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      P-wave dispersion: an update

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          Abstract

          P-wave dispersion (PWD, Pd or Pdis) is a noninvasive electrocardiographic (ECG) marker for atrial remodeling and predictor for atrial fibrillation (AF). PWD is defined as the difference between the widest and the narrowest P-wave duration recorded from the 12 ECG leads. Increased P-wave duration and PWD reflect prolongation of intraatrial and interatrial conduction time with lack of a well-coordinated conduction system within the atrial muscles, with inhomogeneous, asynchronic, pro-inflammatory and anti-inflammatory effect mediated by interleukin-6 (IL-6) in patients with the CG + GG genotype IL-6 -634C/G polymorphism [1] and discontinuous propagation of sinus impulses mainly between the left and right atria, interstitial/extracellular fibroblast activation and collagen deposition with fibrosis (via TGF- β) in atrial tissue, insufficient blood supply, significant not isotropic myoelectric activity, and thin wall thickness and consequent expansion tendency all well-known electrophysiological characteristics in patients with atrial arrhythmias and especially paroxysmal atrial fibrillation (PAF) [2].

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          Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress

          Current therapies for arrhythmia using ion channel blockade, catheter ablation, or an implantable cardioverter defibrillator have limitations, and it is important to search for new antiarrhythmic therapeutic targets. Both atrial fibrillation and heart failure, a condition with increased arrhythmic risk, are associated with excess amount of reactive oxygen species (ROS). There are several possible ways for ROS to induce arrhythmia. ROS can cause focal activity and reentry. ROS alter multiple cardiac ionic currents. ROS promote cardiac fibrosis and impair gap junction function, resulting in reduced myocyte coupling and facilitation of reentry. In order to design effective antioxidant drugs for treatment of arrhythmia, it is essential to explore the molecular mechanisms by which ROS exert these arrhythmic effects. Activation of Ca2+/CaM-dependent kinase II, c-Src tyrosine kinase, protein kinase C, and abnormal splicing of cardiac sodium channels are among the recently discovered molecular mechanisms of ROS-induced arrhythmia.
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            P-WAVE ANALYSIS IN VALVULAR HEART DISEASE.

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              Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance

              Background Anatomic atrial enlargement is associated with significant morbidity and mortality. However, atrial enlargement may not correlate with clinical measures such as electrocardiographic (ECG) criteria. Past studies correlating ECG criteria with anatomic measures mainly used inferior M-mode or two-dimensional echocardiographic data. We sought to determine the accuracy of the ECG to predict anatomic atrial enlargement as determined by volumetric cardiovascular magnetic resonance (CMR). Methods ECG criteria for left (LAE) and right atrial enlargement (RAE) were compared to CMR atrial volume index measurements for 275 consecutive subjects referred for CMR (67% males, 51 ± 14 years). ECG criteria for LAE and RAE were assessed by an expert observer blinded to CMR data. Atrial volume index was computed using the biplane area-length method. Results The prevalence of CMR LAE and RAE was 28% and 11%, respectively, and by any ECG criteria was 82% and 5%, respectively. Though nonspecific, the presence of at least one ECG criteria for LAE was 90% sensitive for CMR LAE. The individual criteria P mitrale, P wave axis 0.04s·mm were 88–99% specific although not sensitive for CMR LAE. ECG was insensitive but 96–100% specific for CMR RAE. Conclusion The presence of at least one ECG criteria for LAE is sensitive but not specific for anatomic LAE. Individual criteria for LAE, including P mitrale, P wave axis 0.04s·mm are highly specific, though not sensitive. ECG is highly specific but insensitive for RAE. Individual ECG P wave changes do not reliably both detect and predict anatomic atrial enlargement.
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                Author and article information

                Contributors
                Journal
                Indian Pacing Electrophysiol J
                Indian Pacing Electrophysiol J
                Indian Pacing and Electrophysiology Journal
                Elsevier
                0972-6292
                20 October 2016
                Jul-Aug 2016
                20 October 2016
                : 16
                : 4
                : 126-133
                Affiliations
                [a ]Design of Studies and Scientific Writing Laboratory in the ABC Medicine Faculty, Santo André, São Paulo, Brazil
                [b ]Program in Molecular and Integrative Physiological Sciences (MIPS), Department of Environmental Health, Harvard T.H. Chan School of Public Health, USA
                [c ]Coronary Center of the Messejana Hospital Dr. Carlos Alberto Studart Gomes, Fortaleza, Ceará, Brazil
                [d ]Electrocardiology Sector, Central Institute of Clínicas Hospital, Faculty of Medicine, University of São Paulo (HCFMUSP), Brazil
                [e ]Division of Cardiology, Queen's University, Kingston, Ontario, Canada
                Author notes
                []Corresponding author. Rua Sebastião Afonso 885, Jd. Miriam, São Paulo, 04417-100, Brazil.Rua Sebastião Afonso 885Jd. MiriamSão Paulo04417-100Brazil riera@ 123456uol.com.br
                Article
                S0972-6292(16)31339-0
                10.1016/j.ipej.2016.10.002
                5197451
                27924760
                25b8d495-6daa-40b8-a9f0-b55ec20f3b67
                Copyright © 2016, Indian Heart Rhythm Society. Production and hosting by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 29 August 2016
                : 20 October 2016
                Categories
                Review Article

                Cardiovascular Medicine
                p-wave dispersion,p-wave duration,intraatrial block,interatrial block,paroxysmal atrial fibrillation

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