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  • Myocardial late gadolinium enhancement is associated with raised serum amino-terminal propeptide of type III collagen concentrations in patients with hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the α tropomyosin gene: magnetic r…

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Scientific letters
Myocardial late gadolinium enhancement is associated with raised serum amino-terminal propeptide of type III collagen concentrations in patients with hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the α tropomyosin gene: magnetic resonance imaging study
  1. P Sipola1,
  2. K Peuhkurinen2,
  3. K Lauerma3,
  4. M Husso1,
  5. P Jääskeläinen2,
  6. M Laakso2,
  7. H J Aronen1,*,
  8. J Risteli4,
  9. J Kuusisto2
  1. 1Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland
  2. 2Department of Medicine, Kuopio University Hospital, Kuopio, Finland
  3. 3Department of Radiology, Helsinki University Central Hospital, Helsinki, Finland
  4. 4Department of Clinical Chemistry, Oulu University Hospital, Oulu, Finland
  1. Correspondence to:
    Dr Johanna Kuusisto
    Kuopio University Hospital, Cardiology Unit, Department of Medicine, Puijonlaaksontie 2, Kuopio FIN-70210, Finland; johanna.kuusisto{at}kuh.fi

https://doi.org/10.1136/hrt.2005.075523

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    Myocardial late gadolinium enhancement in magnetic resonance imaging (MRI) has been proposed to detect myocardial fibrosis in patients with cardiomyopathies, including hypertrophic cardiomyopathy (HCM).1,2 The amino-terminal propeptide of type III collagen (PIIINP) reflects synthesis or turnover of soft-tissue collagen and is a marker of collagen scar formation after acute myocardial infarction.3 No studies have investigated the association of myocardial late gadolinium enhancement with PIIINP concentration in patients with HCM. We therefore investigated the relationship of myocardial late gadolinium enhancement by MRI with serum concentration of PIIINP and other markers of collagen metabolism in patients with HCM attributable to an identical HCM-causing mutation, Asp175Asn in the α tropomyosin gene (TPM1).4

    PATIENTS AND METHODS

    The present study enrolled 21 adult patients (9 men, 12 women, mean age 37 years) with the Asp175Asn mutation of TPM1.4 Seventeen healthy control participants matched for age and sex were also enrolled.

    MRIs were acquired with a 1.5 T clinical scanner (Magnetom Vision; Siemens Medical Systems, Erlangen, Germany) in the left ventricular (LV) short-axis orientation. Late-enhancement images were acquired at the level of the tips of the mitral valve leaflets and at the level of the papillary muscles with a T1-weighted single-shot inversion-recovery fast low angle shot sequence 10–15 min after gadopentetate dimeglumine (Magnevist; Schering AG, Berlin, Germany) injection into the antecubital vein (0.05 …

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    Footnotes

    • ↵* Also the Functional Brain Imaging Unit, Brain Research Center, Helsinki, Finland

    • Supported by Kuopio University Hospital Research Grant 5063502 (PS), the Radiological Society of Finland, Orion Corporation Research Foundation, Aarne and Aili Turunen Foundation, and Finnish Foundation for Cardiovascular Research.

    • Competing interests: None declared.

    • The study protocol was approved by the ethics committee of the University of Kuopio and Kuopio University Hospital. All participants gave written informed consent.