Covariant Stringlike Dynamics of Scroll Wave Filaments in Anisotropic Cardiac Tissue

2007 ◽  
Vol 99 (16) ◽  
Author(s):  
Henri Verschelde ◽  
Hans Dierckx ◽  
Olivier Bernus
Keyword(s):  
Cardiac Tissue ◽  
Scroll Wave

TEMPORAL EVOLUTION OF NONLINEAR DYNAMICS IN VENTRICULAR ARRHYTHMIA

2001 ◽  
Vol 11 (10) ◽  
pp. 2531-2548 ◽  
Author(s):  
MICHAEL SMALL ◽  
DEJIN YU ◽  
ROBERT G. HARRISON ◽  
RICHARD CLAYTON ◽  
TRYGVE EFTESTØL ◽  
...  
Keyword(s):  
Cardiac Tissue ◽  
Surrogate Data ◽  
Mapping Technique ◽  
Ecg Signals ◽  
Return Mapping ◽  
Industrialized Nations ◽  
Spatially Extended ◽  
Observation Function ◽  
Scroll Wave ◽  
Break Up

Ventricular fibrillation (VF) is a rapidly lethal cardiac arrhythmia and one of the leading causes of sudden death in many industrialized nations. VF appears at random, but is produced by a spatially extended excitable system. We generated VF-like "pseudo-ECG" signals from a numerical caricature of cardiac tissue of 100 × 100 × 50 elements. The VF-like "pseudo-ECG" signals represent the propagation and break-up of an excitation scroll wave under FitzHugh–Nagumo dynamics. We use surrogate data and correlation dimension techniques to show that the dynamics observed in these computational simulations is consistent with the evolution of spontaneous VF in humans. Furthermore, we apply a novel adaptation of the traditional first return map technique to show that scroll wave break-up may be represented by a characteristic structural transition in the first return plot. The patterns and features identified by the first return mapping technique are found to be independent of the observation function and location. These methods offer insight into the evolution of VF and hint at potential new methods for diagnosis and analysis of this rapidly lethal condition.

INTERACTIONS BETWEEN VORTICES AND LESIONS AND ECTOPIC FOCI IN A CML MODEL OF CARDIAC TISSUE

1996 ◽  
Vol 06 (10) ◽  
pp. 1935-1946 ◽  
Author(s):  
H. ZHANG
Keyword(s):  
3D Model ◽  
Cardiac Tissue ◽  
Spiral Wave ◽  
Scroll Wave ◽  
Cml Model ◽  
Spatio Temporal

Interactions between a localised lesion, and ectopic focus and vortices are studied in CML models of myocardium. Decrease in the size of a localised lesion may change the motion of a trapped spiral wave from a periodic to a quasiperiodic rotation in 2D models. In a 3D model, a localised lesion gives rise to distortion and then breakdown of a trapped scroll wave, generating spatio-temporal irregularity. The interaction between a spiral wave and an ectopic focus is dependent on the differences in their frequencies and phases.

scholarly journals Scroll Wave Dynamics in a Three-Dimensional Cardiac Tissue Model: Roles of Restitution, Thickness, and Fiber Rotation

2000 ◽  
Vol 78 (6) ◽  
pp. 2761-2775 ◽  
Author(s):  
Zhilin Qu ◽  
Jong Kil ◽  
Fagen Xie ◽  
Alan Garfinkel ◽  
James N. Weiss
Keyword(s):  
Cardiac Tissue ◽  
Three Dimensional ◽  
Tissue Model ◽  
Wave Dynamics ◽  
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.

Cytopathology of Cardiac Tissue from Daunomycin-Treated Mice

1971 ◽  
Vol 29 ◽  
pp. 550-551
Author(s):  
Robert H. Liss ◽  
Frances A. Cotton
Keyword(s):  
Cardiac Tissue ◽  
Cardiac Toxicity ◽  
Drug Distribution ◽  
Personal Communication ◽  
Intravenous Dose ◽  
Single Intravenous Dose ◽  
Physiologic Saline ◽  
Histopathologic Changes ◽  
Distribution Studies ◽  
Lung And Kidney

Daunomycin, an antibiotic used in the clinical management of acute leukemia, produces a delayed, lethal cardiac toxicity. The lethality is dose and schedule dependent; histopathologic changes induced by the drug have been described in heart, lung, and kidney from hamsters in both single and multiple dose studies. Mice given a single intravenous dose of daunomycin (10 mg/kg) die 6-7 days later. Drug distribution studies indicate that the rodents excrete most of a single dose of the drug as daunomycin and metabolite within 48 hours after dosage (M. A. Asbell, personal communication).Myocardium from the ventricles of 6 moribund BDF1 mice which had received a single intravenous dose of daunomycin (10 mg/kg), and from controls dosed with physiologic saline, was fixed in glutaraldehyde and prepared for electron microscopy.

