{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:53:11Z","timestamp":1787017991026,"version":"build-2736575974"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"25","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2001,6,26]]},"abstract":"<jats:p>\n                    <jats:italic>Background<\/jats:italic>\n                    \u2014At one end of the clinical spectrum of coronary artery disease (CAD) are subjects who have had repeated acute ischemic events, and at the other end are those with long-standing angina who have never been unstable. This study tests the hypothesis that a specific biological profile can distinguish these 2 extreme groups and predict acute coronary events.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Methods and Results<\/jats:italic>\n                    \u2014Blood levels of lipoprotein(a), homocysteine, tissue plasminogen activator, plasminogen activator inhibitor-1, C-reactive protein (CRP), fibrinogen, and von Willebrand factor were compared in 3 groups of 50 subjects each: (1) those with previous multiple acute coronary events, (2) age-matched subjects with \u22653 years of stable angina and no prior acute coronary events, and (3) matched controls without evidence of atherosclerotic disease and a normal coronary angiogram. All subjects were followed for 4.0 years. Lipoprotein(a), homocysteine, tissue plasminogen activator, and plasminogen activator inhibitor-1 were similar in both CAD groups and significantly higher than in the control group. However, compared with subjects with long-standing stable angina, those with previous multiple coronary events had higher values of CRP (5.7\u00b15.4 versus 3.0\u00b15.2 mg\/L,\n                    <jats:italic>P<\/jats:italic>\n                    =0.012), fibrinogen (3.38\u00b10.75 versus 2.92\u00b10.64 g\/L,\n                    <jats:italic>P<\/jats:italic>\n                    =0.001), and von Willebrand factor (1.60\u00b10.55 versus 1.25\u00b10.36 U\/mL,\n                    <jats:italic>P<\/jats:italic>\n                    =0.0003). On follow-up, myocardial infarction and unstable angina occurred in 42% of the group with multiple events, 4% of the stable angina group (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.0001), and none of the control subjects. In the 100 patients with CAD, CRP was 4.9 mg\/L in those with and 1.8 mg\/L in those without new instability (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.0001). In a multivariate analysis, only CRP distinguished those with follow-up acute coronary events (adjusted odds ratio 5.9, 95% CI 2.0 to 17.9;\n                    <jats:italic>P<\/jats:italic>\n                    =0.002). A baseline CRP &gt;3.5 mg\/L had a relative risk of 7.6 (2.6 to 21.7,\n                    <jats:italic>P<\/jats:italic>\n                    =0.0002) for subsequent acute events.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Conclusions<\/jats:italic>\n                    \u2014An inflammatory biological profile distinguished patients with previous multiple acute coronary events from those with long-standing stable angina and predicted acute coronary instability.\n                  <\/jats:p>","DOI":"10.1161\/01.cir.103.25.3062","type":"journal-article","created":{"date-parts":[[2012,6,11]],"date-time":"2012-06-11T20:09:32Z","timestamp":1339445372000},"page":"3062-3068","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":74,"title":["Biological Profiles in Subjects With Recurrent Acute Coronary Events Compared With Subjects With Long-Standing Stable Angina"],"prefix":"10.1161","volume":"103","author":[{"given":"Peter","family":"Bogaty","sequence":"first","affiliation":[{"name":"From the Quebec Heart Institute\/Laval Hospital (P.B., P.P., S. Simard, L.B., G.R.D.), Laval University, Ste-Foy; and the Montreal General Hospital (S. Solymoss), McGill University, Montreal, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Poirier","sequence":"additional","affiliation":[{"name":"From the Quebec Heart Institute\/Laval Hospital (P.B., P.P., S. Simard, L.B., G.R.D.), Laval University, Ste-Foy; and the Montreal General Hospital (S. Solymoss), McGill University, Montreal, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Serge","family":"Simard","sequence":"additional","affiliation":[{"name":"From the Quebec Heart Institute\/Laval Hospital (P.B., P.P., S. Simard, L.B., G.R.D.), Laval University, Ste-Foy; and the Montreal General Hospital (S. Solymoss), McGill University, Montreal, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luce","family":"Boyer","sequence":"additional","affiliation":[{"name":"From the Quebec Heart Institute\/Laval Hospital (P.B., P.P., S. Simard, L.B., G.R.D.), Laval University, Ste-Foy; and the Montreal General Hospital (S. Solymoss), McGill University, Montreal, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan","family":"Solymoss","sequence":"additional","affiliation":[{"name":"From the Quebec Heart Institute\/Laval Hospital (P.B., P.P., S. Simard, L.B., G.R.D.), Laval University, Ste-Foy; and the Montreal General Hospital (S. Solymoss), McGill University, Montreal, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilles R.","family":"Dagenais","sequence":"additional","affiliation":[{"name":"From the Quebec Heart Institute\/Laval Hospital (P.B., P.P., S. 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