Scroll wave with negative filament tension in a model of the left ventricle of the human heart and its overdrive pacing

2021 ◽  
Vol 104 (3) ◽  
Author(s):  
Sergei F. Pravdin ◽  
Timofei I. Epanchintsev ◽  
Hans Dierckx ◽  
Alexander V. Panfilov
Keyword(s):  
Left Ventricle ◽  
Human Heart ◽  
Overdrive Pacing ◽  
Scroll Wave

scholarly journals Drift of Scroll Wave Filaments in an Anisotropic Model of the Left Ventricle of the Human Heart

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Sergei Pravdin ◽  
Hans Dierckx ◽  
Vladimir S. Markhasin ◽  
Alexander V. Panfilov
Keyword(s):  
Left Ventricle ◽  
Cardiac Arrhythmias ◽  
Human Heart ◽  
Cardiac Tissue ◽  
Three Dimensional ◽  
Excitable Media ◽  
Filament Dynamics ◽  
Myocardial Wall ◽  
Scroll Wave ◽  
Generic Description

Scroll waves are three-dimensional vortices which occur in excitable media. Their formation in the heart results in the onset of cardiac arrhythmias, and the dynamics of their filaments determine the arrhythmia type. Most studies of filament dynamics were performed in domains with simple geometries and generic description of the anisotropy of cardiac tissue. Recently, we developed an analytical model of fibre structure and anatomy of the left ventricle (LV) of the human heart. Here, we perform a systematic study of the dynamics of scroll wave filaments for the cases of positive and negative tension in this anatomical model. We study the various possible shapes of LV and different degree of anisotropy of cardiac tissue. We show that, for positive filament tension, the final position of scroll wave filament is mainly determined by the thickness of the myocardial wall but, however, anisotropy attracts the filament to the LV apex. For negative filament tension, the filament buckles, and for most cases, tends to the apex of the heart with no or slight dependency on the thickness of the LV. We discuss the mechanisms of the observed phenomena and their implications for cardiac arrhythmias.

The study of scroll wave dynamics in personalized models of the left ventricle of the human heart

2016 ◽  
Vol 31 (5) ◽  
Author(s):  
Konstantin S. Ushenin ◽  
Sergei F. Pravdin ◽  
Yuliya S. Alueva ◽  
Tatyana V. Chumarnaya ◽  
Olga E. Solovyova
Keyword(s):  
Left Ventricle ◽  
Human Heart ◽  
Ultrasound Examination ◽  
Left Ventricular ◽  
Left Ventricular Cavity ◽  
Wave Dynamics ◽  
Wave Drift ◽  
Starting Point ◽  
First Results ◽  
Scroll Wave

AbstractThis paper presents first results on the dynamics of filaments of scroll waves of myocardium excitation obtained for personalized models of the left ventricle of the human heart. The paper describes a mathematical model of the left ventricle of the human heart and its electrical activity, numerical methods for the model calculation within the framework of computer implementation, and also the method of personalization of the model according to data of ultrasound examination. We found that regardless of the starting point of wave the filaments of wave drift along a spiral to the attractor located near the apex of the ventricle. The attractor position was essentially different in models constructed from the data of patients without identified pathology and those for patients with an increased left ventricular cavity.

scholarly journals Anatomy of the lateral, diagonal and anterosuperior arterial branches of the left ventricle of the human heart]]>

2005 ◽  
Vol 20 (2) ◽  
Author(s):  
Jos� R. Ortale ◽  
Jos� Meciano Filho ◽  
Ana M. F. Paccola ◽  
J�lia G. P. G. Leal ◽  
Carolina A. Scaranari
Keyword(s):  
Left Ventricle ◽  
Human Heart

scholarly journals The pattern of intramural veins of the left ventricle of the human heart.

Heart ◽  
1975 ◽  
Vol 37 (1) ◽  
pp. 85-93 ◽  
Author(s):  
G Farrer-Brown ◽  
M H Tarbit
Keyword(s):  
Left Ventricle ◽  
Human Heart

Vasoactive intestinal peptide has a direct positive inotropic effect on isolated human myocardial trabeculae

2001 ◽  
Vol 101 (6) ◽  
pp. 637-643 ◽  
Author(s):  
Ole SAETRUM OPGAARD ◽  
Mikael KNUTSSON ◽  
René DE VRIES ◽  
Beril TOM ◽  
Pramod R. SAXENA ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Vasoactive Intestinal Peptide ◽  
Right Atrium ◽  
Human Heart ◽  
Positive Inotropic Effect ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
The Right ◽  
Ventricular Trabeculae

