In vivo cardiovascular magnetic resonance diffusion tensor imaging shows evidence of abnormal myocardial laminar orientations and mobility in hypertrophic cardiomyopathy

Abstract

BackgroundCardiac 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).MethodsWe 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.ResultsVoxel-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°).ConclusionsIn 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12968-014-0087-8) contains supplementary material, which is available to authorized users.

The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

“…This indicates that the units of aggregated cardiomyocytes in the hypertensive lambs, in general, are more parallel to the epicardium than in controls as seen in the normal diastole (11,16), despite being hypertrophied with a tendency toward greater mural thickness. It can be argued that the change in angulation of the aggregated units could also be caused by pathological dilation of the ventricles, reflecting a contractile state more similar to diastole.…”

“…As seen, the intrusion and unit angles are evenly distributed around zero. Because we are mainly interested in the absolute change in angulation, we allow ourselves to analyze the data statistically as absolute values as has been done by others (11). The results on unit angulations are summarized in Table 2.…”

“…Rearrangement of the units, or so-called sheets, is needed to explain the phenomenon of systolic myocardial thickening (14,15). Changes in angulations have been found through the cardiac cycle in both rats and humans, adding weight to the notion that aggregation into units is needed for optimal and continuous repacking and rearrangement through the cardiac cycle (11,16). Inappropriate repacking, therefore, could well play a significant role in pathology.…”

Review of Journal of Cardiovascular Magnetic Resonance 2015

“…Recent advances reported in the journal have included improved flow mapping, [1–3] real-time imaging, [4] T1 mapping, [5–7] simulations, [8, 9] perfusion, [10–12] coronary imaging, [13] diffusion tensor imaging, [14–16] feature tracking, [17–20] and strain assessment. [21, 22] The full breadth of new developments is described in the papers in the section.…”

Bioprinting in cardiovascular tissue engineering: a review

“…Each distinct layer comprises of myocardial laminar sheets with muscular fibres of three to four cell layer thick [5] . These laminar layers, also known as sheetlets, re-orientates and contributes to wall thickening during systolic shortening [6] . Damaged myocardium cannot be restored on its own as native cardiomyocytes are limited in regenerative abilities.…”