Three-dimensional cartography of the pattern of the myofibres in the second trimester fetal human heart

Jouk, Pierre‐Simon; Usson, Yves; Michalowicz, Gabrielle; Grossi, Laurence

doi:10.1007/s004290000103

Cited by 101 publications

(121 citation statements)

References 18 publications

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“…Computer modeling has shown that tissue polarity, which is propagated at cell junctions, leads to local swirling patterns in the absence of a global polarizing signal (Burak and Shraiman, 2009). This corresponds to our observations in the embryonic heart, and is also consistent in the adult heart with the known architecture of the myofibers, which shows gradual variation and is described as a spiral around the ventricles (Jouk et al, 2000). The pattern of cell coordination that we demonstrate opens perspectives for the understanding of congenital heart diseases, in which myocardial architecture is frequently affected.…”

Section: Research Articlesupporting

confidence: 90%

Quantitative analysis of polarity in 3D reveals local cell coordination in the embryonic mouse heart

et al. 2013

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Anisotropies that underlie organ morphogenesis have been quantified in 2D, taking advantage of a reference axis. However, morphogenesis is a 3D process and it remains a challenge to analyze cell polarities in 3D. Here, we have designed a novel procedure that integrates multidisciplinary tools, including image segmentation, statistical analyses, axial clustering and correlation analysis. The result is a sensitive and unbiased assessment of the significant alignment of cell orientations in 3D, compared with a random axial distribution. Taking the mouse heart as a model, we validate the procedure at the fetal stage, when cardiomyocytes are known to be aligned. At the embryonic stage, our study reveals that ventricular cells are already coordinated locally. The centrosome-nucleus axes and the cell division axes are biased in a plane parallel to the outer surface of the heart, with a minor transmural component. We show further alignment of these axes locally in the plane of the heart surface. Our method is generally applicable to other sets of vectors or axes in 3D tissues to map the regions where they show significant alignment.

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Section: Research Articlesupporting

confidence: 90%

Quantitative analysis of polarity in 3D reveals local cell coordination in the embryonic mouse heart

et al. 2013

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“…It is this distribution of ␣ t that was used in the FIB simulation. Meanwhile, more recent experimental investigations have confirmed the earlier observations by Streeter and colleagues that myofiber orientation in the LV wall has a component in transmural direction (1,13,18,23,24,25,32). Accurate quantification of ␣ t has proven to be difficult, among others, because the unique definition of a wall-bound coordinate system to which the fiber orientation can be referred to is difficult (13).…”

Section: Discussionmentioning

confidence: 79%

“…Accurate quantification of ␣ t has proven to be difficult, among others, because the unique definition of a wall-bound coordinate system to which the fiber orientation can be referred to is difficult (13). Yet, the main experimental findings are that ␣ t is positive in the basal part and negative in the apical part of the LV wall (13,18,32), that ␣ t reaches its extremum closer to the endocardial surface than the epicardial surface (24), and that ␣ t is small (Ͻ5°) in the bulk of the myocardium but certainly not small near the apex and base (23), with some studies (25,32) reporting that the magnitude of ␣ t may increase up to 40°. The distribution of ␣ t in the FIB simulation agrees with these experimental findings.…”

