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    Paroxysmal supraventricular tachycardia (PSVT) hasbeen a well-recognized clinical syndrome and an elec-trocardiographically defined arrhythmia since the earlydays of electrocardiography. The clinical syndrome wasdefined in European literature in the 19th century.In 1867, Cotton reported on an unusually rapid actionof the heart, and this was followed by further observa-tions by French and German scientists.1,2 Variouslyreferred to as Bouverets syndrome and later as paroxysmalatrial tachycardia, it was described classically as a fullyunprovoked tachycardia attack, lasting a few seconds orseveral days, in patients who as a rule have otherwisehealthy hearts.1 It has been electrocardiographicallydefined in the 10th Bethesda Conference on OptimalElectrocardiography as a tachycardia usually charac-terized by an atrial rate of 140 to 240 beats per minute(bpm) and by an abrupt onset and termination. It mayor may not be associated with intact A-V conduction.Specific electrophysiological studies may elicit specificmechanisms such as retrograde and anterograde path-ways and sites of reentry.3

    In the past 25 years, this has been an intensivelystudied arrhythmia, with extensive definition of itsgenesis, presentation, subtypes, and electrophysiology.Pharmacologic therapy and, later, nonpharmacologictherapy have been investigated and refined. This is nowa classic story in the evolution of clinical cardiac elec-trophysiology and forms a fundamental cornerstone inthe modern treatment of cardiac arrhythmias.

    EpidemiologyThe epidemiology of PSVT has not been widely investi-gated in modern times. Early electrocardiographicreports were useful in arrhythmia detection for patientspresenting with sustained palpitations and persistentepisodes of supraventricular tachycardias (SVT) but hadlittle role for this purpose in the large body of patientswith brief SVT events terminating before presentationto the physician.4,5 These efforts were supplemented bythe advent of ambulatory electrocardiography, whichdocumented a large number of cardiac arrhythmias inasymptomatic patients. Conversely, it confirmed thatmany symptoms experienced by patients with or withoutheart disease that are suggestive of tachyarrhythmiasoccur when no arrhythmias or simply premature beatsare documented on monitoring. Epidemiologic dataare extensively colored by the selection criteria and theelectrocardiographic documentation mode used in thestudy. Brodsky and coworkers reported that ambulatoryelectrocardiographic recordings in 50 male medicalstudents detected atrial premature beats in 56%, butonly one had more than 100 beats in 24 hours.6 Thelimited period of observation precludes objectiveassessment of development of SVT events in these sub-jects. Thus, Hinkle et al. in a study of 301 men with amedian age of 56 years, detected various supraventricu-lar arrhythmias in 76% of these individuals.7 However,coronary disease was present in 20% of these patients.

    Chapter 14 Paroxysmal SupraventricularTachycardias and thePreexcitation Syndromes


    Epidemiology: Sanjeev SaksenaAnatomy and Pathology: Saroja BharatiBasic Electrophysiology: Sanjeev SaksenaClinical Presentation: Sanjeev SaksenaElectrocardiography: Bruce D. LindsayDiagnostic Approach: Samuel LevyClinical Electrophysiology: Shih-Ann ChenPrinciples of Management: Sanjeev SaksenaEvidence-Based Therapy: Sanjeev Saksena

  • Clark et al. studied an apparently normal populationranging from 16 to 65 years old and noted a low inci-dence of supraventricular arrhythmias.8,9 In contrast,recent longitudinal studies with telemetric monitoringand even implanted cardiac pacemakers document avery high incidence of asymptomatic and symptomaticatrial arrhythmias, particularly atrial fibrillation inpatients with bradyarrhythmias.10 Thus, it would beappropriate to infer that the true incidence of PSVT inthe general population remains unknown due to itsevanescent nature and limited methods of detection. It would also be appropriate to surmise that the inci-dence may be higher than generally believed over along observation period. Atrial arrhythmias alsoincrease with age.11 In the Cardiovascular Health Study,short runs of PSVT occurred in 50% of men and 48%of women, doubling in prevalence in octagenarians.Twenty-eight percent of nursing home residents demon-strate PSVT.11

