Cellular basis for volume related wall thickness changes in the rat left ventricle

Spotnitz, Henry M.; Spotnitz, William D.; Cottrell, Thomas S.; Spiro, David; Sonnenblick, Edmund H.

doi:10.1016/0022-2828(74)90074-1

Cited by 136 publications

(103 citation statements)

References 29 publications

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“…Keywords cardiac microstructure; sheets LEFT VENTRICULAR (LV) myofibers are connected by an extensive extracellular collagen matrix (3) to form myolaminar "sheets," two-to-four cells thick, which are also interconnected Copyright © 2005 by a collagen network (16). This sheet architecture has been proposed as an anatomic basis for myofiber rearrangement throughout the cardiac cycle (17,22), and sheet deformation is thought to underlie LV mechanics during contraction (6) and relaxation (2).…”

Section: Introductionmentioning

confidence: 99%

Direct measurement of transmural laminar architecture in the anterolateral wall of the ovine left ventricle: new implications for wall thickening mechanics

Harrington

Rodriguez

Cheng

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

108

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Laminar, or sheet, architecture of the left ventricle (LV) is a structural basis for normal systolic and diastolic LV dynamics, but transmural sheet orientations remain incompletely characterized. We directly measured the transmural distribution of sheet angles in the ovine anterolateral LV wall. Ten Dorsett-hybrid sheep hearts were perfusion fixed in situ with 5% buffered glutaraldehyde at end diastole and stored in 10% formalin. Transmural blocks of myocardial tissue were excised, with the edges cut parallel to local circumferential, longitudinal, and radial axes, and sliced into 1-mm-thick sections parallel to the epicardial tangent plane from epicardium to endocardium. Mean fiber directions were determined in each section from five measurements of fiber angles. Each section was then cut transverse to the fiber direction, and five sheet angles (β) were measured and averaged. Mean fiber angles progressed nearly linearly from −41° (SD 11) at the epicardium to +42° (SD 16) at the endocardium. Two families of sheets were identified at approximately +45° (β + ) and −45° (β − ). In the lateral region (n = 5), near the epicardium, sheets belonged to the β + family; in the midwall, to the β − family; and near the endocardium, to the β + family. This pattern was reversed in the basal anterior region (n = 4). Sheets were uniformly β − over the anterior papillary muscle (n = 2). These direct measurements of sheet angles reveal, for the first time, alternating transmural families of predominant sheet angles. This may have important implications in understanding wall mechanics in the normal and the failing heart. Keywords cardiac microstructure; sheets LEFT VENTRICULAR (LV) myofibers are connected by an extensive extracellular collagen matrix (3) to form myolaminar "sheets," two-to-four cells thick, which are also interconnected Copyright © 2005 by a collagen network (16). This sheet architecture has been proposed as an anatomic basis for myofiber rearrangement throughout the cardiac cycle (17,22), and sheet deformation is thought to underlie LV mechanics during contraction (6) and relaxation (2).The three-dimensional geometry of fibers and sheets is critical. Maximum contraction of fibers that lie in planes tangent to the epicardial surface is only 15% along their long axis (21); yet LV ejection fractions of 60% and systolic radial wall thickening of 40% are typically observed. The helical arrangement of the fibers may account for some of this disparity (20), but an additional important mechanism appears to be sheet deformation (19,22). Laminar shear, extension, and thinning or thickening are thought to contribute to wall thickness changes (6,7,24).Fiber orientation, which can be measured directly, has been found in several species to vary from approximately −60° at the epicardium to +60° at the endocardium (4,10,12,14,23,28). Until recently, however, sheet orientation could only be inferred indirectly from the directions of fiber and cleavage planes from three orthogonal views (6). Recently, our group and Ashi...

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Section: Introductionmentioning

confidence: 99%

Direct measurement of transmural laminar architecture in the anterolateral wall of the ovine left ventricle: new implications for wall thickening mechanics

Harrington

Rodriguez

Cheng

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

108

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“…For instance, a recent experimental study demonstrated that myocardial wall thickening is highly heterogeneous despite the absence of any heterogeneity in systolic fiber shortening [121]. These findings support the hypothesis put forward in earlier studies by numerous authors [120,122,123] that rearrangement of laminar sheets of fibers, and thus, the presence of tissue orthotropy, is a key contributor which amplifies systolic fiber shortening into adequate myocardial wall thickening. Finally, the constitutive descriptions are not only spatially varying throughout the heart, they are also temporally varying due to pathologies such as myocardial infarction [124] or dilated cardiomyopathy [125].…”

