through the inhibition of Src family protein tyrosine kinases translocation. Moreover, the concentration of AA increases in the cerebrospinal fluid of patients with SAH, suggesting that this substance has a potential role in the occurrence of cerebral vasospasm following SAH, while EPA is known to change the constitution ratios of AA and EPA in cell membrane phospholipid, resulting in the inhibition of TXA2 synthesis. These observations lead us to hypothesize that EPA may inhibit cerebral vasospasm following SAH through the inhibition of Rho-kinase activation.
Study Started
Dec 31
Primary Completion
Jun 30
Study Completion
Dec 31
Last Update
Sep 03

Drug Eicosapentaenoic acid ethyl ester

Orally administered 900 mg eicosapentaenoic acid ethyl ester three times a day (2700 mg ⁄ day) from the surgery next day to 30 days after the onset of SAH.

  • Other names: EPADEL S900 TM (EPA ethyl ester, purity >98%)

A Experimental

Patients in the group A are orally administered eicosapentaenoic acid ethyl ester.

B No Intervention

Patients in the group B (control) are not administered eicosapentaenoic acid ethyl ester.


Inclusion Criteria:

Subarachnoid hemorrhage (SAH)
The ruptured cerebral aneurysms conformed by cerebral angiography
The patients with treated by craniotomy and clip application within 72h after the onset of SAH

Exclusion Criteria:

Traumatic or mycotic aneurysms
A history or complication of serious stroke
Moya Moya disease
A history of SAH
Complication of serious heart or hepatic disease or infection or renal failure
Malignant tumor
Patients judged to be inappropriate by physician in charge
No Results Posted