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Aberrant myocardial sheetlet mobility in hypertrophic cardiomyopathy detected using in vivo cardiovascular magnetic resonance diffusion tensor imaging
© Ferreira et al.; licensee BioMed Central Ltd. 2014
- Published: 16 January 2014
- Cardiovascular Magnetic Resonance
- Diffusion Tensor Imaging
- Late Gadolinium Enhancement
- Hypertrophic Cardiomyopathy
- Magnetic Resonance Diffusion Tensor Imaging
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 , we hypothesized that cDTI at two cardiac phases would identify changing sheetlet orientations and abnormalities in hypertrophic cardiomyopathy (HCM).
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.
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°).
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 . The persistence of a systolic conformation may provide novel phenotypic insight into diastolic abnormalities arising from sarcomeric dysfunction, with potential therapeutic implications.
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