{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T05:51:31Z","timestamp":1777355491465,"version":"3.51.4"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1998,11]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            \u2014The aim of our study was to characterize the patient profile and prognostic value associated with high positive IgG (&gt;100 GPL) anticardiolipin antibodies (aCL).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            \u2014We studied the clinical, laboratory, radiological, and prospective historical features of ischemic cerebrovascular disease in patients with &gt;100 GPL titers. From our neurology department, 27 consecutive patients were prospectively identified and followed up (mean follow-up time, 34 months).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            \u2014The mean age of our cohort was 41 years. Lupuslike illness occurred in 3; 23 had primary antiphospholipid syndrome, including 3 who met criteria for Sneddon\u2019s syndrome; 1 patient had progressive systemic sclerosis. Cerebral infarcts occurred in 74% and were recurrent in 37%. Systemic ischemic events, most commonly deep vein thrombosis, occurred in 37%. Tobacco use was documented in 85%, hyperlipidemia in 74%, hypertension in 44%, and diabetes mellitus in 7% of patients. A prominent headache history was present in 67%. Lupus anticoagulant (LA) was present in 72%, approximately one half had positive antinuclear antibodies and thrombocytopenia, and one quarter had a false-positive VDRL. We compared mean GPL levels in patients testing positive for specific laboratory features of antiphospholipid syndrome with those testing negative for these parameters. Only the LA(+) group had a significantly higher mean GPL than the LA(-) group (\n            <jats:italic>P<\/jats:italic>\n            =0.006). Brain imaging showed nonlacunar infarcts in 73% and lacunes in 12%. Of 19 cerebral angiograms, 5 (26%) showed large-vessel occlusive disease and 6 (32%) branch obstruction. Echocardiograms were abnormal in 75%: thickened left-sided valves in 33% and vegetations in 12%. Recurrent cerebrovascular ischemic events were observed in 96%, with transient events (mean rate, 25%\/y) occurring 5 times more frequently than strokes (mean rate, 5%\/y). Using a standardized disability scale blinded to aCL titer, neurological impairment was severe in 7%, moderate in 30%, and mild or nonexistent in 63%, and unrelated to mean GPL value (\n            <jats:italic>P<\/jats:italic>\n            =0.567). Titers fluctuated greatly for individual patients, and most did not consistently test as highly positive. An analysis of fluctuation in symptom severity with concurrent GPL values did not show a statistically significant correlation. Compared with historical controls having a wide range of positive titers, the presence of high IgG aCL titers did not confer a worse prognosis for disability and recurrent ischemic events.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014Our data suggest that cerebrovascular events associated with high positive GPL are frequently multiple and minor (with no disability-titer correlation), present in relatively young patients, and often associated with tobacco abuse, hyperlipidemia, LA, systemic ischemic events, and occult cardiac disease.\n          <\/jats:p>","DOI":"10.1161\/01.str.29.11.2245","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"2245-2253","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":89,"title":["Cerebrovascular Ischemic Events With High Positive Anticardiolipin Antibodies"],"prefix":"10.1161","volume":"29","author":[{"given":"Piero","family":"Verro","sequence":"first","affiliation":[{"name":"From the Center for Stroke Research, Department of Neurology, Henry Ford Health Science Center (Detroit Campus of Case Western University), Detroit, Mich."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven R.","family":"Levine","sequence":"additional","affiliation":[{"name":"From the Center for Stroke Research, Department of Neurology, Henry Ford Health Science Center (Detroit Campus of Case Western University), Detroit, Mich."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gretchen E.","family":"Tietjen","sequence":"additional","affiliation":[{"name":"From the Center for Stroke Research, Department of Neurology, Henry Ford Health Science Center (Detroit Campus of Case Western University), Detroit, Mich."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.40.8.1190"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.21.9.2396261"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(89)90335-5"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410250303"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.39.020188.001401"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.29.9.1755"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.40.8.1181"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0733-8619(18)30237-8"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1136\/ard.47.11.947"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410380119"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(83)91267-9"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0307-742X(21)00606-8"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(86)92258-0"},{"key":"e_1_3_2_14_2","doi-asserted-by":"crossref","unstructured":"Asherson RA Harris EN. 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