The differential diagnosis of RVOTVT has also to exclude tachycardia associated withatriofascicular fibers, atrioventricular reentranttachycardia using a right-sided accessory pathway,and VT occurring in patients after repair oftetralogy of Fallot Figure Figure 8. A: sustained ventricular tachycardia VT originating from the right ventricular outflow tract. B: sustained VT due to atriofascicular fibers. Although both VTs present with wide QRS complex and left bundle branch block, the QRS axis in the frontal plane is different, reflecting 2 different mechanisms and origins.
In case A, the VT has a focal source and the ventricular myocardial mass is activated from top to bottom. In case B, the VT is dependent from a reentry circuit and the ventricular myocardial mass is activated in the opposite direction, from the bottom to the top, thus creating a different direction of the QRS axis in the frontal plane. Atriofascicular fibers are uncommon but a very distinct form of accessory pathways.
These accessory pathways arise from the right atrium at the parietal tricuspid ring and terminate in or near the distal part of the right bundle branch. They exhibit slow and exclusively antegrade decremental conduction. Because of the right sidelocation of these pathways, preexcitedQRS complexes show a left bundle branchblock-like morphology.. The tachycardia may be inducible by programmedextrastimuli, by burst pacing the ventricle oratrium or by infusion of isoproterenol duringelectrophysiological study.. If symptoms are very mild or infrequent,no treatment is necessary.
RVOT-VT can bearrested acutely by vagal manoeuvres, carotidsinus massage, intravenous adenosine mg ,and intravenous verapamil mg. Rhythm disturbances may be observed in thenatural history of congenital heart defects CHD ,as well as after open heart surgery. Figure 9. The 12 lead ECG shows an atrialflutter in a year-old female who hadundergone tetralogy of Fallot correction31 years earlier.
The patient was admittedto our center because of palpitations. Atypical counterclockwise right atrial flutter cavo-tricuspid isthmus dependent wasfound during an electrophysiology studyand treated with radiofrequency ablation. A 12 lead ECG after the ablation stillshowed right bundle branch block andright axis deviation, reflecting the rightheart dysfunction.. This condition consists of four features:subpulmonary infundibular stenosis, ventricularseptal defect, overriding aorta, and right ventricularhypertrophy.
The surgical procedure includes a rightventriculotomy and ventricular septal defect patchrepair. These lesions cause the arrhythmia substrate. The ventricular septal defect patch repair providesa fixed anatomic obstacle around which re-entrantarrhythmias may occur.. In these patients, there is a persistent risk of lateSCD, with an estimated incidence rate of 0. Antiarrhythmic drugssuch as amiodarone and sotalol are usually used inthese patients as first-line therapy. In patients withdrug-refractory symptomatic VT, radiofrequencyablation can be performed. Conventional andelectroanatomical mapping are used to identify thereentry circuit.
Electroanatomical mapping may becrucial for success, especially in poorly tolerated VTs. Figure Localization of anatomic boundaries blue line for right ventricular tachycardia after repair of cardiac heart defect and the resulting anatomic isthmuses red lines, numbers from 1 to 4. Modified from Zeppenfeld K et al with permission.. Thispercentage is even higher in young athletes. It has been reported that young athletes die suddenly in Spain each year.
In young, otherwiseapparently healthy subjects, SCD is always a tragicevent and can be even crueller when photographedfor viewing by millions of people. Pre-participationscreening has been shown to decrease SCD amongathletes. Common and training-related abnormalities include sinus bradycardia,first degree and Wenckebach heart blocks,incomplete RBBB, left ventricular hypertrophy andan early repolarization pattern. These physiologicabnormalities reflect the remodelling of the heartand the change in autonomic balance in individualswho train regularly and intensely.
Cardiac genetic disorders ARVD, BS, hypertrophiccardiomyopathy, long-short QT syndrome havevarying levels of environmental contribution that can worsen or even unmask the phenotypicexpression of the disease.
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In patients with ARVD,exercise accelerates the genetically determineddamage of mechanical contacts. The ECG is from an asymptomatic year-old competitive soccer player at rest without evidence of left ventricular hypertrophy or other structural abnormalities on echocardiography. With this ECG pattern the exclusion of life-threatening cardiac conditions such as hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia,dilated cardiomyopathy, aortic valvestenosis, and channelopathies Brugadasyndrome, long and short QT syndrome is mandatory..
ICD implantation should be seriously consideredafter a careful risk stratification. Debate exists asto whether athletes who have received an ICD may or may not continue competitive sports. Accordingto the Bethesda guidelines, patients with an ICDcan participate only in "class IA" activities, suchas bowling or golf. Conversely, more recent datashowed that, although shocks during sports arereported frequently, significant adverse events arerare. Several theoretical and practical reasons existto restrict athletes with ICDs from participationin sports but data actually proving sports to bedangerous for all ICD patients are not available andan informed decision should probably lie with theindividual athlete..
Correspondence: L. Belgium E-mail: luciomassimo hotmail. Home Articles in press Current Issue Archive. ISSN: Previous article Next article. Issue 8. Pages August More article options. Download PDF. This item has received. Article information. Show more Show less. TABLE 1. McKenna et al Historically, left ventricular cardiomyopathy and coronary heart disease have been regarded as the main causes of ventricular arrhythmia and sudden cardiac death. However, within last two decades, arrhythmias originating from the right ventricle have begun to attract the attention of the scientific world for a number of reasons.
Ventricular arrhythmias originating from the right ventricle usually affect younger patients and can lead to sudden cardiac death. The pathophysiologic mechanism of these arrhythmias is not fully understood, which can leave room for a range of different interpretations. Moreover, the intriguing world of genetics is increasingly being drawn into the pathogenesis, diagnosis and prognosis of some of these arrhythmias.
