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      Radiofrequency Catheter Ablation of Idiopathic Right Ventricular Outflow Tract Arrhythmias

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          Abstract

          Idiopathic ventricular arrhythmias (VA) consist of various subtypes of VA that occur in the absence of clinically apparent structural heart disease. Affected patients account for approximately 10% of all patients referred for evaluation of ventricular tachycardia (VT). Arrhythmias arising from the outflow tract (OT) are the most common subtype of idiopathic VA and more than 70-80% of idiopathic VTs or premature ventricular contractions (PVCs) originate from the right ventricular (RV) OT. Idiopathic OT arrhythmias are thought to be caused by adenosine-sensitive, cyclic adenosine monophosphate (cAMP) mediated triggered activity and, in general, manifest at a relatively early age. Usually they present as salvos of paroxysmal ventricular ectopic beats and are rarely life-threatening. When highly symptomatic and refractory to antiarrhythmic therapy or causative for ventricular dysfunction, ablation is a recommended treatment with a high success rate and a low risk of complications.

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          Most cited references79

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          Mapping and ablation of idiopathic ventricular fibrillation.

          Ventricular fibrillation is the main mechanism of sudden cardiac death. The feasibility of eliminating recurrent episodes by catheter ablation has not been reported. Twenty-seven patients without known heart disease (13 men, 14 women, 41+/-14 years of age) were studied after being resuscitated from recurrent (10+/-12) episodes of primary idiopathic ventricular fibrillation; 23 had received a defibrillator. The first initiating beat of ventricular fibrillation had an identical electrocardiographic morphology and coupling interval (297+/-41 ms) to preceding isolated premature beats typically noted in the aftermath of resuscitation. These triggers were localized by mapping the earliest electrical activity and ablated by local radiofrequency delivery. Outcome was assessed by Holter and defibrillator memory interrogation. Premature beats were elicited from the Purkinje conducting system in 23 patients: from the left ventricular septum in 10, from the anterior right ventricle in 9, and from both in 4. The interval from the Purkinje potential to the following myocardial activation varied from 10 to 150 ms during premature beat but was 11+/-5 ms during sinus rhythm, indicating location at peripheral Purkinje arborization. The premature beats originated from the right ventricular outflow tract muscle in 4 patients. The accuracy of mapping was confirmed by acute elimination of premature beats during local radiofrequency delivery. During a follow-up of 24+/-28 months, 24 patients (89%) had no recurrence of ventricular fibrillation without drug. Primary idiopathic ventricular fibrillation is a syndrome characterized by dominant triggers from the distal Purkinje system. These sources can be eliminated by focal energy delivery.
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            Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease.

            The present study evaluated clinical benefits of radiofrequency catheter ablation (RFA) for premature ventricular complexes from right ventricular outflow tract (RVOT-PVC) in patients without structural heart disease. It is unknown whether PVC causes left ventricular (LV) dilation, which is a well-recognized precursor of LV dysfunction and heart failure, and whether eliminating PVC by RFA produces clinical benefits in patients with RVOT-PVC. Frequency of PVC per total heart beats by 24-h Holter monitoring, left ventricular ejection fraction (LVEF), left ventricular end-diastolic internal dimension (LVDd), mitral regurgitation (MR) by echocardiogram, cardiothoracic ratio (CTR) by chest radiogram, and New York Heart Association (NYHA) functional class of 40 patients with RVOT-PVC without structural heart disease were evaluated before and 6 to 12 months after RFA. Before RFA, a subgroup of patients with frequent (>20%) PVC demonstrated significantly enlarged LVDd and CTR, reduced LVEF, increased MR, and deteriorated NYHA functional class as compared to the subgroup with rare ( 20%) RVOT-PVC may be a possible cause of LV dysfunction and/or heart failure, and RFA produces clinical benefits in these patients.
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              Basics of cardiac development for the understanding of congenital heart malformations.

              Cardiovascular development has become a crucial element of transgene technology in that many transgenic and knockout mice unexpectedly present with a cardiac phenotype, which often turns out to be embryolethal. This demonstrates that formation of the heart and the connecting vessels is essential for the functioning vertebrate organism. The embryonic mesoderm is the source of both the cardiogenic plate, giving rise to the future myocardium as well as the endocardium that will line the system on the inner side. Genetic cascades are unravelled that direct dextral looping and subsequent secondary looping and wedging of the outflow tract of the primitive heart tube. This tube consists of a number of transitional zones and intervening primitive cardiac chambers. After septation and valve formation, the mature two atria and two ventricles still contain elements of the primitive chambers as well as transitional zones. An essential additional element is the contribution of extracardiac cell populations like neural crest cells and epicardium-derived cells. Whereas the neural crest cell is of specific importance for outflow tract septation and formation of the pharyngeal arch arteries, the epicardium-derived cells are essential for proper maturation of the myocardium and coronary vascular formation. Inductive signals, sometimes linked to apoptosis, of the extracardiac cells are thought to be instructive for differentiation of the conduction system. In summary, cardiovascular development is a complex interplay of many cell-cell and cell-matrix interactions. Study of both (transgenic) animal models and human pathology is unravelling the mechanisms underlying congenital cardiac anomalies.
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                Author and article information

                Journal
                Indian Pacing Electrophysiol J
                Indian Pacing Electrophysiol J
                Indian Pacing Electrophysiol J
                Indian Pacing and Electrophysiology Journal
                Indian Heart Rhythm Society
                0972-6292
                Jan-Feb 2013
                01 January 2013
                : 13
                : 1
                : 14-33
                Affiliations
                [1 ]Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
                [2 ]Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands
                Author notes
                Address for correspondence: Dr. Zeppenfeld, Leiden University Medical Center, Department of Cardiology, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. K.Zeppenfeld@ 123456lumc.nl
                Article
                ipej130014-00
                3540113
                23329871
                33ea9551-db6b-46e0-a1b7-628d4f714278
                Copyright: © 2013 Calvo et al.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Review Article

                Cardiovascular Medicine
                ventricular arrhythmias,outflow tract,icds,premature ventricular contractions,ablation

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