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A computational study of mother rotor VF in the human ventricles.

Keldermann RH, ten Tusscher KH, Nash MP, Bradley CP, Hren R, Taggart P, Panfilov AV - Am. J. Physiol. Heart Circ. Physiol. (2008)

Bottom Line: We found that, based on these data, mother rotor VF can occur in the human heart and that ablation of the mother rotor terminates VF.Furthermore, we found that both mother rotor and multiple wavelet VF can occur in the same heart depending on the initial conditions at the onset of VF.We conclude that mother rotor fibrillation is a possible mechanism in the human heart.

View Article: PubMed Central - PubMed

Affiliation: Department of Theoretical Biology, Utrecht University, Utrecht, The Netherlands. R.H.Keldermann@uu.nl

ABSTRACT
Sudden cardiac death is one of the major causes of death in the industrialized world. It is most often caused by a cardiac arrhythmia called ventricular fibrillation (VF). Despite its large social and economical impact, the mechanisms for VF in the human heart yet remain to be identified. Two of the most frequently discussed mechanisms observed in experiments with animal hearts are the multiple wavelet and mother rotor hypotheses. Most recordings of VF in animal hearts are consistent with the multiple wavelet mechanism. However, in animal hearts, mother rotor fibrillation has also been observed. For both multiple wavelet and mother rotor VF, cardiac heterogeneity plays an important role. Clinical data of action potential restitution measured from the surface of human hearts have been recently published. These in vivo data show a substantial degree of spatial heterogeneity. Using these clinical restitution data, we studied the dynamics of VF in the human heart using a heterogeneous computational model of human ventricles. We hypothesized that this observed heterogeneity can serve as a substrate for mother rotor fibrillation. We found that, based on these data, mother rotor VF can occur in the human heart and that ablation of the mother rotor terminates VF. Furthermore, we found that both mother rotor and multiple wavelet VF can occur in the same heart depending on the initial conditions at the onset of VF. We studied the organization of these two types of VF in terms of filament numbers, excitation periods, and frequency domains. We conclude that mother rotor fibrillation is a possible mechanism in the human heart.

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Related in: MedlinePlus

Ablation of the mother rotor spiral in the LV (posterior view). The black dashed line denotes the portion of the ventricles that was removed. The first snapshot (left) is at ∼3 s of simulation time (i.e., the time when part of the LV was removed), the second snapshot (middle) is at 3.3 s, and the third snapshot (right) is at 3.5 s, after which there was no longer any wave activity.
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f4: Ablation of the mother rotor spiral in the LV (posterior view). The black dashed line denotes the portion of the ventricles that was removed. The first snapshot (left) is at ∼3 s of simulation time (i.e., the time when part of the LV was removed), the second snapshot (middle) is at 3.3 s, and the third snapshot (right) is at 3.5 s, after which there was no longer any wave activity.

Mentions: To test the hypothesis that the wavebreaks shown in Fig. 3 are driven by the mother rotor, we eliminated the mother rotor spiral 3 s after its onset by removing ∼20% of the LV free wall of the LV that contained this rotor (see Fig. 4). We found that after removal, the wavebreaks did not complete rotation and that the wavetips of the rotors ran into the refractory tails of the waves and disappeared. After 0.5 s, there was no wave activity present in the heart. Thus, the wavebreaks in the RV (Fig. 3) seemed to be driven by the stable spiral wave in the LV, implying that this is indeed mother rotor fibrillation. We tested this removal procedure further by applying it at different phases of the mother rotor rotation and by removing differently sized regions (10–20% of the LV free wall). We found that as soon as the mother rotor activity was eliminated, the wavebreaks in the RV died out.


A computational study of mother rotor VF in the human ventricles.

Keldermann RH, ten Tusscher KH, Nash MP, Bradley CP, Hren R, Taggart P, Panfilov AV - Am. J. Physiol. Heart Circ. Physiol. (2008)

Ablation of the mother rotor spiral in the LV (posterior view). The black dashed line denotes the portion of the ventricles that was removed. The first snapshot (left) is at ∼3 s of simulation time (i.e., the time when part of the LV was removed), the second snapshot (middle) is at 3.3 s, and the third snapshot (right) is at 3.5 s, after which there was no longer any wave activity.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2643893&req=5

f4: Ablation of the mother rotor spiral in the LV (posterior view). The black dashed line denotes the portion of the ventricles that was removed. The first snapshot (left) is at ∼3 s of simulation time (i.e., the time when part of the LV was removed), the second snapshot (middle) is at 3.3 s, and the third snapshot (right) is at 3.5 s, after which there was no longer any wave activity.
Mentions: To test the hypothesis that the wavebreaks shown in Fig. 3 are driven by the mother rotor, we eliminated the mother rotor spiral 3 s after its onset by removing ∼20% of the LV free wall of the LV that contained this rotor (see Fig. 4). We found that after removal, the wavebreaks did not complete rotation and that the wavetips of the rotors ran into the refractory tails of the waves and disappeared. After 0.5 s, there was no wave activity present in the heart. Thus, the wavebreaks in the RV (Fig. 3) seemed to be driven by the stable spiral wave in the LV, implying that this is indeed mother rotor fibrillation. We tested this removal procedure further by applying it at different phases of the mother rotor rotation and by removing differently sized regions (10–20% of the LV free wall). We found that as soon as the mother rotor activity was eliminated, the wavebreaks in the RV died out.

Bottom Line: We found that, based on these data, mother rotor VF can occur in the human heart and that ablation of the mother rotor terminates VF.Furthermore, we found that both mother rotor and multiple wavelet VF can occur in the same heart depending on the initial conditions at the onset of VF.We conclude that mother rotor fibrillation is a possible mechanism in the human heart.

View Article: PubMed Central - PubMed

Affiliation: Department of Theoretical Biology, Utrecht University, Utrecht, The Netherlands. R.H.Keldermann@uu.nl

ABSTRACT
Sudden cardiac death is one of the major causes of death in the industrialized world. It is most often caused by a cardiac arrhythmia called ventricular fibrillation (VF). Despite its large social and economical impact, the mechanisms for VF in the human heart yet remain to be identified. Two of the most frequently discussed mechanisms observed in experiments with animal hearts are the multiple wavelet and mother rotor hypotheses. Most recordings of VF in animal hearts are consistent with the multiple wavelet mechanism. However, in animal hearts, mother rotor fibrillation has also been observed. For both multiple wavelet and mother rotor VF, cardiac heterogeneity plays an important role. Clinical data of action potential restitution measured from the surface of human hearts have been recently published. These in vivo data show a substantial degree of spatial heterogeneity. Using these clinical restitution data, we studied the dynamics of VF in the human heart using a heterogeneous computational model of human ventricles. We hypothesized that this observed heterogeneity can serve as a substrate for mother rotor fibrillation. We found that, based on these data, mother rotor VF can occur in the human heart and that ablation of the mother rotor terminates VF. Furthermore, we found that both mother rotor and multiple wavelet VF can occur in the same heart depending on the initial conditions at the onset of VF. We studied the organization of these two types of VF in terms of filament numbers, excitation periods, and frequency domains. We conclude that mother rotor fibrillation is a possible mechanism in the human heart.

Show MeSH
Related in: MedlinePlus