Supraventricular Arrhythmias: Clinical Framework and Common Scenarios for the Internist

REVIEW

Supraventricular Arrhythmias: Clinical Framework and Common Scenarios for the Internist Christopher V. DeSimone, MD, PhD; Niyada Naksuk, MD; and Samuel J. Asirvatham, MD Abstract Supraventricular arrhythmias can cause uncomfortable symptoms for patients. Often, the first point of contact is in the primary care setting, and thus, it is imperative for the general internist to have a clinical framework in place to recognize this cluster of cardiac arrhythmias, be familiar with immediate and longterm management of supraventricular tachycardias, and understand when cardiac electrophysiologic consultation is necessary. The electrocardiographic characteristics can have subtle but important clues to the diagnosis and initial management. An understanding of the mechanisms of these arrhythmias is essential to provide proper therapy to the patient. In addition, there are common practice strategies that should be emphasized to avoid common misperceptions that could pose risk to the patient. In this review, we provide a framework to more easily recognize and classify these arrhythmias. We also illustrate the mechanism for these arrhythmias to provide an understanding of the interventions generally used. ª 2018 Mayo Foundation for Medical Education and Research

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upraventricular tachycardia (SVT) is an encompassing term referring to fast heart rhythms that involve cardiac tissue above (supra) the ventricles.1 A ventricular rate that exceeds 100 beats/min along with a narrow QRS complex (QRS width, <120 ms) is, in broad strokes, the general way SVTs are identified. Less commonly, a wide QRS complex (QRS width,
120 ms) can also result from an SVT; the increased QRS width is due to concomitant aberrancy of the normal conduction system, such as that associated with bundle branch block. Alternatively, SVTs with a wide QRS complex can involve supraventricular tissue with conduction to the ventricle via abnormal myocardial fibers, such as in the case of an accessory pathway connection.2 Supraventricular tachycardias are classically clustered as regular, narrow complex tachycardias that include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia (AT)3,4 (Figure 1). As SVTs include rhythms with origin above the ventricle, regular, narrow complex tachycardias also include sinus tachycardia and atrial

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flutter. In addition, irregular, narrow complex tachycardias (Figure 2) can be seen and classified as SVTs. This includes atrial fibrillation (AF), multifocal AT, and atrial flutter with variable block. In this review, we discuss each of these rhythms independently to focus on the pathophysiologic basis and mechanism of each arrhythmia (section I). In section II, we provide a classification schema for these arrhythmias and focus on electrocardiographic (ECG) clues and recommend an approach to recognize these rhythms. In section III, we provide a simplified approach to clinical management and interweave clinical pearls into the discussion. In section IV we discuss the management of SVTs.

From the Department of Cardiovascular Diseases (C.V.D., N.N., S.J.A.) and Department of Pediatrics and Adolescent Medicine (S.J.A.), Mayo Clinic, Rochester, MN.

SECTION I: PATHOPHYSIOLOGIC BASIS OF SVTS Atrioventricular Nodal Reentrant Tachycardia Atrioventricular nodal reentrant tachycardia is the most common of the classical SVTs in the general population,5 and its frequency is likely rooted in the origins and anatomical basis of the tachycardia circuit. For example, it is likely

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ARTICLE HIGHLIGHTS d

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The internist requires a fundamental knowledge of the mechanisms and management of these arrhythmias. The electrocardiographic characteristics can have subtle but important clues to the diagnosis and initial management. Patient management may require rate or rhythm control, electrical cardioversion, or even catheter ablation. Understanding downstream therapies helps the internist provide initial counseling to the patient and recognize when to refer to cardiac electrophysiology.

that many patients are born with 2 atrial myocardial inputs into the atrioventricular (AV) node, which have been termed as pathways to the AV node: (1) a slow pathway and (2) a fast pathway6 (Figure 3). Because these pathways set up at least 2 means into and out of the AV node, a reentry circuit can occur under certain conditions. During sinus rhythm, conduction from the atria to the AV node travels down both the fast and slow pathways. However, the fast pathway conduction continues to the AV node and further down the conduction system and it also conducts in a retrograde manner into the slow pathway to extinguish its conduction; this is termed concealed (as it is not manifested on ECG) penetration into the slow pathway.7 Atrioventricular nodal reentrant tachycardia occurs under certain conditions, which create the setup for a reentrant circuit8 (Figure 4). For example, a premature atrial contraction can create an electrical wavefront that can travel antegrade down the slow pathway while the fast pathway is still refractory (unable to conduct) to electrical stimuli from the previous sinus impulse.9 Retrograde conduction to atrial tissue can occur if the fast pathway has recovered from refractoriness and thus allows electrical activation back toward the atrium. The atrial activation wavefront can again conduct antegrade back down the slow pathway and thus create a reentrant loop for tachycardia to sustain10,11 (Figure 4). Atrioventricular Reentrant Tachycardia Atrioventricular reentrant tachycardia is dependent on the presence of an electrical 2

