Probing dynamic myocardial microstructure with cardiac magnetic resonance diffusion tensor imaging

Abstract

This article is an invited editorial comment on the paper entitled "In vivo cardiovascular magnetic resonance diffusion tensor imaging shows evidence of abnormal myocardial laminar orientations and mobility in hypertrophic cardiomyopathy" by Ferreira et al., and published as Journal of Cardiovascular Magnetic Resonance 2014; 16:87.

Figure 1

Myocardial structure and function. (A) Diffusion tensor “fiber” tracking of a canine heart reveals large-scale connectivity of the end-to-end anastomoses of continuously branching myocytes. With sufficiently high spatial resolution (especially required at the apex and base) the principal eigenvector can be tracked from asterisk (*) to asterisk (*) while tracing out aspects of the base, apex, endocardium, and epicardium. (B) A representative sheetlet structure comprised of three myocyte layers. Incompressible myocyte shortening of ~15% gives rise to only ~8% radial wall thickening when sheet-shear is absent. In the presence of sheet shear, which is accommodated by the sheetlets, radial wall thickening increases to >25%.

Figure 2

Schematic representation of architecture of fibers and sheets of normal myocardium (A) and in myocardial fiber disarray (B), and of their respective diffusion tensors. In the normal, fibers are locally parallel, and organized in local planes, sheetlets. Diffusion tensors represent an ellipsoid whose leading eigenvector (v1), the direction of maximum diffusion, is aligned with the mean axis of the myocardial fibers, and whose second eigenvector (v2) indicates the local sheet orientation. These directions are well-defined in the normal heart (A), and their distinctiveness is reduced or lost in fiber disarray. This is reflected in the lengths of the eigenvectors, which become more nearly equal in disarray (B). In maximum disorder, the diffusion tensor is a sphere, without distinguished directions. Details omitted include the facts that myocardial fibers are not isolated but branched syncytia, and that disarray is typically accompanied by increased matrix protein and non-contractile cells.