This review considers the pathogenesis, diagnosis and treatment of arrhythmogenic right ventricular cardiomyopathy or dysplasia ARVD , Brugada syndrome, right ventricular outflow tract ventricular tachycardia, and arrhythmias in the right side of the heart due to congenital heart disease.
Arrhythmogenic right ventricular dysplasia. Palabras clave:. Genetics are also increasinglyhelping to explain the pathogenetic, diagnosticand prognostic aspects of some of thesearrhythmias. As will be discussed, the diseaseshould also be suspected in athletes presenting withsymptoms indicative of arrhythmias palpitations,syncope.
Desmosome integrityis required to maintain the normal function of gapjunctions as intercellular channels responsible forthe electrical coupling and signaling mechanismsin the regulation of cell growth, differentiationand development. Electrocardiologie de cas de dysplasie ventriculaire droite arythmogene.. Arch Mal Coeur Vaiss, 71 , pp. Right ventricular cardiomiopathy and sudden death in young people.. N Engl J Med, , pp. Pathologic evidence of extensive left ventricular involvement in arrhythmogenic right ventricular cardiomyopathy..
Hum Pathol, 23 , pp. Arrhythmogenic right ventricular cardiomyopathy: an update.. Cardiovasc Pathol, 10 , pp. Right ventricular dysplasia: a report of 24 adult cases.. Circulation, 65 , pp.
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Cardiac abnormalities in familial palmoplantar keratosis.. Br Heart J, 56 , pp. Circulation, , pp. E Medline. Mutation in human desmoplakin domain binding to plakoglobin causes a dominant form of arrhythmogenic right ventricular cardiomyopathy.. Am J Hum Genet, 71 , pp. Mutations in the desmosomal protein plakophilin 2 are common in arrhythmogenic right ventricular cardiomiopathy..
Nat Genet, 36 , pp. Human Mutation, 30 , pp. Regulatory mutations in transforming growth factor -beta3 gene cause arrhythmogenic right ventricular cardiomiopathy type Cardiovasc Res, 65 , pp.
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Identification of mutations in the cardiac ryanodine receptor genes infamilies affected with arrhythmogenic right ventricular cardiomiopathy type 2 ARVD Hum Mol Genet, 10 , pp. Arrhythmogenic right ventricular cardiomiopathy type 5 is a fully penetrant, lethal arrhythmic disorder caused by a missense mutation in the TMEM43 gene..
Am J Hum Genet, 82 , pp. J Am Coll Cardiol, 50 , pp. Orphanet J Rare Dis, 14 , pp. J A Coll Cardiol, 30 , pp. Br Heart J, 71 , pp.
J Am Coll Cardiol, 40 , pp. Proposed modification of the Task Force criteria.. Heart Rhythm, 6 , pp. Diagnostic accuracy of right ventriculography in arrhythmogenic right ventricular cardiomyopathy.. Am J Cardiol, 66 , pp. Arrhythmogenic right ventricular dysplasia: MRI findings.. Herz, 25 , pp. Right ventricular arrhythmia: emergence of magnetic resonance imaging as an investigative tool..
Eur Heart J, 18 , pp. Assessment of right ventricular regional contraction and comparison with the left ventricle in normal humans: a cine magnetic resonance study with presaturation myocardial tagging.. Br Heart J, 74 , pp. Am J Cardiol, 97 , pp. Magnetic resonance and computed tomography imaging of arrhythmogenic right ventricular dysplasia..
J Magn Reson Imaging, 19 , pp. Noninvasive detection of myocardial fibrosis in arrhythmogenic right ventricular cardiomyopathy using delayed-enhancement magnetic resonance imaging.. J Am Coll Cardiol, 45 , pp.
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Late enhancement: a new feature in MRI of arrhythmogenic right ventricular cardiomyopathy? J Cardiovasc Magn Reson.. Arrhythmogenic right ventricular cardiomyopathy and fatty replacement of the right ventricular myocardium: are they different diseases? Three-dimensional electroanatomical voltage mapping and histologic evaluation of myocardial substrate in right ventricular outflow tract tachycardia.. J Am Coll Cardiol, 51 , pp. Patients with scar related right ventricular tachycardia: determinans of long-term outcome.. J Cardiovasc Electrophysiol, 20 , pp.
Role of genetic testing in arrhythmogenic right ventricular cardiomiopathy dysplasia: experience from a single center prospective cohort. Clin Genet.. A new diagnostic test for arrhythmogenic right ventricular cardiomiopathy.. Prog Cardiovasc Dis, ,. D2 Medline.
J Am Coll Cardiol, 43 , pp. Circulation, 43 , pp. Efficacy of antiarrhythmic drugs in patients with arrhythmogenic right ventricular disease: results in patients with inducible and noninducible ventricular tachycardia..
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Circulation, 86 , pp. Efficacy of antiarrhythmic drugs in arrhythmogenic right ventricular cardiomiopathy.. J Am Coll Cardiol, 54 , pp. Catheter ablation of ventricular tachycardia in arrhythmogenic right ventricular dysplsia.. J Interv Card Electrophysiol, 25 , pp. Catheter ablation of ventricular tachycardia. Ventricular tachycardia catheter ablation in arrhythmogenic right ventricular dysplasia: a year experience..
Curr Cardiol Rep, 2 , pp. Implantable cardioverter-defibrillator therapy in arrhythmogenic right ventricular cardiomiopathy: a role for genotyping in decision-making? Skip to main content. UC Riverside. Email Facebook Twitter. Clark, Walter A. SpanishDict is the world's most popular Spanish-English dictionary, translation, and learning website.
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