- Poster presentation
- Open Access
In vivo fiber tractography of the right and left ventricles using diffusion tensor MRI of the entire human heart
© Mekkaoui et al.; licensee BioMed Central Ltd. 2014
- Published: 16 January 2014
- Left Ventricle
- Fractional Anisotropy
- Right Ventricle
- Helix Angle
- Sweet Spot
Diffusion Tensor MRI (DTI) tractography of the human heart in vivo has previously been performed with either large slice gaps or limited coverage [1, 2]. The aim of this study was to investigate the feasibility of performing DTI of the entire human heart in vivo without slice gaps. This, we hypothesized, would enhance the characterization of fiber architecture in the left ventricle (LV), allow myofiber organization in the right ventricle (RV) to be characterized in vivo, and further elucidate microstructural differences in the heart between systole and diastole.
DTI was performed on a clinical 3T scanner (Skyra, Siemens) using a fat-suppressed, zone-selected, diffusion-encoded stimulated echo sequence with 10 diffusion encoding directions, TE/TR 33/80 ms, GRAPPA rate 2, b-value 500 s/mm2, resolution 2.8 × 2.8 × 8 mm3, 8 averages and multiple breath-holds. The entire LV and RV were covered in 13 contiguous short-axis slices. Images were acquired in the systolic and diastolic sweet spots  of the cardiac cycle and were spatiotemporally coregistered . Tractography was performed by numerically integrating the primary eigenvector field into streamlines using an adaptive 5th order Runge-Kutta method. The impact of cumulative image averages (1-8) on the reliability of the fractional anisotropy (FA) and fiber helix angle (HA) indices was assessed.
DTI-tractography of the entire human heart can be performed in vivo, without slice gaps, and allows both the LV and the RV to be characterized. A minimum of 5 averages at each slice location is required for accurate quantification. The ability to characterize fiber architecture in the LV and RV in vivo has the potential to provide new insights into a range of diseases affecting both the pulmonary venous and arterial circulations.
R01 HL093038 (D.E.S.), R01HL112831 (D.E.S.), P41RR14075 (Martinos Center).
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