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Translational Insights Into Myocardial Deformation and Fibrosis in Hypertrophic Cardiomyopathy Using Diffusion Tensor
Oumaima Laghzali1, Danielle Kara2, Shi Chen3
1Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility (B.U.F.F.), Berlin, Germany; Charité-Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site BERLIN, Berlin, Germany.
Insights
Fractional anisotropy (FA) from cardiac diffusion tensor imaging (cDTI) detects myocardial remodeling in hypertrophic cardiomyopathy (HCM). This imaging marker shows potential for early risk stratification in HCM patients, even with preserved ejection fraction.
Area of Science:
- Cardiovascular Imaging
- Biomedical Engineering
- Medical Diagnostics
Background:
- Hypertrophic cardiomyopathy (HCM) diagnosis is often delayed until significant myocardial thickening occurs.
- Cardiac diffusion tensor imaging (cDTI) can detect microstructural myocardial remodeling, aiding early risk stratification, particularly in patients with preserved ejection fraction.
Purpose of the Study:
- To evaluate if cDTI-derived fractional anisotropy (FA), mean diffusivity, and helix angle (HA) can identify myocardial disarray and structural remodeling in HCM.
- To assess the utility of these cDTI parameters in both human patients and preclinical mouse models of HCM.
Main Methods:
- Cardiovascular magnetic resonance imaging with cDTI and cine imaging was performed on 10 HCM patients and 10 healthy volunteers.
- A parallel study involved cine-MRI, ex vivo cDTI, scanning electron microscopy, and histology on myosin binding protein C3-knock-in and wild-type mice.
Main Results:
- HCM patients showed significantly reduced FA compared to controls, correlating with impaired strain.
- FA values were lowest in HCM patients with late gadolinium enhancement.
- Knock-in mice exhibited similar FA reductions, along with elevated HA transmurality, systolic dysfunction, and a correlation between FA and interstitial fibrosis.
Conclusions:
- Fractional anisotropy (FA) may serve as a crucial marker for myocardial remodeling in HCM, reflecting fibrosis and mechanical dysfunction.
- The ability of FA to detect abnormalities in patients with preserved ejection fraction highlights its potential as a translational marker for risk stratification and guiding therapy.
Background:
Hypertrophic cardiomyopathy (HCM) diagnosis often occurs after myocardium thickening develops, delaying intervention. Cardiac diffusion tensor imaging (cDTI) detects microstructural myocardial remodeling, offering potential for improved risk stratification, especially in patients with preserved ejection fraction.
Objectives:
The objective of the study was to determine whether cDTI-derived fractional anisotropy (FA), mean diffusivity, and helix angle (HA) identify myocardial disarray and structural remodeling in HCM in patients and in mouse models.
Methods:
Cardiovascular magnetic resonance imaging at 3T with cDTI (FA, mean diffusivity, and HA) and cine imaging was performed in 10 HCM patients with prior late gadolinium enhanced imaging and 10 healthy volunteers. In parallel, 6 myosin binding protein C3-knock-in and 6 wild-type mice (7-8 weeks) underwent cine-cardiovascular magnetic resonance imaging (9.4 T), ex vivo cDTI, scanning electron microscopy, and histology for microstructural, collagen area fraction and fibrosis analysis.
Results:
HCM patients exhibited reduced FA vs controls (0.29 ± 0.03 vs 0.34 ± 0.02; P = 0.002), correlating with strain impairment (R2 = 0.67; P = 0.003) and reaching the lowest value in patients with late gadolinium enhancement (P = 0.02). In knock-in mice, the reduction in FA mirrored the human findings. However, additional alterations were observed, including elevated HA transmurality, significant systolic dysfunction, and a strong correlation between FA and interstitial fibrosis.
Conclusions:
FA may reflect critical aspects of myocardial remodeling in HCM, including fibrosis, and mechanical dysfunction, as demonstrated in both preclinical and clinical settings. Its ability to detect abnormalities even in patients with preserved ejection fraction supports its potential as a translational marker for risk stratification and guiding therapeutic intervention.
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