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Amaurosis Fugax Caused by Heritable Thrombophilia-Hypofibrinolysis in Cases Without Carotid Atherosclerosis

Thromboprophylaxis Prevents Subsequent Transient Monocular Partial Blindness

Cholesterol Center, Jewish Hospital, glueckch{at}healthall.com

Karl Golnik, MD

Department of Ophthalmology, University of Cincinnati Medical Center, Cincinnati, Ohio

Ping Wang

Cholesterol Center, Jewish Hospital

Nineteen patients (age 60 ± 14) with amaurosis fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of amaurosis fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent amaurosis fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for 1 year on therapy, without adverse treatment side effects. When amaurosis fugax occurs without carotid artery atherosclerosis or other known causes, thrombophilia or hypofibrinolysis, or both are nearly universal, safely treatable, reversible pathoetiologies.

Key Words: amaurosis fugax • transient cerebral ischemic attack • thrombophilia • hypofibrinolysis • thromboprophylaxis.

Clinical and Applied Thrombosis/Hemostasis, Vol. 13, No. 2, 124-129 (2007)
DOI: 10.1177/1076029606298735


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