Background
Background: Cardiac diffusion tensor imaging (cDTI) contains information on cross-myocyte components of intramyocardial water diffusion. Assuming these to be constrained by the sheetlet and shear layer microstructure of left ventricular myocardium [1], we hypothesized that cDTI at two cardiac phases would identify changing sheetlet orientations and abnormalities in hypertrophic cardiomyopathy (HCM).
Methods
We performed cDTI in vivo at 3 Tesla at end-systole and late-diastole in 11 healthy controls and 11 patients with HCM, with previous late gadolinium enhancement (LGE) for detection of fibrosis.
Results
Voxel-wise analysis of diffusion tensors relative to ventricular coordinates showed transmural changes of helix-angle, with no differences between phases or between HCM and controls. In controls, the orientation of the second eigenvector of diffusion (E2A), changed from more wall-parallel in diastole to more wall-perpendicular in systole, in accord with the predicted reorientations of sheetlet populations. HCM hearts showed markedly abnormal global E2A in diastole consistent with impaired relaxation (46.8° vs 24.0° controls, p < 0.001), and minor abnormal global E2A in systole consistent with hypercontraction (63.9° vs 56.4° controls, p = 0.026). In hypertrophic regions, sheetlets retained relatively systolic orientations in diastole, independent of fibrosis, which differed from regions of normal wall thickness (LGE present 57.8°, p = 0.0028, LGE absent 54.8°, p = 0.0022 vs normal thickness 38.1°).
Conclusions
In vivo DTI quantifies cross-myocyte diffusion. We are potentially showing impaired in vivo diastolic reorientation of sheetlet populations in HCM, although further investigation is required as myocardial strain is a possible confounder. Current work includes the measurement of 3D strain in all subjects for assessment of contractility and for strain correction of the diffusion tensor [2]. The persistence of a systolic conformation may provide novel phenotypic insight into diastolic abnormalities arising from sarcomeric dysfunction, with potential therapeutic implications.
Funding
This work was supported by the National Institute of Health Research Cardiovascular Biomedical Research Unit at the Royal Brompton Hospital and Imperial College, London.
References
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Ferreira, P., Kilner, P.J., McGill, LA. et al. Aberrant myocardial sheetlet mobility in hypertrophic cardiomyopathy detected using in vivo cardiovascular magnetic resonance diffusion tensor imaging. J Cardiovasc Magn Reson 16 (Suppl 1), P338 (2014). https://doi.org/10.1186/1532-429X-16-S1-P338
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DOI: https://doi.org/10.1186/1532-429X-16-S1-P338