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Postnatal myocardium remodelling generates inhomogeneity in the architecture of the ventricular mass
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Postnatal myocardium remodelling generates inhomogeneity in the architecture of the ventricular mass
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Postnatal myocardium remodelling generates inhomogeneity in the architecture of the ventricular mass
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Journal Article
Postnatal myocardium remodelling generates inhomogeneity in the architecture of the ventricular mass
2018
Overview
BackgroundThe 3D architecture of the ventricular mass is poorly known, although in vivo imaging techniques show the physiological inhomogeneity of ventricular walls mechanics. Polarized light imaging makes it possible to quantitatively analyse the myosin filament orientation.AimsIn this paper, we focus on the study the 3D architecture and regional isotropy of myocardial cells.MethodsTwenty normal human hearts, 10 from the perinatal period and 10 from the post-neonatal period were studied by polarized light microscopy. In each voxel of the ventricular mass (90 × 90 × 500 µm) the principal orientation segment was automatically and unambiguously extracted as well as a regional isotropy index (regional orientation tensor of the voxel neighbourhood).ResultsDuring the first months of postnatal age, the median regional isotropy values decreased in the ventricular mesh. This global decrease was not homogeneous across the ventricular walls. From the perinatal to the neonatal period, this decrease was more marked in the inner two-third of the lateral left ventricular wall and in the right part of the interventricular septum. There was a progressive post-neonatal appearance of a particularly inhomogeneous secondary arrangement of myocardial cells with alternation of thick low-RI and thin high-RI areas.ConclusionsThis study has shown a postnatal change in ventricular myocardial architecture, which became more inhomogeneous. The cell rearrangements responsible for the inhomogeneity in ventricular myocardial architecture are revealed by a variation of the regional isotropy index. These major changes are probably an adaptive consequence of the major haemodynamic changes occurring after birth during the neonatal period that generates major parietal stress variations and parietal remodelling.