Section: Introductionsupporting

confidence: 69%

Cardiovascular Mechanics

SpringerReference

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Modeling in biomechanics plays an important role in simulating biological functions and has great potential to aid medical clinicians in determining the cause of a disease, the type of treatment or by aiding in the training of a surgical procedure. Cardiovascular diseases (CVDs) are the leading cause of mortality today. This work therefore aims at developing a framework for modeling CVDs, such as cerebral aneurysms or heart diseases with increased myofiber dispersion as seen in, e.g., hypertrophic cardiomyopathy.To this end, a three-dimensional growth model of a human saccular cerebral aneurysm is presented that includes the anisotropy of the medial layer. It is shown that including fibers in the media reduces the maximum principal stress, thickness increase and shear stress in the aneurysm wall. It is also shown that the axial pre-stretch has a large impact on the stress levels and thickness increase in the aneurysm wall.In addition, the constituents needed for the numerical implementation of a structurally based constitutive law describing the behavior of passive myocardium is shown. A comparison is made between this invariant based model and a commonly used Green-Lagrange strain component based model and it is shown that using material parameters retrieved when both models is fitted using a simple shear mode experiment, the invariant based model is better suited to predict the stress in the myocardium for other modes of deformation. The passive cardiac model is coupled together with an evolution equation responsible for generating the active stress. A model of the left ventricle (LV) is presented where pressure is calculated as a response to the change in the ventricular volume in order to ensure physiologically realistic pressure-volume loops. The influence of myocardial fiber and sheet distribution is investigated by using two different setups, a generic setup and one based on experiments. The results implies that spatial heterogeneity may play a critical role in mechanical contraction of the LV and that geometrical descriptions of deformation are needed when evaluating the accuracy of a ventricular model.Further, a novel approach to model the dispersion of both the fiber and sheet orientations evident in, especially diseased, myocardium is presented. Analytical and numerical simulations show that the dispersion parameter has great effect on myocardial deformation and stress development. The results also show that the dispersion has a significant impact on pressure-volume loops of an LV, and in future simulations the presented dispersion model for myocardium may advantageously be used together with models of, e.g., growth and remodeling of various cardiac diseases. In cases where fiber-reinforced models are extended to include the effect of distributed fiber orientations, neither the mathematical nor physical motivation for tension-compression fiber switching is clear, and in fact several choices exist for the material modeler. Therefore, methods to study such switching mechanisms is explored by ana...

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“…It is the linkage within the fibrous matrix that permits action as a power train. Taken together, the slippage between the myocardial units accounts for the large changes in shape and dimension of the ventricular mass over the cardiac cycle, underscoring the major transmural gradients of three-dimensional strain, with predominant dimensional changes observed in the inner wall [19]. The marked heterogeneity in the extent of aggregation of the individual cardiomyocytes, furthermore, indicates a local "fingerprint" for each ventricular region, these regions representing the "segments" as identified echocardiographically [17], thus pointing to the well-recognized regional variability in antagonistic function of the wall [11, 12, 20 -22].…”

Section: Histological Findingsmentioning

confidence: 99%

“…In particular, our qualitative observations, supported by our quantitative measurements, reveal a variable mixture of populations of cardiomyocytes aligned in surface-parallel or transmural directions. It is the presence of the spaces between the aggregated cardiomyocytes occupied by loose perimysial tissue that permits their gliding relative to one another during systolic ventricular contraction, thus explaining the paradox of systolic mural thickening [19]. The dense packing of the cardiomyocytes produced by the endomysial component of the fibrous matrix, however, limits the diastolic extension of the myocardium, yet transmits forces and stores energy during systole [19].…”

Section: Histological Findingsmentioning

confidence: 99%

“…It is the presence of the spaces between the aggregated cardiomyocytes occupied by loose perimysial tissue that permits their gliding relative to one another during systolic ventricular contraction, thus explaining the paradox of systolic mural thickening [19]. The dense packing of the cardiomyocytes produced by the endomysial component of the fibrous matrix, however, limits the diastolic extension of the myocardium, yet transmits forces and stores energy during systole [19]. When considered on the basis of continuum mechanics, because of the numerous branchings between the individual cardiomyocytes, the principal stresses occurring during systolic contraction do not coincide with the striation of the myocytes.…”

Section: Histological Findingsmentioning

confidence: 99%

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Pneumatic Distension of Ventricular Mural Architecture Validated Histologically

Burg

Lunkenheimer

Niederer

et al. 2016

Fortschr Röntgenstr

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▼Purpose: There are ongoing arguments as to how cardiomyocytes are aggregated together within the ventricular walls. We used pneumatic distension through the coronary arteries to exaggerate the gaps between the aggregated cardiomyocytes, analyzing the pattern revealed using computed tomography, and validating our findings by histology. Methods: We distended 10 porcine hearts, arresting 4 in diastole by infusion of cardioplegic solutions, and 4 in systole by injection of barium chloride. Mural architecture was revealed by computed tomography, measuring also the angulations of the long chains of cardiomyocytes. We prepared the remaining 2 hearts for histology by perfusion with formaldehyde. Results: Increasing pressures of pneumatic distension elongated the ventricular walls, but produced insignificant changes in mural thickness. The distension exaggerated the spaces between the aggregated cardiomyocytes, compartmenting the walls into epicardial, central, and endocardial regions, with a feathered arrangement of transitions between them. Marked variation was noted in the thicknesses of the parts in the different ventricular segments, with no visible anatomical boundaries between them. Measurements of angulations revealed intruding and extruding populations of cardiomyocytes that deviated from a surface-parallel alignment. Scrolling through the stacks of tomographic images revealed marked spiraling of the aggregated cardiomyocytes when traced from base to apex. Conclusion: Our findings call into question the current assumption that cardiomyocytes are uniformly aggregated together in a tangential fashion. There is marked heterogeneity in the architecture of the different ventricular segments, with the aggregated units never extending in a fully transmural fashion.This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.

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Cellular basis for volume related wall thickness changes in the rat left ventricle

Cited by 136 publications

References 29 publications

Direct measurement of transmural laminar architecture in the anterolateral wall of the ovine left ventricle: new implications for wall thickening mechanics

Direct measurement of transmural laminar architecture in the anterolateral wall of the ovine left ventricle: new implications for wall thickening mechanics

Cardiovascular Mechanics

Pneumatic Distension of Ventricular Mural Architecture Validated Histologically

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