Porous medium finite element model of the beating left ventricle

1992 ◽  
Vol 262 (4) ◽  
pp. H1256-H1267 ◽  
Author(s):  
J. M. Huyghe ◽  
T. Arts ◽  
D. H. van Campen ◽  
R. S. Reneman
Keyword(s):  
Left Ventricle ◽  
Wall Thickness ◽  
Cardiac Cycle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Fiber Direction ◽  
Intraventricular Pressure ◽  
Angle Distribution ◽  
Fiber Angle ◽  
Intramyocardial Pressure

The axisymmetric model described represents myocardial tissue as a spongy anisotropic viscoelastic material. It includes torsion around the axis of symmetry of the ventricle, transmural variation of fiber angle, and redistribution of intracoronary blood in the myocardial wall. In simulations, end-systolic principal strains were equal to 0.45, -0.01, and -0.24 at two-thirds of the wall thickness from the epicardium and 0.26, 0.00, and -0.19 at one-third of the wall thickness from the epicardium. The direction of maximal shortening varied by less than 30 degrees from epicardium to endocardium, whereas fiber direction varied by greater than 100 degrees from epicardium to endocardium. During a normal cardiac cycle peak, equatorial intramyocardial pressure differed by less than 5% from peak intraventricular pressure. When redistribution of intracoronary blood in the ventricular wall was suppressed, peak equatorial intramyocardial pressure was found to exceed peak intraventricular pressure by greater than 30%. Simulated contraction of an unloaded left ventricle (left ventricular pressure = 0 kPa) produced similar magnitude for systolic intramyocardial pressures as the normal cardiac cycle. Transmural systolic fiber stress distribution was very sensitive to the chosen transmural fiber angle distribution.

Electrical activation and mechanical asynchronism in the cardiac cycle of the dog

1959 ◽  
Vol 14 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Philip Samet ◽  
William H. Bernstein ◽  
Robert S. Litwak ◽  
William H. Meyer ◽  
Louis Lemberg
Keyword(s):  
Left Ventricle ◽  
Isometric Contraction ◽  
Cardiac Cycle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Electrical Activation ◽  
Qrs Complex ◽  
Simultaneous Registration ◽  
The Right ◽  
Premature Beats

Dissociation of electrical and mechanical asynchronism in the right and left ventricle of the dog has been studied by simultaneous registration of the precordial electrocardiogram and right and left ventricular pressure curves. Observations were made during sinus rhythm and during digitalis-induced ventricular premature beats with widened aberrant QRS complexes. Measurements were made of the time of onset of isometric contraction in the ventricles, relative to each other, and to the onset of the QRS complex. The results indicate that mechanical asynchronism in onset of isometric contraction is not a necessary consequence of the asynchronous electrical depolarization of ventricular premature systoles. Submitted on November 10, 1958

Interaction Between Intramyocardial Pressure (IMP) and Myocardial Circulation

1985 ◽  
Vol 107 (1) ◽  
pp. 51-56 ◽  
Author(s):  
T. Arts ◽  
R. S. Reneman
Keyword(s):  
Mathematical Model ◽  
Coronary Artery ◽  
Cardiac Cycle ◽  
Animal Experiments ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Intramyocardial Pressure ◽  
Coronary Artery Flow ◽  
Myocardial Fibers ◽  
Artery Flow

In our concept of the interaction between intramyocardial pressure (IMP) and myocardial perfusion, IMP is defined as the hydrostatic pressure in the soft tissue surrounding the myocardial fibers. In a mathematical model of the mechanics of the left ventricle the latter definition results in values for IMP equal to left ventricular pressure in the inner layers of the wall, and a continuous decrease across the wall to zero in the outer layers. Modulation of coronary artery flow during the cardiac cycle is predominantly due to compression of the coronary vasculature by the IMP during the systolic phase of the cardiac cycle, resulting in back-squeezing components in this flow. In a mathematical model of the dynamics of the coronary circulation, containing a large capacitance at the level of the coronary microvasculature, the modulations of coronary artery flow were found to be similar to those found in animal experiments in open-chest dogs.

