QF3-11 - Probing the dynamic of cardiac microarchitecture in vivo using cDTI and DENSE

Background: Global cardiac function and local myocardial deformation arise from the microstructural organization and coordinated contraction of aggregated cardiomyocytes (e.g., “myofibers”)[1]. Measuring “myofiber” orientation in vivo is crucial as it is suspected that transmural cardiomyocyte disarray play a major role in several pathology [2]. This has motivated the development of in vivo cardiac diffusion tensor imaging (cDTI) to measure myofibers orientation [3]. Recently, we developed an approach that combine cDTI and displacement encoding (DENSE) data to compute myofiber strains and mobility during the cardiac cycle [4]. The objective of this work was to characterize myofiber (helix angle, HA) mobility in healthy volunteers using in vivo cDTI and co-registered cine DENSE displacement data.

Methods: Cardiac MRI data were obtained in healthy volunteers (N=3) on a 3T scanner (Prisma, Siemens) after IRB approved informed consent. cDTI was acquired at peak systole (trigger time (TT) ~300ms) in a mid-ventricular slice using a second order motion compensated single-shot spin-echo EPI [3] cardiac sequence at high resolution (TE=61ms, TR=4000ms, 1.6x1.6x8mm, end-respiratory triggering, b-values 0 and 350s/mm², 12 directions, and 5 averages). Two Cine DENSE slices (TE=1ms, TR=15ms, 2.5x2.5x8mm, 30 cardiac phases, free-breathing, Ke= 0.08 cycle/mm, balanced 4-point, 2 averages) were obtained 4mm above and below the location of cDTI.
Cardiomyocyte orientation data was computed throughout systole by combining cDTI data with the CINE DENSE displacement data (Figure 1) using an interpolation technique [4]. Dynamic HA maps were obtained by projecting the myofiber direction on the plane parallel to the epicardial boundary. HA range (HAR) was defined as the HA difference between endocardium and epicardium. Myofiber mobility (DHAR) was defined as the change in HAR relative to the beginning of systole (TT=0ms).

Results: Measured cDTI and DENSE data, together with computed myofiber orientation and displacement data, are shown in Figure 1. Figure 2 shows the HA distribution for one volunteer at two cardiac phases: peak systole (TT=300ms, measured and computed) and beginning of systole (TT=0ms, computed). The HAR variation across volunteers and throughout contraction is shown in Figure 3. HAR gradually increases from early systole (TT=0ms) to peak systole (TT=300ms) resulting in in ΔHAR=16±3°. From end systole to beginning of diastole (TT=450ms) the HAR range decreases leading to ΔHAR=10±6 °.

Conclusion: This study demonstrates distinct changes in the HAR during cardiac contraction. Accordingly, changes in myofiber orientation (i.e., HA) are apparent throughout the cardiac cycle. deformation in healthy and diseased hearts. These findings provide a new link between myocardial deformation and myofiber mobility and therefore point to new mechanistic and clinical insights into LV deformation in healthy and diseased hearts.