Iron storage sites in the myocardium as revealed by cytohistochemistry

1988 ◽  
Vol 46 ◽  
pp. 394-395
Author(s):  
M. Ashraf ◽  
F. Thompson ◽  
S. Miki ◽  
P. Srivastava
Keyword(s):  
Cardiac Tissue ◽  
Coronary Perfusion ◽  
Intracellular Iron ◽  
Ether Anesthesia ◽  
Intense Staining ◽  
Iron Storage ◽  
Thin Sections ◽  
Rat Hearts ◽  
Cacodylate Buffer ◽  
Made In

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).

Immunoelectron microscope detection of C-type natriuretic peptide in normal human atrial tissue

1993 ◽  
Vol 51 ◽  
pp. 388-389
Author(s):  
Chi-Ming Wei ◽  
Margaret Hukee ◽  
Christopher G.A. McGregor ◽  
John C. Burnett
Keyword(s):  
Amino Acid ◽  
Natriuretic Peptide ◽  
Vascular Tone ◽  
Cardiac Tissue ◽  
Ring Structure ◽  
Terminal Amino Acid ◽  
Amino Acid Peptide ◽  
Normal Human ◽  
Terminal Amino ◽  
The Brain

C-type natriuretic peptide (CNP) is a newly identified peptide that is structurally related to atrial (ANP) and brain natriuretic peptide (BNP). CNP exists as a 22-amino acid peptide and like ANP and BNP has a 17-amino acid ring formed by a disulfide bond. Unlike these two previously identified cardiac peptides, CNP lacks the COOH-terminal amino acid extension from the ring structure. ANP, BNP and CNP decrease cardiac preload, but unlike ANP and BNP, CNP is not natriuretic. While ANP and BNP have been localized to the heart, recent investigations have failed to detect CNP mRNA in the myocardium although small concentrations of CNP are detectable in the porcine myocardium. While originally localized to the brain, recent investigations have localized CNP to endothelial cells consistent with a paracrine role for CNP in the control of vascular tone. While CNP has been detected in cardiac tissue by radioimmunoassay, no studies have demonstrated CNP localization in normal human heart by immunoelectron microscopy.

Confocal imaging of calcium in intact ventricular muscle provides a new view of excitation-contraction coupling

1996 ◽  
Vol 54 ◽  
pp. 738-739
Author(s):  
W.G. Wier
Keyword(s):  
Local Control ◽  
Cardiac Tissue ◽  
Cell Function ◽  
Isolated Heart ◽  
Cardiac Cells ◽  
Confocal Imaging ◽  
Ion Concentration ◽  
Heart Cell ◽  
Free Calcium ◽  
Heart Cells

A fundamentally new understanding of cardiac excitation-contraction (E-C) coupling is being developed from recent experimental work using confocal microscopy of single isolated heart cells. In particular, the transient change in intracellular free calcium ion concentration ([Ca2+]i transient) that activates muscle contraction is now viewed as resulting from the spatial and temporal summation of small (∼ 8 μm3), subcellular, stereotyped ‘local [Ca2+]i-transients' or, as they have been called, ‘calcium sparks'. This new understanding may be called ‘local control of E-C coupling'. The relevance to normal heart cell function of ‘local control, theory and the recent confocal data on spontaneous Ca2+ ‘sparks', and on electrically evoked local [Ca2+]i-transients has been unknown however, because the previous studies were all conducted on slack, internally perfused, single, enzymatically dissociated cardiac cells, at room temperature, usually with Cs+ replacing K+, and often in the presence of Ca2-channel blockers. The present work was undertaken to establish whether or not the concepts derived from these studies are in fact relevant to normal cardiac tissue under physiological conditions, by attempting to record local [Ca2+]i-transients, sparks (and Ca2+ waves) in intact, multi-cellular cardiac tissue.

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