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Phenotyping hypertrophic cardiomyopathy using cardiac diffusion magnetic resonance imaging: the relationship between
Arka Das1, Christopher Kelly1, Irvin Teh1
1Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds Teaching Hospitals NHS Trust, Leeds LS2 9JT, UK.
Insights
Hypertrophic cardiomyopathy (HCM) shows altered myocardial microstructure even in normal-appearing segments, indicated by increased diffusion and cardiomyocyte disarray. These microstructural changes, particularly in the subendocardium, correlate with reduced blood flow and may explain clinical decline in HCM patients.
Area of Science:
- Cardiovascular Imaging
- Cardiac MRI
- Diffusion Tensor Imaging
Background:
- Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) predicts clinical decline, but underlying mechanisms are unclear.
- Cardiac diffusion tensor imaging (cDTI) offers in vivo myocardial microstructure characterization using mean diffusivity (MD), fractional anisotropy (FA), and secondary eigenvector angle (E2A).
Purpose of the Study:
- To investigate the relationship between myocardial perfusion and cDTI parameters in HCM.
- To understand the sequence of pathophysiology and the interplay between vascular function and microstructure in HCM.
Main Methods:
- A cardiac magnetic resonance (CMR) study involving 20 HCM patients and 10 controls.
- Utilized 3.0T CMR for spin-echo cDTI, adenosine stress/rest perfusion mapping, cine-imaging, and late gadolinium enhancement (LGE).
- Calculated Myocardial Perfusion Reserve (MPR), MD, FA, and E2A per segment, divided into subendocardial and subepicardial regions. 'Normal' segments were defined by specific criteria (wall thickness ≤11 mm, MPR ≥2.2, no LGE).
Main Results:
- Normal HCM segments exhibited increased MD and E2A, with decreased FA compared to controls, suggesting cardiomyocyte disarray.
- Subendocardial regions in HCM patients showed significantly higher MD and lower MPR than subepicardial regions.
- Increased subendocardial MD correlates with reduced subendocardial blood flow, indicating regional remodeling.
Conclusions:
- Even in HCM segments without wall thickening, scarring, or perfusion deficits, diffusion is more isotropic, pointing to underlying cardiomyocyte disarray.
- Elevated E2A suggests abnormal myocardial sheetlet angulation during systole in HCM.
- Increased subendocardial MD in HCM is linked to regional remodeling and may explain impaired subendocardial blood flow.
Aims:
Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) is predictive of clinical decline, however underlying mechanisms remain unclear. Cardiac diffusion tensor imaging (cDTI) allows in vivo characterization of myocardial microstructure by quantifying mean diffusivity (MD), fractional anisotropy (FA) of diffusion, and secondary eigenvector angle (E2A). In this cardiac magnetic resonance (CMR) study, we examine associations between perfusion and cDTI parameters to understand the sequence of pathophysiology and the interrelation between vascular function and underlying microstructure.
Methods And Results:
Twenty HCM patients underwent 3.0T CMR which included: spin-echo cDTI, adenosine stress and rest perfusion mapping, cine-imaging, and late gadolinium enhancement (LGE). Ten controls underwent cDTI. Myocardial perfusion reserve (MPR), MD, FA, E2A, and wall thickness were calculated per segment and further divided into subendocardial (inner 50%) and subepicardial (outer 50%) regions. Segments with wall thickness ≤11 mm, MPR ≥2.2, and no visual LGE were classified as 'normal'. Compared to controls, 'normal' HCM segments had increased MD (1.61 ± 0.09 vs. 1.46 ± 0.07 × 10-3 mm2/s, P = 0.02), increased E2A (60 ± 9° vs. 38 ± 12°, P < 0.001), and decreased FA (0.29 ± 0.04 vs. 0.35 ± 0.02, P = 0.002). Across all HCM segments, subendocardial regions had higher MD and lower MPR than subepicardial (MDendo 1.61 ± 0.08 × 10-3 mm2/s vs. MDepi 1.56 ± 0.18 × 10-3 mm2/s, P = 0.003, MPRendo 1.85 ± 0.83, MPRepi 2.28 ± 0.87, P < 0.0001).
Conclusion:
In HCM patients, even in segments with normal wall thickness, normal perfusion, and no scar, diffusion is more isotropic than in controls, suggesting the presence of underlying cardiomyocyte disarray. Increased E2A suggests the myocardial sheetlets adopt hypercontracted angulation in systole. Increased MD, most notably in the subendocardium, is suggestive of regional remodelling which may explain the reduced subendocardial blood flow.
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