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Elevated plasma levels of cardiac troponin-I predict left ventricular systolic dysfunction in patients with myotonic dystrophy type 1: A multicentre cohort follow-up study

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  • Mark J Hamilton
  • Yvonne Robb
  • Sarah Cumming
  • Helen Gregory
  • Alexis Duncan
  • Monika Rahman
  • Anne McKeown
  • Catherine McWilliam
  • John Dean
  • Alison Wilcox
  • Maria E Farrugia
  • Anneli Cooper
  • Josephine McGhie
  • Berit Adam
  • Richard Petty
  • Cheryl Longman
  • Iain Findlay
  • Alan Japp
  • Darren G Monckton
  • Martin A. Denvir
  • Scottish Myotonic Dystrophy Consortium

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    Rights statement: Copyright: © 2017 Hamilton et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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    Licence: Creative Commons: Attribution (CC-BY)

Original languageEnglish
Pages (from-to)e0174166
JournalPLoS ONE
Issue number3
Publication statusPublished - 21 Mar 2017


OBJECTIVE: High sensitivity plasma cardiac troponin-I (cTnI) is emerging as a strong predictor of cardiac events in a variety of settings. We have explored its utility in patients with myotonic dystrophy type 1 (DM1).

METHODS: 117 patients with DM1 were recruited from routine outpatient clinics across three health boards. A single measurement of cTnI was made using the ARCHITECT STAT Troponin I assay. Demographic, ECG, echocardiographic and other clinical data were obtained from electronic medical records. Follow up was for a mean of 23 months.

RESULTS: Fifty five females and 62 males (mean age 47.7 years) were included. Complete data were available for ECG in 107, echocardiography in 53. Muscle Impairment Rating Scale score was recorded for all patients. A highly significant excess (p = 0.0007) of DM1 patients presented with cTnI levels greater than the 99th centile of the range usually observed in the general population (9 patients; 7.6%). Three patients with elevated troponin were found to have left ventricular systolic dysfunction (LVSD), compared with four of those with normal range cTnI (33.3% versus 3.7%; p = 0.001). Sixty two patients had a cTnI level < 5ng/L, of whom only one had documented evidence of LVSD. Elevated cTnI was not predictive of severe conduction abnormalities on ECG, or presence of a cardiac device, nor did cTnI level correlate with muscle strength expressed by Muscle Impairment Rating Scale score.

CONCLUSIONS: Plasma cTnI is highly elevated in some ambulatory patients with DM1 and shows promise as a tool to aid cardiac risk stratification, possibly by detecting myocardial involvement. Further studies with larger patient numbers are warranted to assess its utility in this setting.

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