Assessment of Myocardial Viability in Persistent Defects on Thallium-201 SPECT after Reinjection Using Gradient-Echo MRI

1996 ◽  
Vol 35 (05) ◽  
pp. 146-152 ◽  
Author(s):  
A. Kögler ◽  
H.-A. Schmitt ◽  
D. Emrich ◽  
H. Kreuzer ◽  
D. L. Munz ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Myocardial Viability ◽  
Cardiac Cycle ◽  
Single Photon ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Gradient Echo ◽  
Systolic Wall Thickening

SummaryThis prospective study assessed myocardial viability in 30 patients with coronary heart disease and persistent defects despite reinjection on TI-201 single-photon computed tomography (SPECT). In each patient, three observers graded TI-201 uptake in 7 left ventricular wall segments. Gradient-echo magnetic resonance imaging in the region of the persistent defect generated 12 to 16 short axis views representing a cardiac cycle. A total of 120 segments were analyzed. Mean end-diastolic wall thickness and systolic wall thickening (± SD) was 11.5 ± 2.7 mm and 5.8 ± 3.9 mm in 48 segments with normal TI-201 uptake, 10.1 ± 3.4 mm and 3.7 ± 3.1 mm in 31 with reversible lesions, 11.3 ± 2.8 mm and 3.3 ± 1.9 mm in 10 with mild persistent defects, 9.2 ± 2.9 mm and 3.2 ±2.2 mm in 15 with moderate persistent defects, 5.8 ± 1.7 mm and 1.3 ± 1.4 mm in 16 with severe persistent defects, respectively. Significant differences in mean end-diastolic wall thickness (p <0.0005) and systolic wall thickening (p <0.005) were found only between segments with severe persistent defects and all other groups, but not among the other groups. On follow-up in 11 patients after revascularization, 6 segments with mild-to-moderate persistent defects showed improvement in mean systolic wall thickening that was not seen in 6 other segments with severe persistent defects. These data indicate that most myocardial segments with mild and moderate persistent TI-201 defects after reinjection still contain viable tissue. Segments with severe persistent defects, however, represent predominantly nonviable myocardium without contractile function.

Intramyocardial pressure gradients in working and nonworking isolated cat hearts

1994 ◽  
Vol 266 (3) ◽  
pp. H1233-H1241 ◽  
Author(s):  
L. S. Mihailescu ◽  
F. L. Abel
Keyword(s):  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Mechanical Resistance ◽  
Coronary Perfusion ◽  
Pressure Gradients ◽  
Intramyocardial Pressure ◽  
Krebs Henseleit Buffer ◽  
Transmural Gradient

This study presents an improved method for the measurement of intramyocardial pressure (IMP) using the servo-nulling mechanism. Glass micropipettes (20-24 microns OD) were used as transducers, coated to increase their mechanical resistance to breakage, and placed inside the left ventricular wall with a micropipette holder and manipulator. IMP was measured at the base of the left ventricle in working and nonworking isolated cat hearts that were perfused with Krebs-Henseleit buffer. In working hearts a transmural gradient of systolic IMP oriented from endocardium toward the epicardium was found; the endocardial values for systolic IMP were slightly higher than systolic left ventricular pressure (LVP), by 11-18%. Increases in afterload induced increases in IMP, without changing the systolic IMP-to-LVP ratio. In nonworking hearts with drained left ventricles, the systolic transmural gradient for IMP described for working hearts persisted, but at lower values, and was directly dependent on coronary perfusion pressure. Systolic IMP-to-LVP ratios were always > 1. The diastolic IMP of both working and nonworking hearts exhibited irregular transmural gradients. Our results support the view that generated systolic IMP is largely independent of LVP development.

Impact of ejection on magnitude and time course of ventricular pressure-generating capacity

1993 ◽  
Vol 265 (3) ◽  
pp. H899-H909 ◽  
Author(s):  
D. Burkhoff ◽  
P. P. De Tombe ◽  
W. C. Hunter
Keyword(s):  
Time Course ◽  
Cardiac Cycle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Generating Capacity ◽  
Ejection Phase ◽  
Time Point ◽  
Ventricular Dynamics

This study focuses on elucidating how ventricular afterloading conditions affect the time course of change of left ventricular pressure (LVP) throughout the cardiac cycle, with particular emphasis on revealing specific limitations in the time-varying elastance model of ventricular dynamics. Studies were performed in eight isolated canine hearts ejecting into a simulated windkessel afterload. LVP waves measured (LVPm) during ejection were compared with those predicted (LVPpred) according to the elastance theory. LVPm exceeded LVPpred from a time point shortly after the onset of ejection to the end of the beat. The instantaneous difference between LVPm and LVPpred increased steadily as ejection proceeded and reached between 45 and 65 mmHg near end ejection. This was in large part due to an average 35-ms prolongation of the time to end systole (tes) in ejecting compared with isovolumic beats. The time constant of relaxation was decreased on ejecting beats so that, despite the marked prolongation of tes, the overall duration of ejecting contractions was not greater than that of isovolumic beats. The results demonstrate a marked ejection-mediated enhancement and prolongation of ventricular pressure-generating capacity during the ejection phase of the cardiac cycle with concomitant acceleration of relaxation. None of these factors are accounted for by the time-varying elastance theory.

