{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T21:32:26Z","timestamp":1772659946503,"version":"3.50.1"},"reference-count":33,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2017,8,28]],"date-time":"2017-08-28T00:00:00Z","timestamp":1503878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Echocardiography"],"published-print":{"date-parts":[[2017,10]]},"abstract":"Background<\/jats:title>A high proportion of stable hypertrophic cardiomyopathy (HCM<\/jats:styled-content>) patients have elevated serum cardiac troponin I (cTnI<\/jats:styled-content>), but its clinical and echocardiographic determinants are unknown. Our objective was to determine the prevalence and clinical predictors of positive troponin (cTnI<\/jats:styled-content>+) in a well\u2010defined population of HCM<\/jats:styled-content> patients using a highly sensitive assay.<\/jats:p><\/jats:sec>Methods<\/jats:title>We retrospectively interrogated medical records of 167 stable HCM<\/jats:styled-content> patients from 1\/2011 to 3\/2014. cTnI<\/jats:styled-content> >0.04\u00a0ng\/mL<\/jats:styled-content> was considered positive.<\/jats:p><\/jats:sec>Results<\/jats:title>Thirty\u2010four percent were troponin\u2010positive (median cTnI<\/jats:styled-content> was 0.1 [0.07, 0.2] ng\/dL<\/jats:styled-content>). cTnI<\/jats:styled-content> as a continuous variable correlated positively with maximal left ventricular wall thickness (LVT<\/jats:styled-content>), maximal interventricular septal thickness, and global longitudinal strain (GLS<\/jats:styled-content>) (P<\/jats:italic><.001). Unadjusted OR<\/jats:styled-content> (95% CI<\/jats:styled-content>) for positive troponin was 0.5 (0.3\u20130.9, P<\/jats:italic>=.05) for obstructive HCM<\/jats:styled-content>, 3.2 (1.7\u20135.9, P<\/jats:italic><.0001) for increased LVT<\/jats:styled-content>, 0.3 (0.2\u20130.6, P<\/jats:italic><.0001) for \u22125% increase in GLS<\/jats:styled-content>, 0.2 (0.04\u20130.9, P<\/jats:italic>=.04) for moderate\u2010to\u2010severe mitral regurgitation, and 1.9 (0.9\u20133.9, P<\/jats:italic>=.06) for implantable cardioverter defibrillator history. After adjusting for these variables, only maximum LVT<\/jats:styled-content> (OR<\/jats:styled-content> 2.5 [95% CI<\/jats:styled-content>: 1.1\u20135.7, P<\/jats:italic>=.02]) and GLS<\/jats:styled-content> (OR<\/jats:styled-content> 0.3 [95% CI<\/jats:styled-content>: 0.2\u20130.6, P<\/jats:italic>=.001]) were independent predictors. The percentage of patients with a positive cTnI<\/jats:styled-content> increased from 19% to 24% and 57% across tertiles of LVT<\/jats:styled-content> (P<\/jats:italic>=.003) and decreased from 54% to 33% and 14% across tertiles of GLS<\/jats:styled-content> (P<\/jats:italic><.0001).<\/jats:p><\/jats:sec>Conclusion<\/jats:title>In this cohort of HCM<\/jats:styled-content> patients, the association of reduced GLS<\/jats:styled-content> and positive troponin was independent of LVT<\/jats:styled-content>. Further studies are warranted to evaluate whether their combination adds prognostic value in identifying high\u2010risk patients to define effective and early intervention strategies.<\/jats:p><\/jats:sec>","DOI":"10.1111\/echo.13645","type":"journal-article","created":{"date-parts":[[2017,8,29]],"date-time":"2017-08-29T01:20:43Z","timestamp":1503969643000},"page":"1470-1477","source":"Crossref","is-referenced-by-count":11,"title":["Relationship of cardiac troponin to systolic global longitudinal strain in hypertrophic cardiomyopathy"],"prefix":"10.1111","volume":"34","author":[{"given":"Anushree","family":"Agarwal","sequence":"first","affiliation":[{"name":"Aurora Cardiovascular Services Aurora Sinai\/Aurora St. Luke's Medical Centers University of Wisconsin School of Medicine and Public Health Milwaukee WI USA"},{"name":"University of California, San Francisco Division of Cardiology Adult Congenital Cardiology Program, San Francisco CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rayan","family":"Yousefzai","sequence":"additional","affiliation":[{"name":"Aurora Cardiovascular Services Aurora Sinai\/Aurora St. Luke's Medical Centers University of Wisconsin School of Medicine and Public Health Milwaukee WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kambiz","family":"Shetabi","sequence":"additional","affiliation":[{"name":"Aurora Cardiovascular Services Aurora Sinai\/Aurora St. Luke's Medical Centers University of Wisconsin School of Medicine and Public Health Milwaukee WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fatima","family":"Samad","sequence":"additional","affiliation":[{"name":"Aurora Cardiovascular Services Aurora Sinai\/Aurora St. Luke's Medical Centers University of Wisconsin School of Medicine and Public Health Milwaukee WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saurabh","family":"Aggarwal","sequence":"additional","affiliation":[{"name":"Creighton University School of Medicine Omaha NE USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chi","family":"Cho","sequence":"additional","affiliation":[{"name":"Aurora Cardiovascular Services Aurora Sinai\/Aurora St. Luke's Medical Centers University of Wisconsin School of Medicine and Public Health Milwaukee WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michelle","family":"Bush","sequence":"additional","affiliation":[{"name":"Aurora Cardiovascular Services Aurora Sinai\/Aurora St. Luke's Medical Centers University of Wisconsin School of Medicine and Public Health Milwaukee WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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