    More data are available for the preexcitation syn-dromes, particularly the Wolff-Parkinson-White (WPW)syndrome. Electrocardiographic studies of healthy indi-viduals suggest that the incidence of this condition is3 in 1000 of the general population.12 Early studiessuggested that the morbidity and mortality in WPW syn-drome with tachyarrhythmias were greater in adultswith ventricular fibrillation occurring in patients withatrial fibrillation and antegrade preexcitation.13However, Klein et al. have reported on the natural his-tory of asymptomatic WPW syndrome; they noted a verylow incidence of major morbidity and serious sympto-matic arrhythmias including atrial fibrillation with rapidantegrade conduction and mortality.14

    Supraventricular arrhythmias are seen at all ages andare particularly common in infants, children, and youngadults. Age-related behavior of these rhythms has alsobeen the subject of epidemiologic study. In a study ofinfants younger than 1 year of age, Mantakas et al.noted that associated congenital heart disease was pres-ent in 35%, and fully 90% developed SVTs with narrow(35%) or wide QRS (45%) complexes.15 Most patients(90%) improved with growth or remained stable, butpatients with congenital heart disease could haverefractory arrhythmias. The quality and duration oflife in children with WPW syndrome without clinicaldysrhythmias have been reported to be normal.


    In order to understand the pathologic base for atrioventricular (AV) nodal tachycardia and AV reentrytachycardia, the normal anatomy of the AV node and its approaches, including the atria and the AVbundle, is briefly reviewed in the following regions ofinterest: (1) approaches to the AV node including theatrial septum; (2) AV node; and (3) AV nodo-bundlejunction.16-27


    Approaches to the AV node include the atrialmyocardium located in the anterior, superior, midsep-tal, and inferior regions as they converge to the AVnode. The approaches beneath the coronary sinus areamay be called the posterior or inferior approaches.In addition, the approaches also originate from the tri-cuspid valve. The left-sided approaches include thosefrom the left atrial myocardium and the mitral valve.The superior approaches include the pectinate musclesas they merge from the superior, lateral, and posteriorwalls of the right atrium toward the AV nodal area,atrial septum, and Todaros tendon. Approaches to theAV node are formed by different types of myocardialfibers coming from different directions as they mergetoward the AV nodal area (Fig. 14-1). Histologically, ingeneral the cells are relatively loosely arranged withlighter staining smaller cells. The size and shape of themyocardial fibers vary considerably from one approachto the other in the vicinity of the node. In general,there is increase in the elastic collagen connectivetissue intermingling with the cells, fat, and a largeamount of nerve fibers. At the electron microscopic

    250 Cardiac Rhythms and Arrhythmias













    FIGURE 14-1 Schematic representation of the atrioventric-ular (AV) junction depicting the approaches to the AV node.AVN, AV node; CFB, central fibrous body; LA, left atrialmyocardiumleft atrial approaches; LV, left ventricular sideof the septum; MV, approaches from the mitral valve; RA,right atrial myocardiumsuperior approaches; AS, atrial sep-tum; S, superior approaches; I, inferior approaches; RV, rightventricular side of the septumright ventricular approaches;TV, approaches from the tricuspid valve; VS, summit of theventricular septum. Arrows point to the approaches to the AVnode from the tricuspid valve area, right atrial aspect, rightventricular aspect, atrial septal aspect, left atrial aspect, andmitral valvular aspect. (With permission from Bharati S, Lev M: The anatomy of the normal conduction system:Disease-related changes and their relationship to arrhythmo-genesis. In Podrid PJ, Kowey PR [eds]: Cardiac Arrhythmias,Mechanism, Diagnosis and Management. Baltimore, Williams& Wilkins, 1995, p 1.)

  • level, the mitochondria and myofibrils of the atrialmyocardial cells are not as well organized as the ven-tricular cells, and some of them do not have a transversetubular system.16


    The atrial myocardial fibers including the collagen,elastic tissue, and nerve elements in the approaches tothe AV nodal area can vary in size, shape, and direction,suggesting that there may be functional differencesin the speed of conduction.16-20 Anatomically, oneapproach to the AV node may be more dominant thanthe other. For example, dominant posterior approacheswith less prominent superior approaches in the humansuggest the possibility of dominant slow pathway con-duction. Likewise, dominant superior approaches withpractically absent inferior approaches suggest the pos-sibility of dominance of fast pathway conduction orother alterations in AV nodal conduction. Myocardialfibers in the atria may get entrapped within the centralfibrous body and join the AV node. In other instances,approaches to the AV node and the AV node may beentrapped within the tricuspid or mitral valve annulusor the base of the aortic valve. During an altered physio-logic state, these anomalies may form an


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