WPW pattern in the asymptomatic individual: has anything changed? (original) (raw)
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Ventricular Arrhythmias in the Absence of Structural Heart Disease
Ventricular arrhythmia (VA) in structurally normal hearts can be broadly considered under non-life-threatening monomorphic and life-threatening polymorphic rhythms. Monomorphic VA is classified on the basis of site of origin in the heart, and the most common areas are the ventricular outflow tracts and left ventricular fascicles. The morphology of the QRS complexes on electrocardiogram is an excellent tool to identify the site of origin of the rhythm. Although these arrhythmias are common and generally carry an excellent prognosis, rare sudden death events have been reported. Very frequent ventricular ectopy may also result in a cardiomyopathy in a minority of patients. Suppression of VA may be achieved using calcium-channel blockers, beta-adrenergic blockers, and class I or III antiarrhythmic drugs. Radiofrequency ablation has emerged as an excellent option to eliminate these arrhythmias, although certain foci including aortic cusps and epicardium may be technically challenging. Polymorphic ventricular tachycardia (VT) is rare and generally occurs in patients with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and short QT syndrome. Unlike monomorphic VT, these arrhythmic syndromes are associated with sudden death. While the cardiac gross morphology is normal, suggesting a structurally normal heart, abnormalities exist at the molecular level and predispose them to arrhythmias. Another fascinating area, idiopathic ventricular fibrilla-tion and early repolarization syndrome, are undergoing research for a genetic basis. (J Am Coll Cardiol 2012;59:1733-44)
Clinical and Demographic Characteristics of WPW Syndrome Attending Arrhythmia Clinic of NICVD
Bangladesh Medical Journal, 2014
Wolff-Parkinson-White syndrome is a disorder characterized by presence of an accessory pathway which predisposes patients to tachyarrhythmias and sudden death. Among patients with WPW syndrome, atrioventricular reentrant tachycardia (AVRT) is the most common arrhythmia, accounting for 95% of re-entrant tachycardias. It has been estimated that one-third of patients with WPW syndrome have atrial fibrillation (AF). AF is a potentially life-threatening arrhythmia. If an accessory pathway has a short anterograde refractory period, then rapid repetitive conduction to the ventricles during AF can result in a rapid ventricular response with subsequent degeneration to ventricular fibrillation (VF). The study population included a total of 255 patients in whom 175 (68.62%) were men and 80 (31.38%) were women. Demographic data and clinical characteristics are depicted in Table 1. Left and right WPW syndrome were existing in 70.59% and 29.41% of patients respectively. Documented narrow QRS SVT ...
Circulation, 2011
S udden cardiac death (SCD) in the young (SCDY) has a devastating impact on families, care providers, and the community and attracts significant public and media attention. Sudden cardiac death is defined as an abrupt and unexpected death due to a cardiovascular cause, typically occurring Ͻ1 hour from the onset of symptoms. Depending on the source, "young" is variably defined as those less than 25, 30, 35, or 40 years of age. Estimates of the incidence of SCDY (not including infants) vary broadly from 0.6 to 6.2 per 100 000 persons. 1-3 Sudden infant death syndrome (SIDS) may be related to SCD in some infants. Sudden infant death syndrome is defined as the sudden death of an infant Ͻ1 year of age that cannot be explained after a thorough investigation is conducted, including an autopsy, death scene evaluation, and review of the clinical history. The incidence of SIDS ranges from 50 to 100 in 100 000, 4 and emerging data suggest that as many as 10% to 15% of SIDS deaths are associated with functional cardiac ion channelopathy gene variants. 5 The most common diagnoses that increase risk for SCDY include hypertrophic cardiomyopathy (HCM), coronary artery anomalies of wrong sinus origin, myocarditis, arrhythmogenic right ventricular cardiomyopathy, and ion channelopathies. 6 The latter category includes hereditary diseases such as the congenital long-QT syndromes (LQTS), catecholaminergic polymorphic ventricular tachycardia, and Brugada syndrome, among other less common channelopathies. These diseases are typically undetected before the SCD event. Estimated prevalence
Circulation. Arrhythmia and electrophysiology, 2011
S udden cardiac death (SCD) is predominantly related to coronary artery disease and its sequelae, cardiomyopathy, and congenital or valvular heart disease. No structural abnormalities are detectable in 5-8% of SCDs. 1 Identified ion channelopathies such as Brugada syndrome, long-QT syndrome (LQTS), and catecholaminergic polymorphic ventricular tachycardia (CPVT) contribute to this incidence. The diagnosis requires a high level of suspicion because of a resting ECG that is often borderline, intermittently normal, or frankly normal. Genetic testing does not provide a simple solution to this issue, as it is often neither sensitive nor specific even when the phenotype points to a specific entity and may yield results that are difficult to interpret (ie, variants of unknown significance). Pharmacological and/or exercise testing by manipulation/stressing the cardiac action potential can accentuate the desired abnormality or provoke a characteristic arrhythmia response. A systematic approach to clinical testing that includes drug provocation results in unmasking of the cause of apparently unexplained aborted SCD in Ͼ50% of patients and is very helpful in directing genetic testing of the index case and family to diagnose genetically mediated arrhythmia syndromes. 2 This review will seek to highlight the clinical utility of provocative testing and describe how to perform and interpret provocative testing for the diagnosis of Brugada syndrome, LQTS, and CPVT.
