{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T05:53:49Z","timestamp":1790488429722,"version":"4.1.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1998,8]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            \u2014Inflammatory mechanisms have been implicated in the pathogenesis of atherosclerosis. In this study, we investigated whether the extent of inflammatory infiltration in high-grade stenoses of the internal carotid artery (ICA) correlates to clinical features of plaque destabilization.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            \u2014Endarterectomy specimens from 37 consecutive patients undergoing surgery for high-grade ICA stenosis were stained immunocytochemically for macrophages (CD68) and T cells (CD3). The staining was quantified by planimetry of immunostained areas (CD68) or counting individual cells (CD3). Clinical evidence of plaque instability was provided by the preoperative assessment of recent ischemic symptoms attributable to the stenosis and of the occurrence of cerebral microembolism in transcranial Doppler ultrasound monitoring of the ipsilateral middle cerebral artery.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            \u2014The percentage of macrophage-rich areas and number of T cells per mm\n            <jats:sup>2<\/jats:sup>\n            section area were larger in recently symptomatic patients than in asymptomatic patients (macrophages: 18\u00b110% versus 11\u00b14%,\n            <jats:italic>P<\/jats:italic>\n            =0.005; T cells: 71.2\u00b134.4 versus 40.5\u00b131.4 mm\n            <jats:sup>2<\/jats:sup>\n            ,\n            <jats:italic>P<\/jats:italic>\n            =0.005). The presence of microembolism was associated with an increase in macrophage-rich areas (\n            <jats:italic>P<\/jats:italic>\n            =0.011). Macrophage (19\u00b110% versus 9\u00b13%,\n            <jats:italic>P<\/jats:italic>\n            =0.0009) and T cell (71.5\u00b139.0 versus 46.4\u00b122 mm\n            <jats:sup>2<\/jats:sup>\n            ,\n            <jats:italic>P<\/jats:italic>\n            =0.045) infiltration were more pronounced in predominantly atheromatous than in fibrous plaques, but did not correlate significantly to the presence of surface ulceration or luminal thrombosis.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014Our data suggest a role of plaque-infiltrating macrophages and T cells in the clinical destabilization of high-grade ICA stenoses. Inflammatory mechanisms may be a therapeutic target in patients with symptomatic ICA disease.\n          <\/jats:p>","DOI":"10.1161\/01.str.29.8.1625","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"1625-1630","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":139,"title":["Inflammation in High-Grade Carotid Stenosis"],"prefix":"10.1161","volume":"29","author":[{"given":"Sebastian","family":"Jander","sequence":"first","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Sitzer","sequence":"additional","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rene\u0301","family":"Schumann","sequence":"additional","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Schroeter","sequence":"additional","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario","family":"Siebler","sequence":"additional","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helmuth","family":"Steinmetz","sequence":"additional","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guido","family":"Stoll","sequence":"additional","affiliation":[{"name":"From the Department of Neurology, Heinrich Heine University, Du\u0308sseldorf, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/362801a0"},{"key":"e_1_3_2_2_2","first-page":"191","volume":"125","year":"1986","unstructured":"Gown AM, Tsukada T, Ross R. 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