Fiber bundle direction in the mammalian heart

Grimm, Arthur F.; Katele, Kazimieras V.; Lin, Hun-Lin; Fletcher, Joan

doi:10.1007/bf01910776

Cited by 20 publications

(8 citation statements)

References 13 publications

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“…Mammalian hearts have very few overall structural differences (23,24). It is unlikely, therefore, that the neonatal sheep should be any different from other mammals.…”

Section: Discussionmentioning

confidence: 99%

The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

et al. 2015

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BACKGROUND Persistent pulmonary hypertension in the newborn remains a syndrome with high mortality. Knowledge of changes in myocardial architecture in the setting of heart failure in persistent pulmonary hypertension is lacking, and could aid in the explanation of the prevailing high mortality. METHODS Persistent pulmonary hypertension was induced by antenatal ligation of the arterial duct in six ovine fetuses. The hearts were compared ex vivo with five matched control hearts, using diffusion tensor imaging to provide the overall anatomical arrangement, and assessment of the angulations and course of the cardiomyocytes. Fibrosis was assessed with histology. RESULTS We found an overall increase in heart size in pulmonary hypertension, with myocardial thickening confined to the interventricular septum. An increase of 3.5° in angulation of myocyte aggregations was found in hypertensive hearts. In addition, we observed a 2.2% increase in collagen content in the right ventricular free wall. Finally, we found a previously undescribed subepicardial layer of strictly longitudinally oriented cardiomyocytes confined to the right ventricle in all hearts. CONCLUSION Myocardial fibrosis and possibly changes in angulations of myocytes seem to play a part in the etiology of persistent pulmonary hypertension. Moreover, a new anatomical arrangement of right ventricular mural architecture is described.

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“…Mammalian hearts have very few overall structural differences (23,24). It is unlikely, therefore, that the neonatal sheep should be any different from other mammals.…”

Section: Discussionmentioning

confidence: 99%

The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

et al. 2015

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“…The myofiber pattern in the LV of the normal heart has an invariant nature among mammals, including humans 15–17. The orientation of the myofibers varies gradually across the LV wall: subepicardial fibers follow the path of a left‐handed helix around the cavity, fibers in the midwall are circumferentially oriented, and subendocardial fibers follow a right‐handed helical path (Fig.…”

Section: Inner Organ Morphogenesis and Functionmentioning

confidence: 99%

Cardiac Fiber Orientation and the Left‐Right Asymmetry Determining Mechanism

Delhaas

Decaluwe

Rubbens

et al. 2004

Annals of the New York Academy of Sciences

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The invariant nature of body situs within and across vertebrate species implies that a highly conserved pathway controls the specification of the left-right (L/R) axis. Situs-specific morphogenesis begins at the end of this pathway and leads to normal organ arrangement, also known as situs solitus. Occasionally, individuals have a complete, mirror image reversal of this asymmetry, called situs inversus totalis (SIT). In these individuals, gross anatomy is mirror imaged. However, the helical myofiber pattern within the left ventricle (LV) wall is only partially mirror imaged: apical and superficial basal fiber orientation are as in normal persons, whereas the deeper basal layers have an inverted fiber orientation. Because of this bivalent fiber orientation pattern, LV deformation in humans with SIT is mirror imaged only near the base, but near the apex it is as in normal subjects. Apparently, the embryonic L/R controlling genetic pathway does determine situs-specific gross anatomy morphogenesis, but it is not the only factor regulating fiber architecture within the LV wall.

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“…2 Subsequent investigations showed that myocardial microstructure is composed of discrete layers referred to as sheets, which run transmurally across the ventricular wall. 3,4 LeGrice et al 5 provided a more detailed and systematic account of the architecture of these sheets. Finite element (FE) models of the heart incorporate constitutive laws that simulate the anisotropic and nonlinear behavior of the myocardium, which rely on a description of myofiber architecture (i.e.…”

Section: Introductionmentioning

confidence: 99%

Sensitivity of left ventricular mechanics to myofiber architecture: A finite element study

Nikou

Gorman

Wenk

2016

Proc Inst Mech Eng H

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The goal of this study was to investigate the sensitivity of computational models of the heart to their incorporated myofiber architecture during diastole. This architecture plays a critical role in the mechanical and electrical function of the heart and changes after myocardial tissue remodeling, which is associated with some of the most common heart diseases. In this study, a left ventricular finite element model of the porcine heart was created using magnetic resonance imaging, which represents the in vivo geometry. Various myofiber architectures were assigned to the finite element mesh, in the form of fiber and sheet angles. A structural-based material law was used to model the behavior of passive myocardium and its parameters were estimated using measured in vivo strains and cavity volume from magnetic resonance imaging. The final results showed noticeable sensitivity of the stress distribution to both the fiber and sheet angle distributions. This implies that a structural-based material law that takes into account the effect of both fiber and sheet angle distributions should be used. The results also show that although the simulation results improve using available data from histological studies of myocardial structure, the need for individualized myofiber architecture data is crucial.

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Fiber bundle direction in the mammalian heart

Cited by 20 publications

References 13 publications

The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

The myocardial architecture changes in persistent pulmonary hypertension of the newborn in an ovine animal model

Cardiac Fiber Orientation and the Left‐Right Asymmetry Determining Mechanism

Sensitivity of left ventricular mechanics to myofiber architecture: A finite element study

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