Cardiac Arrhythmias, 2018
Primary prevention of ventricular fibrillation is at the heart of the management of Brugada syndrome. Several recent studies have shown that the analysis of simple electrocardiographic criteria could help to stratify the risk of sudden death. In the present work, 12 markers were studied: spontaneous and permanent type 1 pattern, first-degree atrioventricular block, sinus node dysfunction, wide QRS in V2, aVR sign, fragmented QRS, S-waves in DI, early repolarization pattern, atrial fibrillation, type 1 in peripheral leads pattern, and long Tpeak-Tend interval. These electrical markers reflect abnormalities in conduction, depolarization, and repolarization that may indicate the severity of the disease. In this chapter, we carry out a review of these markers, their method of determination on the surface ECG, and the main studies highlighting their prognostic impact. We also review the main underlying pathophysiological hypotheses of Brugada syndrome.
Progress in cardiovascular diseases, 1998
Different polymorphic ventricular tachyarrhythmias may cause syncope or cardiac arrest in patients with no heart disease: (1) Catecholamine-sensitive polymorphic ventricular tachycardia (VT) presents during childhood: the hallmark is the reproducible provocation of atrial and polymorphic ventricular arrhythmias during exercise, despite a normal QT. 13-Blockers are the treatment of choice. (2) In the long QT syndromes (LQTS), malfunction of ion channels leads to prolonged ventdcular repolarization, early afterdepolarizations, and triggered ventricular arrhythmias. Therapeutic options include: 13-blockers, genotype-specific therapy, cardiac sympathetic denervation, and implantation of pacemakers or defibrillators. The "short-coupled variant of torsade de pointes" is a malignant disease that shares several characteristics with idiopathic ventricular fibrillation. Although verapamil is frequently recommended, mortality rates remain high. (4) Idiopathic ventricular fibrillation (VF) with normal electrocardiogram (ECG) strikes young adults of both genders. In contrast to other polymorphic tachyarrhythmias, idiopathic VF is not generally related to stress. Also, familial involvement is rare. Therapeutic options include implantation of defibrillators and therapy with class 1A drugs. (5) The "Brugada syndrome" and the "syndrome of nocturnal sudden death" strike males almost exclusively. Right bundle branch block (RBBB) with ST elevation in the right precordial leads--the "Brugada sign"--is seen in the ECG of both patient populations. Implantation of defibrillators is recommended.
The Asymptomatic Patient with the Wolff-Parkinson-White Electrocardiogram
Pace-pacing and Clinical Electrophysiology, 1997
Sudden death can be the first manifestation of the Wolff-Parkinson-White (WPW) syndrome. The underlying mechanism being atrial fibrillation with a very high ventricular rate, because of a short anterograde refractory period of the accessory atrioventricular pathway (AP), deteriorating into ventricular fibrillation. Information on the anterograde refractory period of the AP is therefore important to recognize asymptomatic people with the WPW ECG at risk for dying suddenly. Several noninvasive tests are available to identify the low risk patient. Decision making when to interrupt the AP in asymptomatic WPW patients not at low risk requires an invasive study to document the electrophysiological properties of the AP and to determine its exact location.
The Wolf-Parkinson-White ECG Pattern – Assessing the Mortality Risk
Journal of Insurance Medicine, 2015
The presence of a Wolf-Parkinson-White (WPW) pattern is not uncommonly discovered on a life insurance applicant’s ECG. How does one determine the appropriate mortality risk in this population? This article will discuss the risk of sudden cardiac death (SCD), the interpretation of electrophysiology testing results, and risk-stratification both for asymptomatic individuals and those who have had ablation treatment.