{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T07:20:15Z","timestamp":1781594415345,"version":"3.54.5"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Background and Purpose<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Ischemic stroke and coronary heart disease (CHD) share risk factors and pathogenic process, ie, atherosclerosis and thrombosis. We examined the relationship between severity of angina pectoris and its accompanying characteristics and the risk of incident ischemic stroke.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Methods<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            We traced 3122 patients with stable CHD, included in a secondary prevention trial of lipid modification, the Bezafibrate Infarction Prevention trial. CHD was documented by a history of myocardial infarction \u22656 months and &lt;5 years before enrollment and\/or stable angina pectoris with evidence of ischemia confirmed by ancillary diagnostic testing. Severity of angina pectoris was assessed according to the Canadian Cardiovascular Society angina classification, and heart failure functional class according to the New York Heart Association (NYHA) classification. Patients with severe heart failure or unstable angina on enrollment were excluded.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Results<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            During a mean follow-up period of 8.2 years, 186 patients developed an ischemic stroke. The cumulative rate of ischemic stroke increased in a dose-response manner from 4.7% in patients with no angina to 5.7%, 8.4%, and 12.9% in patients with angina classes 1, 2, and 3, respectively (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001). Patients with NYHA functional class 1 had a 5.5% rate of ischemic stroke versus 7.3% and 9.6% in patients with classes 2 and 3, respectively (\n            <jats:italic>P<\/jats:italic>\n            =0.05). In a Cox proportional-hazard model adjusting for conventional risk factors and potential confounders, the hazard ratio associated with angina class 1 was 1.20 (95% CI, 0.83 to 1.74); class 2, 1.66 (95% CI, 1.12 to 2.45); and class 3, 2.35 (95% CI, 1.08 to 5.13), as compared with patients with no angina. Hazard ratios of ischemic stroke associated with conventional risk factors were 1.55 for a 10-year age increment, 2.16 for diabetes mellitus, 1.81 for current smoking, and 1.29 for a 20 mm Hg increase in systolic blood pressure.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Conclusions<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Severity of angina pectoris in patients with stable CHD predicts an increased risk of subsequent ischemic stroke. The association between angina class and incident ischemic stroke is independent of traditional vascular risk factors.\n          <\/jats:p>","DOI":"10.1161\/hs0102.101630","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T23:16:47Z","timestamp":1027898207000},"page":"245-250","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["Severity of Angina Pectoris and Risk of Ischemic Stroke"],"prefix":"10.1161","volume":"33","author":[{"given":"David","family":"Tanne","sequence":"first","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Avraham","family":"Shotan","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uri","family":"Goldbourt","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moti","family":"Haim","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina","family":"Boyko","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yehuda","family":"Adler","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lori","family":"Mandelzweig","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Solomon","family":"Behar","sequence":"additional","affiliation":[{"name":"From the Neufeld Cardiac Research Center (A.S., U.G., M.H., V.B., Y.A., L.M., S.B.), and the Stroke Unit, Department of Neurology (D.T.), Chaim Sheba Medical Center, Tel Hashomer, Israel."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410160110"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.17.6.3810707"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.28.5.941"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.52.1.289"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(99)04470-0"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.102.1.21"},{"key":"e_1_3_2_7_2","first-page":"522","volume":"54","year":"1976","unstructured":"Campeasu L. 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