Imaging vortex filaments during cardiac fibrillation

Physics Today ◽  
2018 ◽  
Vol 71 (6) ◽  
pp. 25-25
Author(s):  
Richard J. Fitzgerald
Nature ◽  
2018 ◽  
Vol 555 (7698) ◽  
pp. 667-672 ◽  
Author(s):  
J. Christoph ◽  
M. Chebbok ◽  
C. Richter ◽  
J. Schröder-Schetelig ◽  
P. Bittihn ◽  
...  

1998 ◽  
Vol 08 (04) ◽  
pp. 677-684 ◽  
Author(s):  
V. N. Biktashev

Autowave vortices are topological defects in autowave fields in nonlinear active media of various natures and serve as centers of self-organization in the medium. In three-dimensional media, the topological defects are lines, called vortex filaments. Evolution of three-dimensional vortices, in certain conditions, can be described in terms of evolution of their filaments, analogously to that of hydrodynamical vortices in LIA approximation. In the motion equation for the filament, a coefficient called filament tension, plays a principal role, and determines qualitative long-time behavior. While vortices with positive tension tend to shrink and so either collapse or stabilize to a straight shape, depending on boundary conditions, vortices with negative tension show internal instability of shape. This is an essentially three-dimensional effect, as two-dimensional media with the same parameters do not possess any peculiar properties. In large volumes, the instability of filaments can lead to propagating, nondecremental activity composed of curved vortex filaments that multiply and annihilate in an apparently chaotic manner. This may be related to a mechanism of cardiac fibrillation.


Author(s):  
F.K. Rakhmatullov ◽  
◽  
I.Y. Moiseeva ◽  
A.F. Rakhmatullov ◽  
L.F. Burmistrova ◽  
...  
Keyword(s):  

2021 ◽  
Vol 6 (7) ◽  
Author(s):  
Rodolfo Ostilla-Mónico ◽  
Ryan McKeown ◽  
Michael P. Brenner ◽  
Shmuel M. Rubinstein ◽  
Alain Pumir
Keyword(s):  

AIAA Journal ◽  
1986 ◽  
Vol 24 (8) ◽  
pp. 1290-1297 ◽  
Author(s):  
C. H. Liu ◽  
John Tavantzis ◽  
Lu Ting

2006 ◽  
Vol 43 (5) ◽  
pp. 1434-1439 ◽  
Author(s):  
Teresa S. Miller ◽  
Linda K. Kliment ◽  
Kamran Rokhsaz

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Jaunian Chen ◽  
Johann Schredelseker ◽  
Hirohito Shimizu ◽  
Jie Huang ◽  
Kui Lu ◽  
...  

Abnormal Ca2+ handling in cardiac muscle cells is associated with a wide range of human cardiac diseases, including heart failure and cardiac arrhythmias. Zebrafish tremblor (tre) mutant embryos manifest unsynchronized cardiac contractions due to a Ca2+ extrusion defect in cardiomyocytes and thus are used as an animal model for aberrant Ca2+ homeostasis-induced cardiac arrhythmia. To further dissect molecular mechanisms regulating cardiac Ca2+ homeostasis, we conducted a chemical suppressor screen on tre and found that efsevin, a synthetic compound, potently suppresses cardiac fibrillation and restores rhythmic cardiac contractions in tre embryos. In addition, the treatment with efsevin blocks the propagation of arrhythmogenic Ca2+ waves and accelerates the decay phase of Ca2+ sparks in adult murine cardiomyocytes under Ca2+ overload conditions, demonstrating that efsevin modulates Ca2+ handling in both embryonic and adult cardiac tissues. Through a biochemical pulldown assay, we identified a direct interaction between efsevin and VDAC2, a mitochondrial outer membrane voltage dependent anion channel. Overexpression of VDAC2 restores synchronized cardiac contraction in tre and knocking down VDAC2 activity abolishes the rescue effect of efsevin on tre, suggesting that efsevin modulates cardiac Ca2+ homeostasis by potentiating VDAC2 activity. We further showed that enhancing mitochondria Ca2+ uptake by overexpressing MICU or MCU suppresses cardiac fibrillation in tre just like VDAC2 does. Interestingly, this suppressive effect is absent in tre/vdac2 double deficient embryos and co-expression of VDAC2 and MICU or MCU results in synergistic rescue effect on tre, indicating a critical role for mitochondria in regulating cardiac Ca2+ handling and rhythmicity and suggesting that VDAC2 functions as a gate for transporting Ca2+ across the outer membrane. Taken together, our findings identify efsevin as a potent pharmacological tool to modulate cardiac Ca2+ handling, suggest a critical role of mitochondria in the control of cardiac rhythmicity and establish VDAC2 as a modulator of cardiac Ca2+ handling and a potential therapeutic target for the treatment of arrhythmias.


1965 ◽  
Vol 22 (3) ◽  
pp. 471-479 ◽  
Author(s):  
Robert Betchov

We consider a very thin vortex filament in an unbounded, incompressible and inviscid fluid. The filament is not necessarily plane. Each portion of the filament moves with a velocity that can be approximated in terms of the local curvature of the filament. This approximation leads to a pair of intrinsic equations giving the curvature and the torsion of the filament, as functions of the time and the arc length along the filament. It is found that helicoidal vortex filaments are elementary solutions, and that they are unstable.The intrisic equations also suggest a linear mechanism that tends to produce concentrated torsion and a non-linear mechanism tending to disperse such singularities.


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