ArticleHeart rhythm2009
A mechanism for the upper limit of vulnerability.
Article in Heart rhythm, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Bidomain modeling of electrical and mechanical properties of cardiac tissue.Biophysics reviews · 2021Review
- A Simplified Approach for Simultaneous Measurements of Wavefront Velocity and Curvature in the Heart Using Activation Times.Cardiovascular engineering and technology · 2013Article
- Diastolic field stimulation: the role of shock duration in epicardial activation and propagation.Biophysical journal · 2013Article
- Investigating the role of the coronary vasculature in the mechanisms of defibrillation.Circulation. Arrhythmia and electrophysiology · 2012Article
- How hyperpolarization and the recovery of excitability affect propagation through a virtual anode in the heart.Computational and mathematical methods in medicine · 2011Article
- High defibrillation threshold: the science, signs and solutions.Indian pacing and electrophysiology journal · 2010Article
- Upper limit of vulnerability and heterogeneity.Heart rhythm · 2009Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
backgroundThe strongest shock that induces reentry in the heart is the upper limit of vulnerability (ULV). In order to understand defibrillation, one must know what causes the ULV.
objectiveThe goal of this study was to examine the mechanism of the upper limit of vulnerability.
methodsNumerical simulations of cardiac tissue were performed using the bidomain model. An S2 shock was applied during the refractory period of the S1 action potential, and results using a smooth curving fiber geometry were compared with results using a smooth plus random fiber geometry.
resultsWhen using a smooth fiber geometry only, no ULV was observed. However, when a random fiber geometry was included, the ULV was present. The difference arises from the fate of the shock-induced break wave front when it reaches the edge of the tissue hyperpolarized by the shock (the virtual anode).
conclusionOur numerical simulations suggest that local heterogeneities throughout the tissue may be crucial for determining the fate of the shock-induced wave front at the edge of the virtual anode, and therefore play an important role in the mechanism underlying the ULV.
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Registered trials
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