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      Calcium Dynamics and Cardiac Arrhythmia

      editorial
      1 , 2 , 3
      Clinical Medicine Insights. Cardiology
      SAGE Publications

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          Abstract

          This Special Collection will gather all studies highlighting recent advances in theoretical and experimental studies of arrhythmia, with a specific focus on research seeking to elucidate links between calcium homeostasis in cardiac cells and organ-scale disruption of heart rhythm.

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          Most cited references19

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          Cellular and molecular electrophysiology of atrial fibrillation initiation, maintenance, and progression.

          Atrial fibrillation (AF) is the most common clinically relevant arrhythmia and is associated with increased morbidity and mortality. The incidence of AF is expected to continue to rise with the aging of the population. AF is generally considered to be a progressive condition, occurring first in a paroxysmal form, then in persistent, and then long-standing persistent (chronic or permanent) forms. However, not all patients go through every phase, and the time spent in each can vary widely. Research over the past decades has identified a multitude of pathophysiological processes contributing to the initiation, maintenance, and progression of AF. However, many aspects of AF pathophysiology remain incompletely understood. In this review, we discuss the cellular and molecular electrophysiology of AF initiation, maintenance, and progression, predominantly based on recent data obtained in human tissue and animal models. The central role of Ca(2+)-handling abnormalities in both focal ectopic activity and AF substrate progression is discussed, along with the underlying molecular basis. We also deal with the ionic determinants that govern AF initiation and maintenance, as well as the structural remodeling that stabilizes AF-maintaining re-entrant mechanisms and finally makes the arrhythmia refractory to therapy. In addition, we highlight important gaps in our current understanding, particularly with respect to the translation of these concepts to the clinical setting. Ultimately, a comprehensive understanding of AF pathophysiology is expected to foster the development of improved pharmacological and nonpharmacological therapeutic approaches and to greatly improve clinical management.
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            Rotors and the dynamics of cardiac fibrillation.

            The objective of this article is to present a broad review of the role of cardiac electric rotors and their accompanying spiral waves in the mechanism of cardiac fibrillation. At the outset, we present a brief historical overview regarding reentry and then discuss the basic concepts and terminologies pertaining to rotors and their initiation. Thereafter, the intrinsic properties of rotors and spiral waves, including phase singularities, wavefront curvature, and dominant frequency maps, are discussed. The implications of rotor dynamics for the spatiotemporal organization of fibrillation, independent of the species being studied, are described next. The knowledge gained regarding the role of cardiac structure in the initiation or maintenance of rotors and the ionic bases of spiral waves in the past 2 decades, as well as the significance for drug therapy, is reviewed subsequently. We conclude by examining recent evidence suggesting that rotors are critical in sustaining both atrial and ventricular fibrillation in the human heart and its implications for treatment with radiofrequency ablation.
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              • Article: not found

              Ventricular arrhythmias and the His-Purkinje system.

              Ventricular arrhythmias are a major cause of sudden death, which accounts for approximately half of cardiac mortality. The His-Purkinje system is composed of specialized cells responsible for the synchronous activation of the ventricles. However, experimental studies show that the Purkinje system can be arrhythmogenic during electrolyte imbalance, after exposure to various drugs, and in myocardial ischaemia, during which Purkinje cells can survive in anaerobic conditions. Purkinje cells can generate both automatic and triggered focal rhythms, and their network configuration can accommodate re-entrant circuits. In humans, a variety of monomorphic ventricular tachycardias can be sustained within the architecture of the Purkinje branches. Furthermore, discrete Purkinje sources can serve as critical triggers of ventricular fibrillation in a wide spectrum of patients with structural heart disease or with an apparently normal heart. In drug-resistant cases of monomorphic and polymorphic Purkinje-related ventricular tachycardias, catheter ablation is a very effective treatment. The specific transcriptional signatures and functional properties of Purkinje cells, including their intracellular calcium dynamics, underlie their extreme arrhythmogenicity. However, the identification of vulnerable individuals remains challenging, and the molecular mechanisms of Purkinje-related arrhythmias have to be characterized further to enable the development of interventions to prevent lethal cardiac arrhythmias.
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                Author and article information

                Journal
                Clin Med Insights Cardiol
                Clin Med Insights Cardiol
                CIC
                spcic
                Clinical Medicine Insights. Cardiology
                SAGE Publications (Sage UK: London, England )
                1179-5468
                03 December 2017
                2017
                : 11
                : 1179546817739523
                Affiliations
                [1 ]Department of Engineering, Norfolk State University, Norfolk, VA, USA
                [2 ]Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA, USA
                [3 ]Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA
                Author notes
                [*]Makarand Deo, Department of Electronics Engineering, Norfolk State University, 700 Park Ave, Norfolk, VA 23504, USA. Email: mdeo@ 123456nsu.edu
                Article
                10.1177_1179546817739523 CIC-43933
                10.1177/1179546817739523
                5718302
                939aef5d-caee-43bf-9a03-4158272ad661
                © The Author(s) 2017

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Categories
                Guest Editorial: CMC-11 Special Collection
                Custom metadata
                January-December 2017

                Cardiovascular Medicine
                Cardiovascular Medicine

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