Join the 200th Anniversary Celebration

Correspondence

Amaurosis Fugax

N Engl J Med 1994; 330:143-144January 13, 1994

Article

To the Editor:

In his editorial (Aug. 5 issue),1 Dr. Gautier reviewed the causes and mechanisms of amaurosis fugax. He included atherosclerosis and other lesions of the internal carotid artery as the main possible cause, especially in patients over 40 years of age, but he did not mention embolization of atherosclerotic material from the ascending aorta and aortic arch. Atherosclerotic changes of the ascending aorta and aortic arch should be considered in the differential diagnosis as a possible source of amaurosis fugax or other systemic embolization, especially if the cause is unexplained. Atherosclerotic disease of this portion of the aorta is common in the elderly2,3. Transthoracic and transesophageal echocardiography are the preferred methods of evaluation3,4. If possible, an invasive diagnostic procedure should be avoided3. The treatment is not well established, but even graft replacement may be considered, especially in patients undergoing cardiac surgery5.

Miralem Pasic, M.D., Sc.D.
Thierry Carrel, M.D.
Marko Turina, M.D.
University Hospital Zurich, CH-8091 Zurich, Switzerland

5 References
  1. 1

    Gautier J-C. Amaurosis fugax. N Engl J Med 1993;329:426-428
    Full Text | Web of Science | Medline

  2. 2

    Amarenco P, Duyckaerts C, Tzourio C, Henin D, Bousser M-G, Hauw J-J. The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med 1992;326:221-225
    Full Text | Web of Science | Medline

  3. 3

    Karalis DG, Chandrasekaran K, Victor MF, Ross JJ Jr, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;17:73-78
    CrossRef | Web of Science | Medline

  4. 4

    Tunick PA, Kronzon I. Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography. Am Heart J 1990;120:658-660
    CrossRef | Web of Science | Medline

  5. 5

    Wareing TH, Davila-Roman VG, Barzilai E, Murphy SF, Kouchoukos NT. Management of the severely atherosclerotic ascending aorta during cardiac operation: a strategy for detection and treatment. J Thorac Cardiovasc Surg 1992;103:453-462
    Web of Science | Medline

To the Editor:

We were intrigued by the report by Winterkorn et al. (Aug. 5 issue)1 regarding nine patients with apparent vasospastic amaurosis fugax that was responsive to calcium-channel blockers. Seven of these patients had a possible inflammatory or immune-complex process (lupus erythematosus or elevated erythrocyte sedimentation rate) or a coagulation diathesis (false positive Venereal Disease Research Laboratory test, postive test for anticardiolipin antibody, or low protein C and S levels).

It is not clear that every patient was tested for each of the proteins and antibodies listed. Since the broadening spectrum of symptoms potentially associated with antiphospholipid antibody includes recurrent migraines2 and amaurosis fugax,3 both of which were present in this small series of patients, we wonder whether these vasospastic episodes were actually associated with antiphospholipid antibody.

In one review of the prevalence and clinical importance of antiphospholipid antibodies, Love and Santoro4 stated that neurologic disorders of vascular origin, such as stroke, retinal-artery occlusion, or amaurosis fugax, appear to be associated with antiphospholipid antibodies. Yet in many of the reported cases that they reviewed, insufficient data were available for an adequate assessment of the clinical importance of these antibodies.

Although the formation of arterial and venous thrombus is widely believed to underlie most antiphospholipid-antibody-mediated disease, it has also been suggested that an interference with prostacyclin release at the level of the endothelial cell may be involved5. Since prostacyclin has a vasodilatory effect, we hypothesize that local reductions in relative prostacyclin concentration or activity may promote vasoconstriction or even vasospasm.

Robert M. McLean, M.D.
Yale School of Medicine, New Haven, CT 06510

Thomas P. Greco, M.D.
St. Mary's Hospital, Waterbury, CT 06706

5 References
  1. 1

    Winterkorn JMS, Kupersmith MJ, Wirtschafter JD, Forman S. Treatment of vasospastic amaurosis fugax with calcium-channel blockers. N Engl J Med 1993;329:396-398
    Full Text | Web of Science | Medline

  2. 2

    Chancellor AM, Cull RE, Kilpatrick DC, Warlow CP. Neurological disease associated with anticardiolipin antibodies in patients without systemic lupus erythematosus: clinical and immunological features. J Neurol 1991;238:401-407
    CrossRef | Web of Science | Medline

  3. 3

    Pope JM, Canny CLB, Bell DA. Cerebral ischemic events associated with endocarditis, retinal vascular disease, and lupus anticoagulant. Am J Med 1991;90:299-309
    Web of Science | Medline

  4. 4

    Love PE, Santoro SA. Antiphospholipid antibodies: anticardiolipin and the lupus anticoagulant in systemic lupus erythematosus (SLE) and in non-SLE disorders: prevalence and clinical significance. Ann Intern Med 1990;112:682-698
    Web of Science | Medline

  5. 5

    Watson KV, Schorer AE. Lupus anticoagulant inhibition of in vitro prostacyclin release is associated with a thrombosis-prone subset of patients. Am J Med 1991;90:47-53
    CrossRef | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: Pasic and colleagues are quite right. Theoretically, embolization from the aortic arch could cause amaurosis fugax; however, I do not know of a reported case.

J.C. Gautier, M.D.
Hopital de la Salpetriere, 75651 Paris, France

Author/Editor Response

We appreciate the letter from Drs. McLean and Greco, in which they support our observation that some of our younger patients, whose amaurosis fugax was unresponsive to aspirin but resolved during treatment with calcium-channel blockers, had autoimmune diatheses, including antiphospholipid hypercoagulability syndrome. The mechanism they suggest may be one explanation, but not necessarily the only explanation, for the development of amaurosis fugax in these patients.

Jacqueline S. Winterkorn, Ph.D., M.D.
Jonathan D. Wirtschafter, M.D.
North Shore University Hospital, Manhasset, NY 11030

Citing Articles (1)

Citing Articles

  1. 1

    P. V. Markov, J. Pepin, E. Frost, S. Deslandes, A.-C. Labbe, O. G. Pybus. (2009) Phylogeography and molecular epidemiology of hepatitis C virus genotype 2 in Africa. Journal of General Virology 90:9, 2086-2096
    CrossRef

Trends: Most Viewed (Last Week)

More Trends