Section: Discussionmentioning

confidence: 99%

Determinants of left ventricular shear strain

Bovendeerd¹,

Kroon²,

Delhaas³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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matical models of cardiac mechanics can potentially be used to relate abnormal cardiac deformation, as measured noninvasively by ultrasound strain rate imaging or magnetic resonance tagging (MRT), to the underlying pathology. However, with current models, the correct prediction of wall shear strain has proven to be difficult, even for the normal healthy heart. Discrepancies between simulated and measured strains have been attributed to 1) inadequate modeling of passive tissue behavior, 2) neglecting active stress development perpendicular to the myofiber direction, or 3) neglecting crossover of myofibers in between subendocardial and subepicardial layers. In this study, we used a finite-element model of left ventricular (LV) mechanics to investigate the sensitivity of midwall circumferential-radial shear strain (Ecr) to settings of parameters determining passive shear stiffness, cross-fiber active stress development, and transmural crossover of myofibers. Simulated time courses of midwall LV Ecr were compared with time courses obtained in three healthy volunteers using MRT. Ecr as measured in the volunteers during the cardiac cycle was characterized by an amplitude of ϳ0.1. In the simulations, a realistic amplitude of the Ecr signal could be obtained by tuning either of the three model components mentioned above. However, a realistic time course of Ecr, with virtually no change of Ecr during isovolumic contraction and a correct base-to-apex gradient of Ecr during ejection, could only be obtained by including transmural crossover of myofibers. Thus, accounting for this crossover seems to be essential for a realistic model of LV wall mechanics. magnetic resonance tagging; finite-element model; cardiac mechanics; myofiber angle DEFORMATION OF THE CARDIAC WALL can be assessed noninvasively using ultrasound strain rate imaging (11) or magnetic resonance tagging (MRT) (4). The deformation patterns acquired may deviate from normal in the case of cardiac pathology, e.g., aortic stenosis, ischemia, or conduction disorders (39,40,43). The analysis of abnormal deformation patterns toward the underlying pathology is not straightforward: the relation between the change in the deformation pattern and the pathology is complex, and the criteria for normal and abnormal strain patterns have not yet been defined. A mathematical model capable of predicting the forward relation between pathology and deformation could, if used in an inverse analysis, be a useful clinical tool, not only in diagnosis but also in intervention selection and planning, by simulating candidate interventions beforehand.Several models describing the deformation of cardiac walls have been proposed (5,6,14,19,20,28,35,41,42,45), but none of these models have already been used as a diagnostic tool. As a first step toward this application, one would require the models to be able to correctly predict deformation in the wall of the healthy heart. Most models are able to correctly predict circumferential, longitudinal, and radial strain (5,14,28,41,42,45). However, ...

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“…26), coinciding with establishment of the coronary circulation. From ED16 in the mouse and the 4th mo of gestation in human, the compact layer forms most of the ventricular myocardium, although its structural complexity continues to develop (12). Noncompaction of the myocardium presents serious functional consequences for the heart.…”

Section: Myocardial Compactionmentioning

confidence: 99%

Developmental anatomy of the heart: a tale of mice and man

Wessels

Sedmera

2003

Physiological Genomics

221

189

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Because of the increasing availability of tools for genetic manipulation, the mouse has become the most popular animal model for studying normal and abnormal cardiac development. However, despite the enormous advances in mouse genetics, which have led to the production of numerous mutants with cardiac abnormalities resembling those seen in human congenital heart disease, relatively little comparative work has been published to demonstrate the similarities and differences in the developmental cardiac anatomy in both species. In this review we discuss some aspects of the comparative anatomy, with emphasis on the atrial anatomy, the valvuloseptal complex, and ventricular myocardial development. From the data presented it can be concluded that, apart from the obvious differences in size, the mouse and human heart are anatomically remarkably similar throughout development. The partitioning of the cardiac chambers (septation) follows the same sequence of events, while also the maturation of the cardiac valves and myocardium is quite similar in both species. The major anatomical differences are seen in the venous pole of the heart. We conclude that, taking note of the few anatomical “variations,” the use of the mouse as a model system for the human heart is warranted. Thus the analysis of mouse mutants with impaired septation will provide valuable information on cellular mechanisms involved in valvuloseptal morphogenesis (a process often disrupted in congenital heart disease), while the study of embryonic lethal mouse mutants that present with lack of compaction of ventricular trabeculae will ultimately provide clues on the etiology of this abnormality in humans.

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Three-dimensional cartography of the pattern of the myofibres in the second trimester fetal human heart

Cited by 101 publications

References 18 publications

Quantitative analysis of polarity in 3D reveals local cell coordination in the embryonic mouse heart

Quantitative analysis of polarity in 3D reveals local cell coordination in the embryonic mouse heart

Determinants of left ventricular shear strain

Developmental anatomy of the heart: a tale of mice and man

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