In vivo cardiovascular magnetic resonance diffusion tensor imaging shows evidence of abnormal myocardial laminar orientations and mobility in hypertrophic cardiomyopathy.
BACKGROUND
Cardiac diffusion tensor imaging (cDTI) measures the magnitudes and directions of intramyocardial water diffusion. Assuming the cross-myocyte components to be constrained by the laminar microstructures of myocardium, we hypothesized that cDTI at two cardiac phases might identify any abnormalities of laminar orientation and mobility 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, as well as late gadolinium enhancement (LGE) for detection of regional fibrosis.


RESULTS
Voxel-wise analysis of diffusion tensors relative to left ventricular coordinates showed expected transmural changes of myocardial helix-angle, with no significant differences between phases or between HCM and control groups. In controls, the angle of the second eigenvector of diffusion (E2A) relative to the local wall tangent plane was larger in systole than diastole, in accord with previously reported changes of laminar orientation. HCM hearts showed higher than normal global E2A in systole (63.9° vs 56.4° controls, p=0.026) and markedly raised E2A in diastole (46.8° vs 24.0° controls, p<0.001). In hypertrophic regions, E2A retained a high, systole-like angulation even in diastole, independent of LGE, while regions of normal wall thickness did not (LGE present 57.8°, p=0.0028, LGE absent 54.8°, p=0.0022 vs normal thickness 38.1°).


CONCLUSIONS
In healthy controls, the angles of cross-myocyte components of diffusion were consistent with previously reported transmural orientations of laminar microstructures and their changes with contraction. In HCM, especially in hypertrophic regions, they were consistent with hypercontraction in systole and failure of relaxation in diastole. Further investigation of this finding is required as previously postulated effects of strain might be a confounding factor.
Pedro F
PF
Ferreira
Philip J
PJ
Kilner
Laura-Ann
LA
McGill
Sonia
S
Nielles-Vallespin
Andrew D
AD
Scott
Siew Y
SY
Ho
Karen P
KP
McCarthy
Margarita M
MM
Haba
Tevfik F
TF
Ismail
Peter D
PD
Gatehouse
Ranil
R
de Silva
Alexander R
AR
Lyon
Sanjay K
SK
Prasad
National Institute of Health Research Cardiovascular Biomedical Research Unit, Royal Brompton Hospital and Imperial College, London, UK. d.firmin@ic.ac.uk.
David N
DN
Firmin
Dudley J
DJ
Pennell
D000368:Aged; D002312:Cardiomyopathy, Hypertrophic / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D038524:Diffusion Magnetic Resonance Imaging; D056324:Diffusion Tensor Imaging; D005260:Female; D005355:Fibrosis; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D011237:Predictive Value of Tests; D016277:Ventricular Function, Left