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- HCM, hypertrophic cardiomyopathy
- ICTP, carboxy-terminal telopeptide of type I collagen
- LV, left ventricular
- MRI, magnetic resonance imaging
- PICP, carboxy-terminal propeptide of type I collagen
- PIIINP, amino-terminal propeptide of type III collagen
- PINP, amino-terminal propeptide of type I collagen
- SI, signal intensity
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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