Short Amicar Protocol May Cut Aneurysm Rerupture Rate

SAN FRANCISCO - Once abandoned because of adverse reactions, Amicar is showing new success in preventing the secondary rupture of aneurysms, a retrospective study has shown.

Most clinicians have moved away from using Amicar (epsilon aminocaproic acid) and other antifibrinolytic agents, such as tranexamic acid, in these patients since the mid- to late 1980s after studies found that they contributed to high rates of vasospasm and shunt-dependent hydrocephalus. However, Amicar has regained favor with clinicians at Emory University in Atlanta who used an intravenous drip preparation of the drug in a short-term protocol that calls for a 5-g bolus followed by a drip at 1 g/hr for 72 hours or until aneurysm treatment, whichever came first, said Dr. Albert Jesse Schuette, an interventional neuroradiologist at Emory.

Epsilon aminocaproic acid acts as an inhibitor of plasminogen activators and has some antiplasmin activity, according to its product label.

Dr. Schuette and his colleagues reviewed 454 patients with aneurysmal subarachnoid hemorrhage who received treatment with the drug under the short-term protocol during 2005-2007 and compared them with control patients who received the same overall care except for administration of Amicar.

Overall, aneurysms reruptured in 14 (7%) of 210 patients who did not get Amicar, compared with 6 (2%) of 244 patients who got Amicar. The rerupture rate was higher for patients who did not receive Amicar, regardless of their Fisher grade or Hunt and Hess grade.

Patients on Amicar did not have higher rates of ischemic events, vasospasm, or ventriculoperitoneal shunting, Dr. Schuette reported at the annual meeting of the Congress of Neurological Surgeons.

Based on these findings, he recommended that medical centers treating aneurysm patients begin a clot-stabilizing regimen with Amicar or another antifibrinolytic agent such as tranexamic acid during transfer to a high-volume tertiary care center.

None of the investigators reported relevant disclosures.

SAN FRANCISCO - Once abandoned because of adverse reactions, Amicar is showing new success in preventing the secondary rupture of aneurysms, a retrospective study has shown.

Most clinicians have moved away from using Amicar (epsilon aminocaproic acid) and other antifibrinolytic agents, such as tranexamic acid, in these patients since the mid- to late 1980s after studies found that they contributed to high rates of vasospasm and shunt-dependent hydrocephalus. However, Amicar has regained favor with clinicians at Emory University in Atlanta who used an intravenous drip preparation of the drug in a short-term protocol that calls for a 5-g bolus followed by a drip at 1 g/hr for 72 hours or until aneurysm treatment, whichever came first, said Dr. Albert Jesse Schuette, an interventional neuroradiologist at Emory.

Epsilon aminocaproic acid acts as an inhibitor of plasminogen activators and has some antiplasmin activity, according to its product label.

Dr. Schuette and his colleagues reviewed 454 patients with aneurysmal subarachnoid hemorrhage who received treatment with the drug under the short-term protocol during 2005-2007 and compared them with control patients who received the same overall care except for administration of Amicar.

Overall, aneurysms reruptured in 14 (7%) of 210 patients who did not get Amicar, compared with 6 (2%) of 244 patients who got Amicar. The rerupture rate was higher for patients who did not receive Amicar, regardless of their Fisher grade or Hunt and Hess grade.

Patients on Amicar did not have higher rates of ischemic events, vasospasm, or ventriculoperitoneal shunting, Dr. Schuette reported at the annual meeting of the Congress of Neurological Surgeons.

Based on these findings, he recommended that medical centers treating aneurysm patients begin a clot-stabilizing regimen with Amicar or another antifibrinolytic agent such as tranexamic acid during transfer to a high-volume tertiary care center.

None of the investigators reported relevant disclosures.

SAN FRANCISCO - Once abandoned because of adverse reactions, Amicar is showing new success in preventing the secondary rupture of aneurysms, a retrospective study has shown.

Most clinicians have moved away from using Amicar (epsilon aminocaproic acid) and other antifibrinolytic agents, such as tranexamic acid, in these patients since the mid- to late 1980s after studies found that they contributed to high rates of vasospasm and shunt-dependent hydrocephalus. However, Amicar has regained favor with clinicians at Emory University in Atlanta who used an intravenous drip preparation of the drug in a short-term protocol that calls for a 5-g bolus followed by a drip at 1 g/hr for 72 hours or until aneurysm treatment, whichever came first, said Dr. Albert Jesse Schuette, an interventional neuroradiologist at Emory.

Epsilon aminocaproic acid acts as an inhibitor of plasminogen activators and has some antiplasmin activity, according to its product label.

Dr. Schuette and his colleagues reviewed 454 patients with aneurysmal subarachnoid hemorrhage who received treatment with the drug under the short-term protocol during 2005-2007 and compared them with control patients who received the same overall care except for administration of Amicar.

Overall, aneurysms reruptured in 14 (7%) of 210 patients who did not get Amicar, compared with 6 (2%) of 244 patients who got Amicar. The rerupture rate was higher for patients who did not receive Amicar, regardless of their Fisher grade or Hunt and Hess grade.

Patients on Amicar did not have higher rates of ischemic events, vasospasm, or ventriculoperitoneal shunting, Dr. Schuette reported at the annual meeting of the Congress of Neurological Surgeons.

Based on these findings, he recommended that medical centers treating aneurysm patients begin a clot-stabilizing regimen with Amicar or another antifibrinolytic agent such as tranexamic acid during transfer to a high-volume tertiary care center.

None of the investigators reported relevant disclosures.