Myocardial volume change during cardiac cycle derived from three orthogonal systolic strains: towards a quality assessment of strains

2018 ◽  
Vol 60 (3) ◽  
pp. 286-292 ◽  
Author(s):  
Laurent Bonnemains ◽  
Anne Sophie Guerard ◽  
Paul Soulié ◽  
Freddy Odille ◽  
Jacques Felblinger
Keyword(s):  
Left Ventricle ◽  
Quality Assessment ◽  
Healthy Volunteers ◽  
Volume Change ◽  
Cardiac Cycle ◽  
Mean Value ◽  
Left Ventricular ◽  
Strain Measurements ◽  
Significant Difference ◽  
Standard Deviations

Background The relative modification of the myocardial volume between end-systole and end-diastole ([Formula: see text]) has already been assessed with different methods and falls in a range of 0.9–0.97 (mean value = 0.93). Purpose To estimate [Formula: see text] from the three longitudinal ([Formula: see text], circumferential ([Formula: see text]), and radial ([Formula: see text]) strains of the left ventricle using the formula: [Formula: see text] and to test whether this estimate of [Formula: see text] can be used as a marker of the echocardiography quality. Material and Methods Two hundred manuscripts, including a total of 34,690 patients or healthy volunteers, were identified in the Medline database containing values of [Formula: see text], [Formula: see text], and [Formula: see text] measured from echocardiography. Results The median value of was 0.93, in accordance with the literature, with no significant difference between patients or healthy volunteers ( P = 0.38). The proportion of studies with [Formula: see text] was 79%. When only considering groups of healthy volunteers, the studies failing this test had higher standard deviations for the three individual strains: 0.038 vs. 0.029 ( P = 0.02) for [Formula: see text]; 0.060 vs. 0.034 ( P < 10–6) for [Formula: see text], and 0.243 vs. 0.101 ( P < 10–14) for [Formula: see text]. Conclusion The median ratio of the left ventricular myocardial volumes between end-systole and end-diastole in the investigated studies was [Formula: see text]. The formula [Formula: see text] could be used to detect studies with inaccurate strain measurements.

scholarly journals P955 left ventricle cardiac remodeling among lithuanian football versus basketball players

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A Aldujeli ◽  
J Laukaitiene ◽  
R Unikas
Keyword(s):  
Left Ventricle ◽  
Wall Thickness ◽  
Cardiac Remodeling ◽  
Interventricular Septum ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Relative Wall Thickness ◽  
Football Players ◽  
Basketball Players ◽  
Lv Mass

Abstract Background Regular physical exercise causes a continuous gradual increase of the cardiac left ventricular (LV) mass known as physiological adaptive hypertrophy. The extent of LV remodeling depends on the type, amount, and intensity of the exercise. Purpose The aim of this study was to compare structural changes of the heart among Lithuanian football, basketball players and unathletic controls. Methods A total of 50 Lithuanian males aged between 20-29 years volunteered to participate in the study. Football players (n = 15) playing for local II league football clubs,and Basketball players (n = 15) playing for local minor league basketball teams. All athletes had been regularly engaged in their sport for at least three years. Inactive healthy volunteers (n = 20) of similar age served as controls. Routine transthoracic echocardiographic examinations to measure end-diastolic LV dimensions were performed by cardiology fellow under the supervision of a fully licensed cardiologist. Statistical analyses were performed using the SPSS 20.0 software. The value of p &lt; 0,05 was considered as statistically significant. Results No structural or functional pathologies were evident during the echocardiographic examination in any of the subjects. Absolute interventricular septum (IVS) thickness and LV posterior wall thickness, but not LV diameter, were higher in athletes than in inactive controls (P &lt; 0,001). Indexed LV diameter was higher in football players as compared with non-athlete controls and basketball players (P &lt; 0,05). Left ventricular mass of all athletes were higher as compared with controls (p &lt; 0.001). Relative wall thickness was not increased in football players but was higher in basketball players as compared with controls (p &lt; 0.05). Conclusion Cardiac remodeling in Lithuanian football players resulted in left ventricle eccentric hypertrophy due to the LV dilation, increased LV mass and relatively normal relative wall thickness. However in Lithuanian basketball players we noticed an increase in both relative wall thickness and LV mass resulting in LV concentric hypertrophy. Echocardiographic characteristics Groups n End-diastolic LV diameter(mm) End-diastolic Interventricular septum (mm) End-diastolic LV posterior wall LV mass Football Players 15 56.9 10.8 10.8 242 Basketball players 15 53.6 11.5 11.3 254 Inactive individuals 20 53.2 9.1 9.5 182 P value 0.01 &lt;0.001 &lt;0.001 &lt;0.01 Abstract P955 Figure.

