The feasibility of a novel limited field of view spiral cine DENSE sequence to assess myocardial strain in dilated cardiomyopathy

Abstract

Objective Develop an accelerated cine displacement encoding with stimulated echoes (DENSE) cardiovascular magnetic resonance (CMR) sequence to enable clinically feasible myocardial strain evaluation in patients with dilated cardiomyopathy (DCM). Materials and methods A spiral cine DENSE sequence was modified by limiting the field of view in two dimensions using in-plane slice-selective pulses in the stimulated echo. This reduced breath hold duration from 20RR to 14RR intervals. Following phantom and pilot studies, the feasibility of the sequence to assess peak radial, circumferential, and longitudinal strain was tested in control subjects ( n = 18) and then applied in DCM patients ( n = 29). Results DENSE acquisition was possible in all participants. Elements of the data were not analysable in 1 control (6%) and 4 DCM r(14%) subjects due to off-resonance or susceptibility artefacts and low signal-to-noise ratio. Peak radial, circumferential, short-axis contour strain and longitudinal strain was reduced in DCM patients ( p < 0.001 vs. controls) and strain measurements correlated with left ventricular ejection fraction (with circumferential strain r = − 0.79, p < 0.0001; with vertical long-axis strain r = − 0.76, p < 0.0001). All strain measurements had good inter-observer agreement (ICC > 0.80), except peak radial strain. Discussion We demonstrate the feasibility of CMR strain assessment in healthy controls and DCM patients using an accelerated cine DENSE technique. This may facilitate integration of strain assessment into routine CMR studies. Electronic supplementary material The online version of this article (10.1007/s10334-019-00735-5) contains supplementary material, which is available to authorized users.

Fully-automated global and segmental strain analysis of DENSE cardiovascular magnetic resonance using deep learning for segmentation and phase unwrapping

“…For images with SNR typical of routine DENSE protocols [ 15 , 39 ] (phase SNR of approximately 22), MSE referenced to ground truth were evaluated for the proposed U-Net and the path-following method. Similar to the phase SNR of velocity-encoded phase contrast imaging [ 40 ], we calculated the DENSE phase SNR as …”

“…While low-rank [ 13 , 14 ] and reduced field-of-view [ 15 ] methods have been developed recently to accelerate data acquisition for DENSE, there remains a need and opportunity to accelerate DENSE strain analysis and to eliminate all steps that require user assistance. Image analysis of cine DENSE to compute LV whole-slice (global) and segmental strain requires the following steps: (a) segmentation of the LV myocardium, (b) identification of the anterior right-ventricular (RV) insertion point into the LV to align the American Heart Association 16-segment model [ 16 ], (c) unwrapping of potentially wrapped displacement-encoded phase values of the myocardium, (d) computation of the spatiotemporal displacement field, and (e) computation of strain.…”

Predictors of left ventricular remodelling in patients with dilated cardiomyopathy – a cardiovascular magnetic resonance study

“…All patients underwent baseline assessment of myocardial strain using a modified cine spiral DENSE sequence . Images were acquired at the mid‐ventricular short‐axis level and two long‐axis planes (horizontal and vertical) at rest and during the 10 μg/kg/min dobutamine dose.…”

Scanning Electron Microscopic Investigations to Clarify the Role Played by the Endocardium in the Origin of Dilated Cardiomyopathy(DCM)

“…The detection of involvement of the endocardium tissue in DCM suggests that pathophysiological processes similar to the degeneration of heart valves play a major etiological role in the development of DCM. Parallel to assumed pathophysiological processes of the heart valves, collagen substance transition disorders based on endothelial dysfunction could lead to pathologically increased stress on the extracellular matrix, which causes a similar response of the endothelium and the extracellular matrix as in the degeneration of aortic and mitral valve disease [30,31]. Further investigations are necessary to clarify the role of a possible infection aetiology.…”