The aim of the present study was to assess the inotropic effects of vasoactive intestinal peptide (VIP) on isolated myocardial trabeculae from the right atrium and the left ventricle of human hearts. Furthermore, using reverse transcriptase-PCR, we wanted to determine the presence of mRNAs encoding the three cloned human VIP receptors, VPAC1, VPAC2 and PAC1. The trabeculae were paced at 1.0Hz in tissue baths, and changes in isometric contractile force upon exposure to agonist were studied. VIP had a potent positive inotropic effect in some of the atrial and ventricular trabeculae tested. This effect was almost completely blocked by the VIP-receptor antagonist VIP-(6-28). mRNAs encoding the human VPAC1, VPAC2 and PAC1 receptors were detected in human myocardial trabeculae from both the right atrium and the left ventricle. In conclusion, VIP has a direct positive inotropic effect in both the atria and the ventricles of the human heart. The presence of mRNAs for the VPAC1, VPAC2 and PAC1 receptors suggest that VIP may mediate its effect via these receptors.

Anizotropy characteristics of the left ventricle false chordae tendineae as one of varieties of myoendocardial formations of the human heart

2018 ◽  
Author(s):  
Sergey B. Yermolenko ◽  
Myhajlo S. Gavrylyak ◽  
Dmitrij N. Burkovets ◽  
Yulija Y. Malyk ◽  
Olexander V. Tsyhykalo ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Human Heart ◽  
Chordae Tendineae

Abstract 238: Single-Cell Transcriptomic Analysis and Patient-Specific IPSCs Reveal Dysregulated Cell Cycle in Coronary Endothelial Cell in Hypoplastic Left Heart Syndrome

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Mingxia Gu ◽  
Yifei Miao ◽  
Xin Zhou ◽  
Lei Tian ◽  
Marcy Martin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endothelial Cell ◽  
Left Ventricle ◽  
Single Cell ◽  
Hypoplastic Left Heart Syndrome ◽  
Human Heart ◽  
G1 Phase ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Left Heart Syndrome

Hypoplastic left heart syndrome (HLHS) is a single ventricle congenital heart disease that results in severe underdevelopment of the left ventricle, mitral valve, aortic valve, and ascending aorta. Early serial postmortem examinations also revealed a high rate of coronary anomalies in HLHS, which included multiple ventriculo-coronary arterial connections as well as thick-walled and kinked coronary arteries. A previous study showed that fetal hypoplastic left hearts had a reduced endothelial cell (EC) population and lower capillary density compared with normal hearts. However, the mechanism underlying coronary abnormalities associated with HLHS remains unknown. Thus, we generated induced pluripotent stem cells derived ECs (iPSC-ECs) from three HLHS patients and three age-matched controls. Single Cell RNA-Seq (scRNA-seq) profiling identified both endocardial (NPR3 + /CDH5 + ) and coronary endothelial populations (APLN + /CDH5 + ) from the heterogeneous iPSC-ECs. Intriguingly, a subcluster of the coronary endothelial cells (CECs) with cell cycle arrest was specifically enriched in HLHS patients. Further cell cycle analysis showed that 30.6% of the HLHS cells were trapped in the G1 phase, while the majority of the control CECs entered cell cycle normally. Additionally, the cell cycle differences between control and HLHS was only seen in CECs, not in the endocardial population. To verify our transcriptomic analysis, we applied negative cell sorting (NPR3 - /CDH5 + ) on iPSC-ECs to purify CECs (iCECs) and confirmed that HLHS iCECs showed profound reduction of cell cycle/proliferative genes ( KI67, PCNA, CCNA2, CCNB1 ) and abnormal induction of CCND2 , which is the hallmark of G1 phase. BrdU assays also indicated suppressed proliferation in HLHS iCECs. Furthermore, we profiled the transcriptome from a human heart with an underdevelopment left ventricle (ULV) at single cell resolution. When compared to the normal human heart, pathway enrichment analysis of differentially expressed genes in ULV hearts demonstrated reduced cell proliferation in the CEC subpopulation. Here, we identified that CECs from HLHS patients exerted proliferative defects that can potentially impede the development of vascular/capillary structure and cause related functional deficiencies. Reformation of the coronary defect provides a promising therapeutic strategy to prevent HLHS deterioration.

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