In patients with hypertrophic cardiomyopathy, cardiac diffusion tensor imaging revealed markedly raised secondary eigenvector angles in diastole (46.8° vs 24.0° in controls, p < 0.001), indicating abnormal myocardial laminar orientations.
Case-Control (n=22)
No
Does cardiac diffusion tensor imaging identify abnormalities of laminar orientation and mobility in hypertrophic cardiomyopathy compared to healthy controls?
In vivo cardiac diffusion tensor imaging reveals abnormal myocardial laminar orientations in hypertrophic cardiomyopathy, consistent with hypercontraction in systole and failure of relaxation in diastole.
Absolute Event Rate: 46.8% vs 24%
p-value: p=<0.001
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.
Ferreira et al. (Wed,) conducted a case-control in Hypertrophic cardiomyopathy (n=22). Cardiac diffusion tensor imaging (cDTI) vs. Healthy controls was evaluated on Global angle of the second eigenvector of diffusion (E2A) in diastole (p=<0.001). In patients with hypertrophic cardiomyopathy, cardiac diffusion tensor imaging revealed markedly raised secondary eigenvector angles in diastole (46.8° vs 24.0° in controls, p < 0.001), indicating abnormal myocardial laminar orientations.