{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T15:11:26Z","timestamp":1770995486213,"version":"3.50.1"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,6,5]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The joint effect of atherosclerosis and CRP (C\u2010reactive protein) on risk of ischemic stroke (\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              ) and myocardial infarction (\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              ) has been sparsely studied. The aim of this study was to explore whether\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              mediates the risk of events in subjects with prevalent carotid plaque, examine synergism, and test whether\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              and carotid plaque add to risk prediction beyond traditional risk factors.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              and carotid total plaque area (\n              <jats:styled-content style=\"fixed-case\">TPA<\/jats:styled-content>\n              ) were measured in 10 109 participants in the Troms\u00f8 Study from 1994 to 2008. Incident\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              (n=671) and\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              (n=1079) were registered until December 31, 2013. We calculated hazard ratios (HRs) of\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              according to categories of\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              (&lt;1, 1\u20133, and &gt;3\u00a0mg\/L) and plaque status (no plaque and\n              <jats:styled-content style=\"fixed-case\">TPA<\/jats:styled-content>\n              below and above median) in Cox proportional hazard models with time\u2010varying covariates. Multivariable\u2010adjusted\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              &gt;3 versus &lt;1\u00a0mg\/L was associated with risk of\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              (\n              <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>\n              , 1.84; 95% confidence interval, 1.49\u20132.26) and\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              (\n              <jats:styled-content style=\"fixed-case\">HR,<\/jats:styled-content>\n              1.46; 95% confidence interval, 1.23\u20131.73).\n              <jats:styled-content style=\"fixed-case\">TPA<\/jats:styled-content>\n              above median versus no plaque was associated with risk for\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              (\n              <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>\n              , 1.65; 95% confidence interval, 1.36\u20132.01) and\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              (\n              <jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>\n              , 1.64; 95% confidence interval, 1.41\u20131.92). In participants with plaque, adjustment for\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              minimally attenuated the risk estimates. The highest incidence rates for\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              were seen in the group with both\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              &gt;3\u00a0mg\/L and TPA is above the median.\n              <jats:styled-content style=\"fixed-case\">TPA<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              combined added to risk prediction beyond traditional risk factors.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The simultaneous presence of subclinical atherosclerosis and elevated\n              <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n              was associated with increased risk of\n              <jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n              . The combined assessment of subclinical atherosclerosis and inflammatory biomarkers may improve cardiovascular disease risk stratification.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.118.008951","type":"journal-article","created":{"date-parts":[[2018,5,17]],"date-time":"2018-05-17T09:15:20Z","timestamp":1526548520000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":16,"title":["Joint Effect of Carotid Plaque and C\u2010Reactive Protein on First\u2010Ever Ischemic Stroke and Myocardial Infarction?"],"prefix":"10.1161","volume":"7","author":[{"given":"Agnethe","family":"Eltoft","sequence":"first","affiliation":[{"name":"Department of Clinical Medicine, UiT The Arctic University of Norway, Troms\u00f8, Norway"},{"name":"Department of Neurology, University Hospital of North Norway, Troms\u00f8, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kjell Arne","family":"Arntzen","sequence":"additional","affiliation":[{"name":"Department of Clinical Medicine, UiT The Arctic University of Norway, Troms\u00f8, Norway"},{"name":"Department of Neurology, University Hospital of North Norway, Troms\u00f8, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tom","family":"Wilsgaard","sequence":"additional","affiliation":[{"name":"Department of Community Medicine, UiT The Arctic University of Norway, Troms\u00f8, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John\u2010Bjarne","family":"Hansen","sequence":"additional","affiliation":[{"name":"Department of Clinical Medicine, K.G. 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