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.
This work was supported by the National Institute of Health Research Cardiovascular
Biomedical Research Unit at the Royal Brompton Hospital and Imperial College, London.
Averaged magnitude image and the respective E2 angle maps for a control and 2 HCM
examples with anteroseptal hypertrophy at the 2 imaged cardiac phases. Additionally
the 2 HCM examples also have on the right the matching LGE images. E2A differences
between controls and HCM can be seen in the hypertrophied regions, mainly in the diastolic
phase. The non-hypertrophic lateral wall in both HCM hearts approaches the absolute
E2A angles measured in the control heart.
Scatter plots showing the E2 mobility (mean absolute E2 angle change between diastole
and systole) for all subjects at the two imaged cardiac phases. A) Global mean E2A
values. B) Global controls vs HCM cohort with the myocardium divided into three different
regions: regions with hypertrophy and LGE (H+LG+), regions with hypertrophy but no
LGE (H+LG-), and regions with no hypertrophy or LGE (H-LG-). In all plots the median
and interquartile range are shown. Of note, it shows the most abnormal orientations,
inclined steeply inward from the wall plane with low mobility, in the hypertrophic
regions, whether not there is LGE evidence of fibrosis. *P-value multiplied by 2 for
Bonferroni correction for 2 tests. †P-value multiplied by 3 for Bonferroni correction
for 3 tests.