Epicardial Suction: A New Approach to Mechanical Testing of the Passive Ventricular Wall

2000 ◽  
Vol 122 (5) ◽  
pp. 479-487 ◽  
Author(s):  
R. J. Okamoto ◽  
M. J. Moulton ◽  
S. J. Peterson ◽  
D. Li ◽  
M. K. Pasque ◽  
...  

The lack of an appropriate three-dimensional constitutive relation for stress in passive ventricular myocardium currently limits the utility of existing mathematical models for experimental and clinical applications. Previous experiments used to estimate parameters in three-dimensional constitutive relations, such as biaxial testing of excised myocardial sheets or passive inflation of the isolated arrested heart, have not included significant transverse shear deformation or in-plane compression. Therefore, a new approach has been developed in which suction is applied locally to the ventricular epicardium to introduce a complex deformation in the region of interest, with transmural variations in the magnitude and sign of nearly all six strain components. The resulting deformation is measured throughout the region of interest using magnetic resonance tagging. A nonlinear, three-dimensional, finite element model is used to predict these measurements at several suction pressures. Parameters defining the material properties of this model are optimized by comparing the measured and predicted myocardial deformations. We used this technique to estimate material parameters of the intact passive canine left ventricular free wall using an exponential, transversely isotropic constitutive relation. We tested two possible models of the heart wall: first, that it was homogeneous myocardium, and second, that the myocardium was covered with a thin epicardium with different material properties. For both models, in agreement with previous studies, we found that myocardium was nonlinear and anisotropic with greater stiffness in the fiber direction. We obtained closer agreement to previously published strain data from passive filling when the ventricular wall was modeled as having a separate, isotropic epicardium. These results suggest that epicardium may play a significant role in passive ventricular mechanics. [S0148-0731(00)00305-8]

2004 ◽  
Vol 286 (2) ◽  
pp. H640-H647 ◽  
Author(s):  
Hiroshi Ashikaga ◽  
John C. Criscione ◽  
Jeffrey H. Omens ◽  
James W. Covell ◽  
Neil B. Ingels

Early relaxation in the cardiac cycle is characterized by rapid torsional recoil of the left ventricular (LV) wall. To elucidate the contribution of the transmural arrangement of the myofiber to relaxation, we determined the time course of three-dimensional fiber-sheet strains in the anterior wall of five adult mongrel dogs in vivo during early relaxation with biplane cineangiography (125 Hz) of implanted transmural markers. Fiber-sheet strains were found from transmural fiber and sheet orientations directly measured in the heart tissue. The strain time course was determined during early relaxation in the epicardial, midwall, and endocardial layers referenced to the end-diastolic configuration. During early relaxation, significant circumferential stretch, wall thinning, and in-plane and transverse shear were observed ( P < 0.05). We also observed significant stretch along myofibers in the epicardial layers and sheet shortening and shear in the endocardial layers ( P < 0.01). Importantly, predominant epicardial stretch along the fiber direction and endocardial sheet shortening occurred during isovolumic relaxation ( P < 0.05). We conclude that the LV mechanics during early relaxation involves substantial deformation of fiber and sheet structures with significant transmural heterogeneity. Predominant epicardial stretch along myofibers during isovolumic relaxation appears to drive global torsional recoil to aid early diastolic filling.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yaghoub Dabiri ◽  
Alex Van der Velden ◽  
Kevin L. Sack ◽  
Jenny S. Choy ◽  
Julius M. Guccione ◽  
...  

AbstractAn understanding of left ventricle (LV) mechanics is fundamental for designing better preventive, diagnostic, and treatment strategies for improved heart function. Because of the costs of clinical and experimental studies to treat and understand heart function, respectively, in-silico models play an important role. Finite element (FE) models, which have been used to create in-silico LV models for different cardiac health and disease conditions, as well as cardiac device design, are time-consuming and require powerful computational resources, which limits their use when real-time results are needed. As an alternative, we sought to use deep learning (DL) for LV in-silico modeling. We used 80 four-chamber heart FE models for feed forward, as well as recurrent neural network (RNN) with long short-term memory (LSTM) models for LV pressure and volume. We used 120 LV-only FE models for training LV stress predictions. The active material properties of the myocardium and time were features for the LV pressure and volume training, and passive material properties and element centroid coordinates were features of the LV stress prediction models. For six test FE models, the DL error for LV volume was 1.599 ± 1.227 ml, and the error for pressure was 1.257 ± 0.488 mmHg; for 20 LV FE test examples, the mean absolute errors were, respectively, 0.179 ± 0.050 for myofiber, 0.049 ± 0.017 for cross-fiber, and 0.039 ± 0.011 kPa for shear stress. After training, the DL runtime was in the order of seconds whereas equivalent FE runtime was in the order of several hours (pressure and volume) or 20 min (stress). We conclude that using DL, LV in-silico simulations can be provided for applications requiring real-time results.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Maryse Lapierre-Landry ◽  
Hana Kolesová ◽  
Yehe Liu ◽  
Michiko Watanabe ◽  
Michael W. Jenkins

