Drift of scroll waves of electrical excitation in an isotropic model of the cardiac left ventricle

2016 ◽  
Vol 31 (5) ◽  
Author(s):  
Sergei F. Pravdin ◽  
Hans Dierckx ◽  
Alexander Panfilov
Keyword(s):  
Left Ventricle ◽  
Wall Thickness ◽  
Cell Model ◽  
Rotation Velocity ◽  
Initial Position ◽  
Electrical Excitation ◽  
Isotropic Model ◽  
Wave Rotation ◽  
Cardiac Left Ventricle ◽  
Scroll Waves

AbstractThe dynamics of scroll waves in a symmetric isotropic model of the human cardiac left ventricle is considered. The position of the attractor and the wave rotation velocity over the attractor were determined depending on the wall thickness, parameters of the cell model, chirality of the wave, and the initial position. Mechanisms of observed phenomena are discussed.

Drift of scroll waves in a generic axisymmetric model of the cardiac left ventricle

2019 ◽  
Vol 120 ◽  
pp. 222-233 ◽  
Author(s):  
Sergei F. Pravdin ◽  
Hans Dierckx ◽  
Alexander V. Panfilov
Keyword(s):  
Left Ventricle ◽  
Axisymmetric Model ◽  
Cardiac Left Ventricle ◽  
Scroll Waves

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 < 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 < 0,001). Indexed LV diameter was higher in football players as compared with non-athlete controls and basketball players (P < 0,05). Left ventricular mass of all athletes were higher as compared with controls (p < 0.001). Relative wall thickness was not increased in football players but was higher in basketball players as compared with controls (p < 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 <0.001 <0.001 <0.01 Abstract P955 Figure.

AUTOMATIC METHODS TO ANALYZE AND QUANTIFY CARDIAC LEFT VENTRICLE PARAMETERS BY MEANS OF SPECT

2005 ◽  
pp. 61-88
Author(s):  
MARCO A. GUTIERREZ ◽  
SÉERGIO S. FURUIE ◽  
MARINA S. REBELO ◽  
JOSÉ C. MENEGHETTI
Keyword(s):  
Left Ventricle ◽  
Automatic Methods ◽  
Cardiac Left Ventricle

scholarly journals Role of Oxidation-Dependent CaMKII Activation in the Genesis of Abnormal Action Potentials in Atrial Cardiomyocytes: A Simulation Study

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Na Zhao ◽  
Qince Li ◽  
Haibo Sui ◽  
Henggui Zhang
Keyword(s):  
Oxidative Stress ◽  
Action Potential ◽  
Intracellular Calcium ◽  
Action Potentials ◽  
Cell Model ◽  
Atrial Arrhythmia ◽  
Electrical Excitation ◽  
Calcium Cycling ◽  
Simulation Results ◽  
Camkii Activation

Atrial fibrillation is a common cardiac arrhythmia with an increasing incidence rate. Particularly for the aging population, understanding the underlying mechanisms of atrial arrhythmia is important in designing clinical treatment. Recently, experiments have shown that atrial arrhythmia is associated with oxidative stress. In this study, an atrial cell model including oxidative-dependent Ca2+/calmodulin- (CaM-) dependent protein kinase II (CaMKII) activation was developed to explore the intrinsic mechanisms of atrial arrhythmia induced by oxidative stress. The simulation results showed that oxidative stress caused early afterdepolarizations (EADs) of action potentials by altering the dynamics of transmembrane currents and intracellular calcium cycling. Oxidative stress gradually elevated the concentration of calcium ions in the cytoplasm by enhancing the L-type Ca2+ current and sarcoplasmic reticulum (SR) calcium release. Owing to increased intracellular calcium concentration, the inward Na+/Ca2+ exchange current was elevated which slowed down the repolarization of the action potential. Thus, the action potential was prolonged and the L-type Ca2+ current was reactivated, resulting in the genesis of EAD. Furthermore, based on the atrial single-cell model, a two-dimensional (2D) ideal tissue model was developed to explore the effect of oxidative stress on the electrical excitation wave conduction in 2D tissue. Simulation results demonstrated that, under oxidative stress conditions, EAD hindered the conduction of electrical excitation and caused an unstable spiral wave, which could disrupt normal cardiac rhythm and cause atrial arrhythmia. This study showed the effects of excess reactive oxygen species on calcium cycling and action potential in atrial myocytes and provided insights regarding atrial arrhythmia induced by oxidative stress.

