{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T02:20:12Z","timestamp":1768789212202,"version":"3.49.0"},"reference-count":19,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,8,11]],"date-time":"2014-08-11T00:00:00Z","timestamp":1407715200000},"content-version":"vor","delay-in-days":41,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Academic Emergency Medicine"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>With clinical use of high\u2010sensitivity troponin I (hsTnI), more frequent troponin elevations will occur. However, the burden and implications of these elevations are not well understood. The authors quantified the prevalence of elevated hsTnI in patients presenting with possible acute coronary syndrome (ACS) who do not have elevated troponin with a current generation assay (cardiac troponin I [<jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content>]) and determined the association of these newly detected elevations with a composite of all\u2010cause mortality and subsequent cardiac hospitalization.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This was a prospective observational study of 808 subjects evaluated for possible ACS and followed for up to 1\u00a0year. Troponin values were measured with hsTnI (Abbott Laboratories) and <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> (Abbott and Beckman Coulter). Cardiac hospitalization was defined as hospitalization for ACS, revascularization, acute heart failure (AHF), or tachy\/brady arrhythmia that occurred after the index emergency department (ED) visit or hospital discharge.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Forty subjects (5%) were diagnosed with ACS (26 myocardial infarction and 14 unstable angina). On the initial sample, the prevalence of elevated hsTnI among subjects with nonelevated <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> was 9.2% using a gender\u2010neutral cutoff (95% confidence interval [CI]\u00a0=\u00a07.1% to 11.4%) and 11.1% using a gender\u2010specific cutoff (95% CI\u00a0=\u00a08.8% to 13.4%). Adjudicated diagnoses for subjects whose initial samples had elevated hsTnI but nonelevated <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> (gender\u2010neutral cutoff) were as follows: three (4.6%) ACS, 15 (23.1%) AHF, three (4.6%) volume overload etiology unclear\/noncardiac, three (4.6%) cardiac (non\u2010ACS), and 41 (63.1%) other. Of the 65 patients whose initial samples had hsTnI but nonelevated <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content>, eight developed <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> elevation on subsequent serial sampling. After traditional cardiovascular risk factors and renal function were adjusted for, subjects with elevated initial hsTnI but nonelevated <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> (initial and serial sampling) had a higher risk of all\u2010cause mortality and subsequent cardiac hospitalization than subjects with both nonelevated hsTnI and nonelevated <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> (hazard ratio [HR]\u00a0= 1.91, 95% CI\u00a0=\u00a01.14 to 3.19).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>On the initial sample, 9% to 11% of subjects without <jats:styled-content style=\"fixed-case\">cTnI<\/jats:styled-content> elevation had hsTnI elevation. Although the majority of the patients with these newly detected hsTnI elevations did not have ACS, they had a higher risk for all\u2010cause mortality and subsequent cardiac hospitalization.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acem.12417","type":"journal-article","created":{"date-parts":[[2014,8,11]],"date-time":"2014-08-11T21:43:27Z","timestamp":1407793407000},"page":"727-735","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Troponin Elevations Only Detected With a High\u2010sensitivity Assay: Clinical Correlations and Prognostic Significance"],"prefix":"10.1111","volume":"21","author":[{"given":"Frederick K.","family":"Korley","sequence":"first","affiliation":[{"name":"The Department of Emergency Medicine Baltimore MD"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven P.","family":"Schulman","sequence":"additional","affiliation":[{"name":"The Division of Cardiology Baltimore MD"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lori J.","family":"Sokoll","sequence":"additional","affiliation":[{"name":"The Department of Medicine Division of Clinical Chemistry Department of Pathology Baltimore MD"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew P.","family":"DeFilippis","sequence":"additional","affiliation":[{"name":"The Division of Cardiovascular Medicine Baltimore MD"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew I.","family":"Stolbach","sequence":"additional","affiliation":[{"name":"The Department of Emergency Medicine Baltimore MD"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jamil D.","family":"Bayram","sequence":"additional","affiliation":[{"name":"The Department of Emergency Medicine Baltimore MD"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mustapha O.","family":"Saheed","sequence":"additional","affiliation":[{"name":"The Department of Emergency 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