Abstract While major coronary artery development and pathologies affecting them have been extensively studied, understanding the development and organization of the coronary microvasculature beyond the earliest developmental stages requires new tools. Without techniques to image the coronary microvasculature over the whole heart, it is likely we are underestimating the microvasculature’s impact on normal development and diseases. We present a new imaging and analysis toolset to visualize the coronary microvasculature in intact embryonic hearts and quantify vessel organization. The fluorescent dyes DiI and DAPI were used to stain the coronary vasculature and cardiomyocyte nuclei in quail embryo hearts during rapid growth and morphogenesis of the left ventricular wall. Vessel and cardiomyocytes orientation were automatically extracted and quantified, and vessel density was calculated. The coronary microvasculature was found to follow the known helical organization of cardiomyocytes in the ventricular wall. Vessel density in the left ventricle did not change during and after compaction. This quantitative and automated approach will enable future cohort studies to understand the microvasculature’s role in diseases such as hypertrophic cardiomyopathy where misalignment of cardiomyocytes has been observed in utero.


1991 ◽  
Vol 261 (3) ◽  
pp. H918-H928 ◽  
Author(s):  
J. H. Omens ◽  
K. D. May ◽  
A. D. McCulloch

Three-dimensional myocardial strains in seven isolated, potassium-arrested dog hearts were measured by biplane radiography of 3 transmural columns of 4-6 radiopaque beads implanted in the midanterior left ventricular free wall. Transmural distributions of strain during inflation of a left ventricular balloon to 20-30 mmHg were computed with respect to the zero pressure state. Magnitudes of the 3 principal strains increased in proportion to ventricular volume (0.0088, 0.0037, and -0.0059 ml-1). At a left ventricular pressure of 8 +/- 4 mmHg, mean circumferential (E11) and longitudinal strains (E22) were similar, increasing from epicardium (0.058 +/- 0.055 and 0.036 +/- 0.024) to subendocardium (0.139 +/- 0.102 and 0.120 +/- 0.084) as did the transmural (wall thinning) strain E33 (-0.053 +/- 0.071 to -0.128 +/- 0.083). Negative in-plane shear E12 was small (-0.008 to -0.052), consistent with a left-handed torsion of the left ventricular wall. Mean transverse shear strains E13 and E23 were small (-0.029 to 0.007) but showed considerable variability between hearts. Fiber strain had no significant transmural variation (P = 0.57). The principal axis of greatest strain was close to the fiber orientation on the epicardium (-15 degrees) but closer to the cross-fiber direction near the endocardium (-40 degrees). Therefore, the end-diastolic fiber lengths are maximized on the epicardium and minimized on the endocardium.


2004 ◽  
Vol 287 (6) ◽  
pp. H2697-H2704 ◽  
Author(s):  
Scott D. Zimmerman ◽  
John Criscione ◽  
James W. Covell

Changes in the structure of the “normal” ventricular wall adjacent to an infarcted area involve all components of the myocardium (myocytes, fibroblasts and the extracellular matrix, and the coronary vasculature) and their three-dimensional structural relationship. Assessing changes in these components requires tracking material markers in the remodeling tissue over long periods of time with a three-dimensional approach as well as a detailed histological evaluation of the remodeled structure. The purpose of the present study was to examine the hypotheses that changes in the tissue adjacent to an infarct are related to myocyte elongation, myofiber rearrangement, and changes in the laminar architecture of the adjacent tissue. Three weeks after myocardial infarction, noninfarcted tissue adjacent to the infarct remodeled by expansion along the direction of the fibers and in the cross fiber direction. These changes are consistent with myocyte elongation and myofiber rearrangement (slippage), as well as a change in cell shape to a more elliptical cross section with the major axis in the epicardial tangent plane, and indicate that reorientation of fibers either via “cell slippage” or changes in orientation of the laminar structure of the ventricular wall are quantitatively important aspects of the remodeling of the normally perfused myocardium.


1999 ◽  
Vol 276 (2) ◽  
pp. H595-H607 ◽  
Author(s):  
Kevin D. Costa ◽  
Yasuo Takayama ◽  
Andrew D. McCulloch ◽  
James W. Covell

Previous studies suggest that the laminar architecture of left ventricular myocardium may be critical for normal ventricular mechanics. However, systolic three-dimensional deformation of the laminae has never been measured. Therefore, end-systolic finite strains relative to end diastole, from biplane radiography of transmural markers near the apex and base of the anesthetized open-chest canine anterior left ventricular free wall ( n = 6), were referred to three-dimensional laminar microstructural axes reconstructed from histology. Whereas fiber shortening was uniform [−0.07 ± 0.04 (SD)], radial wall thickening increased from base (0.10 ± 0.09) to apex (0.14 ± 0.13). Extension of the laminae transverse to the muscle fibers also increased from base (0.08 ± 0.07) to apex (0.11 ± 0.08), and interlaminar shear changed sign [0.05 ± 0.07 (base) and −0.07 ± 0.09 (apex)], reflecting variations in laminar architecture. Nevertheless, the apex and base were similar in that at each site laminar extension and shear contributed ∼60 and 40%, respectively, of mean transmural thickening. Kinematic considerations suggest that these dual wall-thickening mechanisms may have distinct ultrastructural origins.


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