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Anticardiolipin Antibodies and the Risk for Ischemic Stroke and Venous Thrombosis

Katherine S. Ginsburg, MD; Matthew H. Liang, MD; Laura Newcomer, BS; Samuel Z. Goldhaber, MD; Peter H. Schur, MD; Charles H. Hennekens, MD; and Meir J. Stampfer, MD
[+] Article and Author Information

The On Being A Doctor selection in this issue is written in memory of Dr. Ginsburg.

Grant Support: In part by National Institutes of Health research grants AR07530, AR36308, CA42182, HL26490, HL34595, CA34944, and CA40360.

Requests for Reprints: Meir J. Stampfer, MD, DrPH, Channing Laboratory, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.

Current Author Addresses: Drs. Liang and Schur: Department of Rheumatology and Immunology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.

Ms. Newcomer, Department of Epidemiology, University of Washington, SC-36, Seattle, WA 98195.

Dr. Stampfer: Channing Laboratory, Brigham and Women's Hospital, 180 Longwood Avenue, Boston, MA 02115.

Dr. Goldhaber: Department of Cardiology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.

Dr. Hennekens: Channing Laboratory, Brigham and Women's Hospital, 900 Commonwealth Avenue East, Boston, MA 02115-1204.


For current author affiliations and addresses, see end of text.†Deceased.


© 1992 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1992;117(12):997-1002. doi:10.7326/0003-4819-117-12-997
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Objective: To determine whether the presence of anticardiolipin antibodies is a risk factor for ischemic stroke and venous thrombosis in healthy adult men.

Design: A nested, case-control study in a prospective cohort.

Setting: A nationwide study of physicians.

Participants: The study sample was drawn from the Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in 22 071 male physicians. At entry, 68% of the participants submitted plasma samples that were subsequently frozen at -80 °C. During 60.2 months of follow-up, follow-up for nonfatal outcomes was 99.7% complete and ascertainment of fatal outcomes was 100% complete. We identified men with documented ischemic stroke, deep venous thrombosis of the leg, or pulmonary embolus and for whom a plasma sample was available. A control was matched by age, smoking history, and length of follow-up to each of the 100 patients with ischemic stroke and the 90 patients with deep venous thrombosis or pulmonary embolus.

° Measurements: Plasma samples were assessed for IgG anticardiolipin antibodies by enzyme-linked immunosorbent assay. The mean anticardiolipin antibody titers of the case patients in the two diagnostic groups (ischemic stroke; venous thrombosis or pulmonary embolus) were compared with those of the control groups, and relative risks were calculated for patients in increasing percentile categories of anticardiolipin antibodies by conditional logistic regression.

° Results: The anticardiolipin antibody titers were higher in case patients with deep venous thrombosis and pulmonary embolus than in their matched controls (P = 0.01). Persons with anticardiolipin antibody titers above the 95th percentile had a relative risk for developing deep venous thrombosis or pulmonary embolus of 5.3 (95% Cl, 1.55 to 18.3; P = 0.01). The anticardiolipin antibody titers in case patients with ischemic stroke and controls were not significantly different (P > 0.2), and no clear trend of higher risks among those with elevated levels of anticardiolipin antibodies was observed.

Conclusion: An anticardiolipin antibody level above the 95th percentile is an important risk factor for deep venous thrombosis or pulmonary embolus but not for ischemic stroke in healthy adult men.

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