Biomedical subjects

Jiangang Dou

Publications and source records attributed to Jiangang Dou.

4 recordsLinked to original sources

PubMed2006

Imaging myocardial fiber disarray and intramural strain hypokinesis in hypertrophic cardiomyopathy with MRI.

PURPOSE: To examine the relationship between myofiber disarray and myocardial hypokinesis in human hypertrophic cardiomyopathy (HCM) using noninvasive cardiac diffusion and strain MRI. MATERIALS AND METHODS: Five patients with a diagnosis of HCM and five age-matched healthy volunteers were studied and compared. Cardiac diffusion MRI was applied to map in vivo myocardial fiber architecture. Cardiac strain MRI was applied to map myocardial motion. By acquiring registered diffusion and strain MRI images in vivo on both normal and HCM hearts, we investigated in HCM the relationship between myofiber disarray and systolic strain components, including radial, fiber, and cross-fiber strains, and sought to determine the mechanism behind disarray-related myocardial dysfunction in HCM. RESULTS: Regionally disordered fiber orientation and reduced diffusion fractional anisotropy (FA) were found in HCM, demonstrating myofiber disarray. Intramural myocardial strain hypokinesis (reduced radial, fiber, and cross-fiber strains) was also observed in HCM in the same region, and was found to be correlated with FA. The correlation between FA and hypokinesis was found to be stronger in the cross-fiber direction (part of the passive myocardial function) compared to the fiber direction (part of the active myocardial function). This is consistent with the hypothesis that the principal feature of HCM is the reduction of myocardium passive compliance. The angle between principal shortening and fiber orientation was markedly disordered in HCM, indicating an abnormal transmural coupling. CONCLUSION: Myofiber disarray in HCM is correlated with abnormalities of both passive and active myocardial function, and the normal patterns of fiber shortening and wall thickening are deranged in HCM.

Adult↗

PubMed2003

Combined diffusion and strain MRI reveals structure and function of human myocardial laminar sheets in vivo.

The mechanism of ventricular thickening in normal humans was investigated using in vivo MRI. The hypothesis that myocardial laminar sheets contribute to ventricular thickening predominantly via sheet shear and sheet extension, as previously found invasively in canine studies at particular ventricular sites, was tested. In normal human subjects, registered images of myocardial sheet architecture and strain at the mid-left ventricle (mid-LV) at mid-systole were acquired with diffusion and strain MRI. Sheet function was analyzed by computing myocardial strain in the local fiber-sheet coordinates. In general, myocardial sheets contribute to ventricular thickening through all three cross-fiber strain components: sheet shear, sheet extension, and sheet-normal thickening (previously undocumented). Each of these components demonstrated substantial spatial heterogeneity, with sheet shear and sheet extension usually predominant in the anterior free wall, and sheet-normal thickening predominant near the right ventricular (RV) insertions. However, considerable intersubject variability was also found. In all cases, the contributions to thickening of fiber strains were small. Sheet function in normal humans was found to be heterogeneous and variable, contrasting with the uniform and symmetric ventricular patterns of fiber shortening and wall thickening. The study demonstrates that noninvasive NMR imaging is a promising tool for investigations of myocardial sheet architecture and function, and is particularly suited to the evident complexity of this field of study.

Diastole↗

PubMed2002

Phase contrast MRI of myocardial 3D strain by encoding contiguous slices in a single shot.

Quantitative measurements of inherently three-dimensional (3D) cardiac strain and strain rate require 3D data; MRI provides uniquely high sensitivity to material strain by combining phase contrast with single-shot acquisition methods, such as echo-planar imaging (EPI). Previous MRI methods applied to 3D strain used multiple two-dimensional (2D) acquisitions and suffered loss of sensitivity due to magnification within the strain calculation of physiologic noise related to cardiac beat-to-beat variability. In the present work, each single-shot acquisition generates 3D image data by acquiring two contiguous 2D Fourier transform (FT) images in a single echo train of an EPI readout. Although strain encoding divides across multiple EPI shots, each strain component is computed only within single-shot data, avoiding noise magnification. Strain tensor maps are displayed using iconic 3D graphics or a simple color code of tensor shape. In a deforming gel phantom, gradient-recalled echo (GRE) MRI movies of 3D strain rates match expected strain fields. In normal human subjects, 3D strain rate tensor movies of heart and brain comprising seven slices in each of seven cardiac phases were completed in 56 heartbeats. Stimulated echo (STE) MRI of net systolic 3D strain was also demonstrated. Two-slices-in-one-shot spatial encoding permits a complete quantitative survey of ventricular 3D strain in under a minute, with routine patient supervision and turnkey image processing.

Brain↗

PubMed2002

Cardiac diffusion MRI without motion effects.

We present a method for diffusion tensor MRI in the beating heart that is insensitive to cardiac motion and strain. Using a stimulated echo pulse sequence with two electrocardiogram (ECG) triggers, diffusion-encoding bipolar gradient pulses are applied at identical phases in consecutive cardiac cycles. In this experiment, diffusion is encoded at a single phase in the cardiac cycle of less than 30 ms in duration. This encoding produces no phase shifts for periodic motion and is independent of intervening strains. Studies in a gel phantom with cyclic deformation confirm that by using this sequence we can map the diffusion tensor free of effects of cyclic motion. In normal human subjects, myocardial diffusion eigenvalues measured with the present method showed no significant change between acquisitions encoded at maximum contractile velocity (peak) vs. at myocardial standstill (end-systole), demonstrating motion independence of in vivo diffusion measurements. Diffusion tensor images acquired with the present method agree with registered data acquired with a previous cardiac diffusion MRI method that was shown to be valid in the normal heart, strongly supporting the validity of MRI diffusion measurement in the beating heart. Myocardial sheet and fiber dynamics measured during systole showed that normal human myocardial sheet orientations tilt toward the radial during systole, and fiber orientations tilt toward the longitudinal, in qualitative agreement with previous invasive studies in canines. These results demonstrate the technique's ability to measure myocardial diffusion accurately at any point in the cardiac cycle free of measurable motion effect, as if the heart were frozen at the point of acquisition.

Diffusion↗