Structure and torsion in the normal and situs inversus totalis cardiac left ventricle. II. Modeling cardiac adaptation to mechanical load

2008 ◽  
Vol 295 (1) ◽  
pp. H202-H210 ◽  
Author(s):  
Wilco Kroon ◽  
Tammo Delhaas ◽  
Peter Bovendeerd ◽  
Theo Arts
Keyword(s):  
Left Ventricle ◽  
Situs Inversus ◽  
Mechanical Load ◽  
Systolic Pressure ◽  
Situs Inversus Totalis ◽  
Cardiac Structure ◽  
Mechanical Stimuli ◽  
Model Study ◽  
Cardiac Adaptation ◽  
Cardiac Left Ventricle

Mathematical models provide a suitable platform to test hypotheses on the relation between local mechanical stimuli and responses to cardiac structure and geometry. In the present model study, we tested hypothesized mechanical stimuli and responses in cardiac adaptation to mechanical load on their ability to estimate a realistic myocardial structure of the normal and situs inversus totalis (SIT) left ventricle (LV). In a cylindrical model of the LV, 1) mass was adapted in response to myofiber strain at the beginning of ejection and to global contractility (average systolic pressure), 2) cavity volume was adapted in response to fiber strain during ejection, and 3) myofiber orientations were adapted in response to myofiber strain during ejection and local misalignment between neighboring tissue parts. The model was able to generate a realistic normal LV geometry and structure. In addition, the model was also able to simulate the instigating situation in the rare SIT LV with opposite torsion and transmural courses in myofiber direction between the apex and base [Delhaas et al. ( 6 )]. These results substantiate the importance of mechanical load in the formation and maintenance of cardiac structure and geometry. Furthermore, in the model, adapted myocardial architecture was found to be insensitive to fiber misalignment in the transmural direction, i.e., myofiber strain during ejection was sufficient to generate a realistic transmural variation in myofiber orientation. In addition, the model estimates that, despite differences in structure, global pump work and the mass of the normal and SIT LV are similar.

scholarly journals CMR Assessment of the Left Ventricle Apical Morphology in Subjects with Giant T-wave Inversions and Without Apical Wall Thickness>15mm

2016 ◽  
Vol 18 (S1) ◽  
Author(s):  
Minjie Lu ◽  
Bailing Wu ◽  
Yan Zhang ◽  
Peter Kellman ◽  
Mehul B Patel ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Wall Thickness ◽  
T Wave

Cardiac hypertrophy and telemetered blood pressure 6 wk after baroreceptor denervation in normotensive rats

1996 ◽  
Vol 271 (6) ◽  
pp. R1759-R1769 ◽  
Author(s):  
B. N. Van Vliet ◽  
L. Hu ◽  
T. Scott ◽  
L. Chafe ◽  
J. P. Montani
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Left Ventricle ◽  
Arterial Pressure ◽  
Wall Thickness ◽  
Free Wall ◽  
Long Evans ◽  
The Right ◽  
Rule Out

We investigated cardiac morphometry 6 wk after sinoaortic baroreceptor denervation (SAD) in Long-Evans rats. SAD (n = 19) was associated with an 11% increase in the weight of the left ventricle (LV) plus septum (P < 0.001) and a 39% increase in that of the right ventricular (RV) free wall (P < 0.001), relative to sham-operated rats (n = 18). RV wall thickness was significantly increased in SAD animals, but there was no difference in the LV wall thickness and volumes of the RV and LV between groups. Constrictor responses to methoxamine and dilation responses to acetylcholine were assessed in an in vitro perfused mesenteric circulation preparation, but neither response was affected by SAD. Baroreceptor denervation was associated with marked and significant increases in the variability (2.8-fold) and daily peak (39 mmHg) levels of telemetered mean arterial pressure (MAP) and small (5%) but significant increases in the daily mean MAP level. Our results are consistent with an effect of increased MAP variability on ventricular weight but cannot rule out possible contributions from other mechanisms.

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