Heart failure & cardiomyopathies
Translational Insights Into Myocardial Deformation and Fibrosis in Hypertrophic Cardiomyopathy Using Diffusion Tensor MRI
Authors' conclusion
FA may reflect critical aspects of myocardial remodeling in HCM, including fibrosis, and mechanical dysfunction, as demonstrated in both preclinical and clinical settings.
Study context
- Population
- Patients with hypertrophic cardiomyopathy and healthy volunteers; MYBPC3-knock-in and wild-type mice
- Participants
- 10 / 10 / 6 / 6
- Comparison
- Hypertrophic cardiomyopathy (HCM) vs healthy controls; MYBPC3 knock-in vs wild-type mice
- HCMn = 10
- Controlsn = 10reference
- Knock-in micen = 6
- Wild-type micen = 6reference
- Outcome
- cDTI-derived fractional anisotropy (FA), mean diffusivity and helix angle (HA)
Methodological detailshuman and mouse model, 3T CMR with cardiac diffusion tensor imaging (cDTI)
- Human and mouse model
- 3T CMR with cDTI
Main finding
As reported in the abstract
Fractional anisotropy
HCM
0.29
± 0.03
Controls
0.34
± 0.02
P = 0.002
Further findings
Fractional anisotropy (FA) vs strain impairment (HCM)
- FA correlated with strain impairment, R2 = 0.67
- P = 0.003
- Lowest FA in patients with late gadolinium enhancement
- P = 0.02
Knock-in vs wild-type mice
- Reduction in FA mirrored the human findings
- Elevated helix angle (HA) transmurality, significant systolic dysfunction, strong correlation between FA and interstitial fibrosis
Original publication
Translational Insights Into Myocardial Deformation and Fibrosis in Hypertrophic Cardiomyopathy Using Diffusion Tensor MRI. JACC Adv. Published 15 November 2025. doi:10.
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