PubMed · 12497881
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S Betocchi, M Chiariello. 1999. [Failure resulting from diastolic dysfunction].. https://pubmed.ncbi.nlm.nih.gov/12497881/
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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.