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. 2016 Oct;9(10):e005018.
doi: 10.1161/CIRCIMAGING.116.005018.

Studying Dynamic Myofiber Aggregate Reorientation in Dilated Cardiomyopathy Using In Vivo Magnetic Resonance Diffusion Tensor Imaging

Constantin von Deuster  1 , Eva Sammut  1 , Liya Asner  1 , David Nordsletten  1 , Pablo Lamata  1 , Christian T Stoeck  1 , Sebastian Kozerke  2 , Reza Razavi  1
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Studying Dynamic Myofiber Aggregate Reorientation in Dilated Cardiomyopathy Using In Vivo Magnetic Resonance Diffusion Tensor Imaging

Constantin von Deuster et al. Circ Cardiovasc Imaging. 2016 Oct.

Abstract

Background: The objective of this study is to assess the dynamic alterations of myocardial microstructure and strain between diastole and systole in patients with dilated cardiomyopathy relative to healthy controls using the magnetic resonance diffusion tensor imaging, myocardial tagging, and biomechanical modeling.

Methods and results: Dual heart-phase diffusion tensor imaging was successfully performed in 9 patients and 9 controls. Tagging data were acquired for the diffusion tensor strain correction and cardiac motion analysis. Mean diffusivity, fractional anisotropy, and myocyte aggregate orientations were compared between both cohorts. Cardiac function was assessed by left ventricular ejection fraction, torsion, and strain. Computational modeling was used to study the impact of cardiac shape on fiber reorientation and how fiber orientations affect strain. In patients with dilated cardiomyopathy, a more longitudinal orientation of diastolic myofiber aggregates was measured compared with controls. Although a significant steepening of helix angles (HAs) during contraction was found in the controls, consistent change in HAs during contraction was absent in patients. Left ventricular ejection fraction, cardiac torsion, and strain were significantly lower in the patients compared with controls. Computational modeling revealed that the dilated heart results in reduced HA changes compared with a normal heart. Reduced torsion was found to be exacerbated by steeper HAs.

Conclusions: Diffusion tensor imaging revealed reduced reorientation of myofiber aggregates during cardiac contraction in patients with dilated cardiomyopathy relative to controls. Left ventricular remodeling seems to be an important factor in the changes to myocyte orientation. Steeper HAs are coupled with a worsening in strain and torsion. Overall, the findings provide new insights into the structural alterations in patients with dilated cardiomyopathy.

Keywords: diffusion tensor imaging; dilated cardiomyopathy; magnetic resonance imaging; myocardium; myofiber architecture.

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Figures

Figure 1.
Figure 1.
A, Idealized left ventricular models used for biomechanical modeling of healthy and dilated cardiomyopathy (DCM) hearts. B, Idealized helix angle maps based on average end-diastolic measurements in controls and patients with DCM.
Figure 2.
Figure 2.
Comparison of helix angle (A) and E2A angle (B) maps acquired in diastole and systole from control vs patient with dilated cardiomyopathy (DCM).
Figure 3.
Figure 3.
Histograms of diastolic and systolic helix angles for controls (A) and patients with dilated cardiomyopathy (DCM; B). Although a shift toward steeper helix angles is seen in the systolic healthy heart, systolic and diastolic distributions are similar in the DCM case. Error bars indicate interquartile ranges across the subjects. C, Corresponding transmural helix angle slopes in diastole vs systole for the control and DCM groups. D, Diastolic and systolic helix angles for control and DCM modeling when compared with the data.
Figure 4.
Figure 4.
Histograms of diastolic and systolic E2A sheet angles for controls (A) and patients with dilated cardiomyopathy (DCM; B). The sheet angle distribution is broader in the systolic healthy heart compared with diastole, whereas systolic and diastolic distributions are similar in the DCM case. Histograms of change between diastolic and systolic E2A distributions for controls (C) and patients with DCM (D). Controls exhibit a marked change in E2A as opposed to little change in patients with DCM. Model results follow a similar trend. Error bars indicate interquartile ranges across the subjects.
Figure 5.
Figure 5.
Time course of myocardial torsion (A), radial (B), circumferential (C), and longitudinal (D) strain for dilated cardiomyopathy (DCM) and control. Error bars indicate interquartile ranges across the subjects.
Figure 6.
Figure 6.
Peak torsion (A), left ventricular ejection fraction (LVEF; B), and (negative) longitudinal strain (C) as a function of normalized helix angle (HA) slope. A trend toward lower torsion (A), LVEF (B), and longitudinal strain (C) with increasing HA slope is seen in the dilated cardiomyopathy (DCM) group.
Figure 7.
Figure 7.
Change in helix angle slope caused by passive inflation of the control left ventricular model to dilated cardiomyopathy (DCM) model cavity volume when compared with measured difference in control and DCM helix angle slopes. Volume change alone does not explain observed differences between the 2 cohorts.
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