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Cardiac troponin I in three cat breeds with hypertrophic cardiomyopathy
  1. R. Langhorn, DVM, PhD,
  2. J. L. Willesen, DVM, PhD,
  3. I. Tarnow, DVM, PhD,
  4. M. Kjelgaard-Hansen, DVM, PhD and
  5. J. Koch, DVM, PhD
  1. Department of Veterinary Clinical and Animal Sciences, University of Copenhagen, Dyrlaegevej 16, Frederiksberg C DK-1870, Denmark
  1. Correspondence to E-mail for correspondence: rel{at}

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HYPERTROPHIC cardiomyopathy (HCM) is the most common cardiac disease in cats, associated with severe myocardial structural and ultrastructural changes (Abbott 2010, Christiansen and others 2015). In human beings, HCM is frequently inherited as an autosomal dominant trait caused by mutations in genes encoding sarcomeric proteins, including the myosin-binding protein C (MYBPC3) and the cardiac troponins (Gomes and Potter 2004, Cambronero and others 2009). In cats, familial mutations have been described in the MYBPC3 protein in Maine Coons (A31P) and ragdolls (R820W) (Meurs and others 2005, 2007). Cats homozygous for these mutations have a high risk of developing a fatal, progressive HCM (Meurs and others 2005, Borgeat and others 2014b). While additional causative mutations associated with feline HCM have yet to be discovered, several other breeds are considered predisposed.

Cardiac troponin I (cTnI) is a sensitive and specific marker of cardiomyocyte injury. Serum cTnI is generally increased in HCM patients and is associated with increased risk of mortality (Borgeat and others 2014a, Langhorn and others 2014). The cause of myocardial injury is believed to be mild chronic ischaemia due to a range of neurohormonal, inflammatory and vascular factors (Langhorn and others 2014). Additionally, effects of specific mutations and sex on myocardial injury in HCM have been suspected in human studies (Cambronero and others 2009, Kubo and others 2010), and one study on ragdolls similarly reported a difference in cTnI concentration between mutation-positive and mutation-negative cats (Borgeat and others 2015). The aim of this study was …

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  • Part of the troponin I data reported in this study has been previously published as the baseline data in a prospective cohort study: Langhorn and others (2014).

  • Provenance: Not commissioned; externally peer reviewed.

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