Df. Kallmes et al., Adjuvant use of epsilon-aminocaproic acid (Amicar) in the endovascular treatment of cranial arteriovenous fistulae, NEURORADIOL, 42(4), 2000, pp. 302-308
We report our experience with the use of the antifibrinolytic agent epsilon
-aminocaproic acid (EACA), Amicar, as an adjuvant to endovascular treatment
of cranial arteriovenous fistulae. We also review applications of antifibr
inolytic agents to neurovascular disorders and discuss the mechanism of act
ion, dosing strategy, contraindications, and possible complications associa
ted with the use of EACA. We identified 13 patients with cranial arterioven
ous fistulae (five direct carotid cavernous fistulae [CCF], seven dural art
eriovenous fistulae [DAVF], and one vein of Galen malformation) who receive
d EACA as an adjunct to endovascular treatment. In all cases embolic coils
were the primary embolic agent. We reviewed the modes of initial endovascul
ar therapy and angiographic findings immediately thereafter and the respons
e to EACA. Two direct CCF and two DAVF were completely thrombosed on follow
-up angiography, and two DAVF demonstrated diminished flow after EACA thera
py. Seven fistulae did not respond to EACA. Four of eight tightly coiled fi
stulae thrombosed, while none of five loosely coiled fistulae thrombosed. N
one of four cases with a residual fistula separate from the coil mass under
went thrombosis with EACA, while four of nine cases without a separate fist
ula thrombosed. There was no morbidity related to EACA therapy. EACA may th
us be useful as an adjunct to endovascular treatment of cranial arterioveno
us fistulae. Loose or incomplete coil packing of the fistula predicts a poo
r response to EACA therapy.