134 Non-invasive Interrogation of Myocardial Disarray in Hypertrophic Cardiomyopathy

Introduction Hypertrophic cardiomyopathy (HCM) is an inheritable cardiomyopathy characterised by left ventricular hypertrophy (LVH). In contrast to other aetiologies of LVH, the HCM myocyte microstructure displays disarray, the ability to detect disarray non-invasively could therefore assist the diagnosis in equivocal cases. In vivo Diffusion tensor imaging (DTI) is a novel cardiovascular magnetic resonance technique, which exploits the fact that intra-myocardial water diffusion reflects the shape and orientation of the underlying microstructure. DTI can characterise the myocardial microstructure with novel parameters: Myocyte orientation can be depicted by the helical angle gradient (HAG); the degree of myocardial organisation can be assessed by fractional anisotropy (FA); and mean diffusivity (MD) quantifies the ease of myocardial water passage. We sought to determine whether DTI could detect myocardial micro-structural differences compared with patients with hypertension and healthy controls. Methods We recruited 25 patients with HCM, 13 patients with HTN and 14 healthy, age matched controls for DTI at 3T. Three short axis mid-ventricular slices were acquired during the systolic pause, with a diffusion-weighted stimulated echo sequence, as previously described. Data was post-processed to calculate global FA, HAG and MD values. Statistical comparison between the 3 cohorts was made with one way ANOVA, followed by students t-tests were ANOVA was significant. Results There was no significant difference in FA between cohorts ( HCM: 0.44 ± 0.05, HTN: 0.47 ± 0.06 and Control: 0.46 ± 0.05, p = 0.20). MD was greater in HCM compared to controls (ANOVA p = 0.002, HCM 1.07 ± 0.13 vs Controls: 0.91 ± 0.13×10–3mm 2 s 1 , p 2 s 1 , p = 0.15). The HAG was less in HCM compared to both HTN and Controls (HCM: -6.2 ± 1.0, HTN: -7.4 ± 0.9 and Controls: -8.6 ± 0.8, p Summary DTI was unable to detect a significant disarray in HCM via fractional anisotropy. Explanations include the limited resolution of our sequence, the small study sample and potential regionality of disarray. The higher MD observed in HCM compared to controls may be attributable to a greater extracellular volume as a result of fibrosis. Technical factors such as myocardial strain and heterogeneity of SNR may also have contributed. The HAG was correlated with maximal wall thickness, with reduction in the rate of angular change as the wall thickness increases. Conclusion DTI provides novel myocardial tissue characterisation, however in its current form it is unable to detect disarray in HCM. Further assessment following technical development is required.