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Differentiation of Myocardial Properties in Physiological Athletic Cardiac Remodeling and Mild Hypertrophic Cardiomyopathy.
Klaeboe, Lars G; Lie, Øyvind H; Brekke, Pål H; Bosse, Gerhard; Hopp, Einar; Haugaa, Kristina H; Edvardsen, Thor.
Afiliación
  • Klaeboe LG; Precision Health Center for Optimized Cardiac Care (ProCardio), Department of Cardiology, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.
  • Lie ØH; Precision Health Center for Optimized Cardiac Care (ProCardio), Department of Cardiology, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.
  • Brekke PH; Precision Health Center for Optimized Cardiac Care (ProCardio), Department of Cardiology, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.
  • Bosse G; Division of Radiology and Nuclear Medicine, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.
  • Hopp E; Division of Radiology and Nuclear Medicine, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.
  • Haugaa KH; Precision Health Center for Optimized Cardiac Care (ProCardio), Department of Cardiology, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.
  • Edvardsen T; Faculty of Medicine, University of Oslo, 0316 Oslo, Norway.
Biomedicines ; 12(2)2024 Feb 12.
Article en En | MEDLINE | ID: mdl-38398022
ABSTRACT
Clinical differentiation between athletes' hearts and those with hypertrophic cardiomyopathy (HCM) can be challenging. We aimed to explore the role of speckle tracking echocardiography (STE) and cardiac magnetic resonance imaging (CMR) in the differentiation between athletes' hearts and those with mild HCM. We compared 30 competitive endurance elite athletes (7% female, age 41 ± 9 years) and 20 mild phenotypic mutation-positive HCM carriers (15% female, age 51 ± 12 years) with left ventricular wall thickness 13 ± 1 mm. Mechanical dispersion (MD) was assessed by means of STE. Native T1-time and extracellular volume (ECV) were assessed by means of CMR. MD was higher in HCM mutation carriers than in athletes (54 ± 16 ms vs. 40 ± 11 ms, p = 0.001). Athletes had a lower native T1-time (1204 (IQR 1191, 1234) ms vs. 1265 (IQR 1255, 1312) ms, p < 0.001) and lower ECV (22.7 ± 3.2% vs. 25.6 ± 4.1%, p = 0.01). MD > 44 ms optimally discriminated between athletes and HCM mutation carriers (AUC 0.78, 95% CI 0.65-0.91). Among the CMR parameters, the native T1-time had the best discriminatory ability, identifying all HCM mutation carriers (100% sensitivity) with a specificity of 75% (AUC 0.83, 95% CI 0.71-0.96) using a native T1-time > 1230 ms as the cutoff. STE and CMR tissue characterization may be tools that can differentiate athletes' hearts from those with mild HCM.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biomedicines Año: 2024 Tipo del documento: Article País de afiliación: Noruega Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biomedicines Año: 2024 Tipo del documento: Article País de afiliación: Noruega Pais de publicación: Suiza