Ionic mechanisms of arrhythmogenesis

Anumonwo, Justus M.B.; Pandit, Sandeep V.

doi:10.1016/j.tcm.2015.01.005

Cited by 29 publications

(16 citation statements)

References 61 publications

(122 reference statements)

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“…Several studies have suggested myocardial ischemia as a variant of progressive prolongation of QT interval and the corresponding action potential duration, which may cause fatal arrhythmias, such as TdP and sudden cardiac death (9)(10)(11). According to these studies, TdP episodes, which are triggered by ischemia or other conditions, may either terminate spontaneously producing some misleading symptoms, similar to the present case (with transient seizure episodes at admission), or may lead to more lethal arrhythmias.…”

Section: Discussionsupporting

confidence: 67%

Torsade de Pointes with Presentation of Seizure in the Ischemic Heart Disease Context: A Case Report

et al. 2017

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Introduction: Torsade de pointes (TdP) is a devastating form of ventricular arrhythmia, mainly associated with prolongation of corrected QT (QTc) interval. In general, a TdP episode terminates spontaneously, produces syncopal episodes, or degenerates lethal arrhythmias. There are few reports on TdP in the context of ischemic heart disease (IHD). The present report describes a case of TdP in an IHD patient with presentation of seizure. Case Presentation: We describe the case of a 64-year-old man with a history of diabetes, complaint of chest discomfort, and diagnosis of unstable angina. The patient experienced recurrent myoclonic jerks, as well as transient, but progressive changes in consciousness; however, they were related to cardiac arrhythmia rather than a brain disorder. Conclusions: Cardiac arrhythmias, similar to TdP episodes, should be taken into consideration in the management of IHD patients with seizure.

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Section: Discussionsupporting

confidence: 67%

Torsade de Pointes with Presentation of Seizure in the Ischemic Heart Disease Context: A Case Report

et al. 2017

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“…The current flow in the ventricular tissue was driven by active ion exchange across the cell membrane. Many researchers have made a great contribution in developing mathematical models of these ionic properties in the cardiac myocyte [9–14]. In this study, we adopted the ionic myocyte model from Ten Tusscher et al [12].…”

Section: Methodsmentioning

confidence: 99%

The effect of electrical conductivity of myocardium on cardiac pumping efficacy: a computational study

Yuniarti

Lim

2017

BioMed Eng OnLine

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Background and aims The existence of non-excitable cells in the myocardium leads to the increasing conduction non-uniformity and decreasing myocardial electrical conductivity. Slowed myocardial conduction velocity (MCV) believed to enhance the probability of cardiac arryhthmia and alter the cardiac mechanical pumping efficacy, even in sinus rhythm. Though several studies on the correlation between MCV and cardiac electrical instabilities exist, there has been no study concerning correlation or causality between MCV and cardiac mechanical pumping efficacy, due to the limitation in clinical methods to document and evaluate cardiac mechanical responses directly. The goal of this study was to examine quantitatively the cardiac pumping efficacy under various MCV conditions using three-dimensional (3D) electromechanical model of canine’s failing ventricle.Methods The electromechanical model used in this study composed of the electrical model coupled with the mechanical contraction model along with a lumped model of the circulatory system. The electrical model consisted of 241,725 nodes and 1,298,751 elements of tetrahedral mesh, whereas the mechanical model consisted of 356 nodes and 172 elements of hexahedral mesh with Hermite basis. First, we performed the electrical simulation for five different MCV conditions, from 30 to 70 cm/s with 10 cm/s interval during sinus pacing. Then, we compared the cardiac electrical and mechanical responses of each MCV condition, such as the electrical activation time (EAT), pressure, volume, and energy consumption of the myocardium. The energy consumption of the myocardium was calculated by integrating ATP consumption rate of each node in myofilament model.ResultsThe result showed that under higher MCV conditions, the EAT, energy consumption, end diastolic and systolic volume are gradually decreased. Meanwhile, the systolic pressure, stroke volume, stroke work, and stroke work to ATP are increased as the MCV values increased. The cardiac functions and performances are more efficient under higher MCV conditions by consuming smaller energy (ATP) while carrying more works.ConclusionIn conclusion, this study reveals that MCV has strong correlation with the cardiac pumping efficacy. The obtained results provide useful information to estimate the effect of MCV on the electro-physiology and hemodynamic responses of the ventricle and can be used for further study about arrhythmogeneis and heart failure.

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“…We will focus on the roles of intracellular Ca + dynamics, gap junctions, myofibroblasts, and cell‐structural and histoanatomic features of the myocardium in the genesis of cardiac arrhythmias. The updated, general principles of electro‐centric arrhythmogenesis can be assessed by reference to another review article …”

Section: Introductionmentioning

confidence: 99%

“…The updated, general principles of electro-centric arrhythmogenesis can be assessed by reference to another review article. 13…”

Section: Introductionmentioning

confidence: 99%

Towards an integrated understanding of cardiac arrhythmogenesis − Growing roles of experimental pathology

Tanaka

Matsuyama

Takamatsu

2016

Pathology International

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Cardiac arrhythmias have long been regarded as derangement of electrical impulse initiation and conduction within the heart. However, underlying mechanisms for arrhythmogenesis are not fully understood solely from the electrophysiological viewpoint. This review article discusses pathogenesis of arrhythmias from non-electrical aspects, which were elucidated by spatiotemporal imaging of functional molecules in combination with morphological analysis of living heart tissues. Intracellular Ca ([Ca ] ) overload, caused by myocardial injury, provokes Ca waves that could lead to abnormal excitations, i.e., triggered arrhythmias. Depressed Ca release from the sarcoplasmic reticulum, caused by ischemia, heart failure, or T-tubular remodeling, results in spatiotemporally inhomogeneous [Ca ] dynamics that could disturb impulse conduction, leading to reentrant tachyarrhythmias. Impairment of the gap junction-mediated intercellular communications, which provokes derangement of impulse propagation of the myocardium, also leads to reentrant arrhythmias. Interpositions of non-cardiomyocytes, especially fibroblasts, in the myocardium could also contribute to arrhythmogenesis via heterocellular gap-junctional coupling with cardiomyocytes. Furthermore, alterations in myocardial histology, e.g., density and arrangements of myocytes in association with gap-junctional distributions, could constitute important pathologic bases of atrial fibrillation. Integration of these molecular, functional, and morphological features of the myocardium, unveiled by experimental pathological approaches, would pave a new way for understanding pathogenesis of cardiac arrhythmias.

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Ionic mechanisms of arrhythmogenesis

Cited by 29 publications

References 61 publications

Torsade de Pointes with Presentation of Seizure in the Ischemic Heart Disease Context: A Case Report

Torsade de Pointes with Presentation of Seizure in the Ischemic Heart Disease Context: A Case Report

The effect of electrical conductivity of myocardium on cardiac pumping efficacy: a computational study

Towards an integrated understanding of cardiac arrhythmogenesis − Growing roles of experimental pathology

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