Thoracic Vein Arrhythmias

Chen, Yi Jen; Chen, Shih Ann

doi:10.1253/circj.71.a20

Cited by 5 publications

(3 citation statements)

References 67 publications

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“…Atrial arrhythmia can originate at the pulmonary veins [ 69 ]. Other veinous structures have also been found to serve as the initiation sites for arrhythmias [ 70 ]. The simulations shown here demonstrate how a reduction in the dimensionality of the system can lower the number of myocytes needed for the generation of an arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?

Ullah

Hoang-Trong

Lederer

et al. 2022

Cells

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Cardiovascular disease is the leading cause of death worldwide due in a large part to arrhythmia. In order to understand how calcium dynamics play a role in arrhythmogenesis, normal and dysfunctional Ca2+ signaling in a subcellular, cellular, and tissued level is examined using cardiac ventricular myocytes at a high temporal and spatial resolution using multiscale computational modeling. Ca2+ sparks underlie normal excitation–contraction coupling. However, under pathological conditions, Ca2+ sparks can combine to form Ca2+ waves. These propagating elevations of (Ca2+)i can activate an inward Na+–Ca2+ exchanger current (INCX) that contributes to early after-depolarization (EADs) and delayed after-depolarizations (DADs). However, how cellular currents lead to full depolarization of the myocardium and how they initiate extra systoles is still not fully understood. This study explores how many myocytes must be entrained to initiate arrhythmogenic depolarizations in biophysically detailed computational models. The model presented here suggests that only a small number of myocytes must activate in order to trigger an arrhythmogenic propagating action potential. These conditions were examined in 1-D, 2-D, and 3-D considering heart geometry. The depolarization of only a few hundred ventricular myocytes is required to trigger an ectopic depolarization. The number decreases under disease conditions such as heart failure. Furthermore, in geometrically restricted parts of the heart such as the thin muscle strands found in the trabeculae and papillary muscle, the number of cells needed to trigger a propagating depolarization falls even further to less than ten myocytes.

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Section: Discussionmentioning

confidence: 99%

Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?

Ullah

Hoang-Trong

Lederer

et al. 2022

Cells

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“…In our experience, the challenges inherent in approaching LV summit arrhythmias accounts for the majority of OT VA procedural failures in the present era. Alternative ablation techniques such as intracoronary ethanol infusion may provide enhanced procedural success in selected patients …”

Section: Specific Challengesmentioning

confidence: 99%

An Organized Approach to the Localization, Mapping, and Ablation of Outflow Tract Ventricular Arrhythmias

Hutchinson

García

2013

Cardiovasc electrophysiol

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The outflow tract (OT) regions of the right and left ventricles, common sites of origin for idiopathic ventricular arrhythmias (VA), have complex three-dimensional anatomical relationships. The understanding of in situ or "attitudinal" relationships not only informs the electrocardiographic interpretation of VA site of origin, but also facilitates their catheter-based mapping and ablation strategies. By viewing each patient as his or her own "control," the expected changes in ECG morphology (i.e., frontal plane QRS axis and precordial transition) between adjacent intracardiac structures (e.g., RVOT and aortic root) can be reliably predicted. Successful mapping of OT VAs involve a combination of activation and pacemapping guided by fluoroscopy, electroanatomical mapping, and intracardiac echocardiography. The purpose of this manuscript is to provide a simple, reliable strategy for catheter based mapping and ablation of OT VAs. We also discuss 2 specific challenges in OT VA mapping: (1) differentiating posterior RVOT from right coronary cusp VA origin; and (2) mapping VAs originating from the LV summit.

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“…Premature atrial contraction that triggers AF is not always identified during procedures, and a proportion of trigger ectopics originate from non-PV regions [10,11]. In such cases, additional ablation of non-PV foci has demonstrated efficacy in improving AFfree survival; however, there is a lack of consensus regarding the most appropriate method for identifying non-PV foci.…”

Section: Introductionmentioning

confidence: 99%

Fibrillatory pattern of dissociated venous activity after pulmonary vein isolation: Novel characteristics for remnant foci of a trigger ectopy for atrial fibrillation

Okada

Hirata

Kashiwase

et al. 2017

Journal of Cardiology

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Thoracic Vein Arrhythmias

Cited by 5 publications

References 67 publications

Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?

Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?

An Organized Approach to the Localization, Mapping, and Ablation of Outflow Tract Ventricular Arrhythmias

Fibrillatory pattern of dissociated venous activity after pulmonary vein isolation: Novel characteristics for remnant foci of a trigger ectopy for atrial fibrillation

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