Fluid-Structure Interaction Simulation of Blood Flow Inside a Diseased Left Ventricle With Obstructive Hypertrophic Cardiomyopathy in Early Systole

2009 ◽  
Author(s):  
Ahmad Moghaddaszade-Kermani ◽  
Peter Oshkai ◽  
Afzal Suleman
Keyword(s):  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Left Ventricle ◽  
Fluid Structure Interaction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Systolic Phase

Mitral-Septal contact has been proven to be the cause of obstruction in the left ventricle with hypertrophic cardiomyopathy (HC). This paper presents a study on the fluid mechanics of obstruction using two-way loosely coupled fluid-structure interaction (FSI) methodology. A parametric model for the geometry of the diseased left ventricular cavity, myocardium and mitral valve has been developed, using the dimensions extracted from magnetic resonance images. The three-element Windkessel model [1] was modified for HC and solved to introduce pressure boundary condition to the aortic aperture in the systolic phase. The FSI algorithm starts at the beginning of systolic phase by applying the left ventricular pressure to the internal surface of the myocardium to contract the muscle. The displacements of the myocardium and mitral leaflets were calculated using the nonlinear finite element hyperelastic model [2] and subsequently transferred to the fluid domain. The fluid mesh was moved accordingly and the Navier-Stokes equations were solved in the laminar regime with the new mesh using the finite volume method. In the next time step, the left ventricular pressure was increased to contract the muscle further and the same procedure was repeated for the fluid solution. The results show that blood flow jet applies a drag force to the mitral leaflets which in turn causes the leaflet to deform toward the septum thus creating a narrow passage and possible obstruction.

scholarly journals Transmural distribution of three-dimensional strain in the isolated arrested canine left ventricle

1991 ◽  
Vol 261 (3) ◽  
pp. H918-H928 ◽  
Author(s):  
J. H. Omens ◽  
K. D. May ◽  
A. D. McCulloch
Keyword(s):  
Three Dimensional ◽  
Left Ventricular Pressure ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Fiber Direction ◽  
Plane Shear ◽  
Left Handed ◽  
Longitudinal Strains ◽  
Transverse Shear Strains ◽  
Principal Strains

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.

Asynchrony and ryanodine modulate load-dependent relaxation in the canine left ventricle

1995 ◽  
Vol 268 (1) ◽  
pp. H17-H24 ◽  
Author(s):  
W. Y. Lew
Keyword(s):  
Left Ventricle ◽  
Time Constant ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Pressure Load ◽  
Single Cardiac Cycle ◽  
Anesthetized Dogs ◽  
Pressure Fall

Load-dependent relaxation was studied in six anesthetized dogs by inflating an intra-aortic balloon to increase peak left ventricular (LV) pressure by 1–20 mmHg within a single cardiac cycle. A series of timed and graded pressure loads was produced by inflating the balloon either during diastole (early loads) or midsystole (midsystolic pressure loads). The rate of LV pressure fall was measured with the time constant (tau). There was a significant increase in tau with 63 midsystolic pressure load [tau increased 1.4 +/- 0.1% (SE)/mmHg increase in peak LV pressure] but not with 67 early pressure loads (-0.5 +/- 0.1%/mmHg). This difference remained with LV pacing-induced asynchrony (tau increased 1.8 +/- 0.1%/mmHg with 54 midsystolic pressure loads compared with -0.2 +/- 0.1%/mmHg with 56 early pressure loads) and after 5 micrograms/kg of intravenous ryanodine (tau increased 1.0 +/- 0.2%/mmHg with 58 midsystolic pressure loads compared with -0.7 +/- 0.1%/mmHg with 59 early pressure loads). When compared with control, asynchrony significantly augmented and ryanodine significantly attenuated the effects of midsystolic pressure loads. In conclusion, asynchrony and ryanodine modulate the extent of load-dependent relaxation in the intact left ventricle.

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