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connection between the atrium to the ventricle in addition to that of the normal conduction system and AV node (which serves to slow conduction from the atrium to the ventricle).12 This is a connection of the atrium to the ventricle via muscle fibers and is termed an accessory pathway. These muscle fibers are located across the valvular annuli and can occur at several locations. This connection bypasses the normal conduction system (and is thus sometimes referred to as a bypass tract), and most importantly the AV node. These muscle fibers can conduct electrical activity in an antegrade manner from the atrium to the ventricle, or in a retrograde manner from the ventricle to the atrium, and some can conduct in both directions.13 Tachycardias related to an accessory pathway can occur from a reentrant circuit using the normal AV conduction system as one limb and an accessory pathway as the other limb of the circuit.8,11 If the electrical wavefront travels down the AV node to reach the ventricle and returns to the atria via an accessory pathway connection, the tachycardia is termed orthodromic reentrant tachycardia (ORT) (Figure 3). If the antegrade limb is down the accessory pathway to reach the ventricle and returns to the atrium in a retrograde fashion from the conduction system, the tachycardia is termed antidromic reentrant tachycardia (ART) (Figure 3). Of note, ART, which bypasses the AV node (normal conduction system) to reach the ventricle, causes a wide QRS complex tachycardia. Alternatively, ORT engages the conduction tissue to reach the ventricle, and then returns to the atrium via the pathway, and thus presents on the ECG as a narrow complex tachycardia. In practice, ORT is much more common than ART.11 Atrial Tachycardia Although AT may at times be a nonspecific term, it is generally used to refer to focal spontaneous depolarization of the atria at a site not at the sinus node14,15 (Figure 3). Focal AT can be caused by stressors to the body, which heightens autonomic tone and thus firing of a specific collection of cells/tissue located in the atria.14 Alternatively, these can originate from abnormal cells that can automatically fire, similar to the normal pacemaker cells XXX 2018;nn(n):1-17

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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST

Regular, narrow complex tachycardia (QRS width <120 ms, HR >100 beats/min)

Long RP interval

Short RP interval RP interval V1

I

RP interval

Sinus tachycardia Sinus P-wave morphology (positive P waves in leads II, III, and aVF; biphasic P wave with terminal negative deflection in lead V1) Focal atrial tachycardia Non-sinus P-wave morphology

AVNRT Pseudo-R' in leads V1 or pseudo-S' in leads II, II, and aVF

ORT Possible retrograde P waves (negative P waves in leads II, III, and aVF)

FIGURE 1. Supraventricular tachycardias (SVTs) with regular, narrow QRS complexes. SVTs with successive QRS complexes that are regular and have a narrow QRS width (<120 ms) with a heart rate (HR) greater than 100 beats/min are further subclassified on the basis of the RP interval. The RP interval represents the time from ventricular activation (R from the QRS complex) to atrial activation (P wave). The long RP tachycardias (including sinus tachycardia and focal atrial tachycardia) are separated from SVTs, which have a short RP interval (atrioventricular nodal reentrant tachycardia [AVNRT] and orthodromic reciprocating tachycardia [ORT]). Note that SVTs with short RP intervals involve the atrioventricular node as part of the tachycardia circuits and thus provide an initial insight into tachycardia mechanisms. Sinus tachycardia has a P wave morphology reflective of the site of the sinus node, with the P wave being positive in leads II, III, and aVF and biphasic in lead V1 with a terminal negative deflection. Focal atrial tachycardias have P waves that can be subtly or vastly different from those of the sinus node, depending on the site of origin. Close inspection reveals that AVNRT can sometimes have a “pseudo-R0 ” wave in lead V1 and a “pseudo-S0 ” wave in leads II, III, and aVF. In ORT, clues may include negative P waves in leads II, III, and aVF, which represent retrograde activation of the atria from the ventricle.

located in the sinus node.14 The origin of this arrhythmia can technically be anywhere above the ventricle, but common locations include the crista terminalis, coronary sinus, pulmonary veins, tricuspid or mitral annulus, or atrial septum.16 It is important to differentiate AT from sinus tachycardia, which is a normal physiologic response1 and treatment is aimed at correcting the underlying cause (anemia, fever, infection, hyperthyroidism, hypoxia, etc).17 The origin of sinus tachycardia is at the sinus node, located in the superior posterolateral aspect of the right atrium. Multifocal AT Multifocal AT is usually seen in patients with chronic lung conditions such as chronic Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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obstructive pulmonary disease as a result of right atrial enlargement, hypercapnia, decreased oxygen, or, in other cases, drugs used to treat lung diseases, such as inhaled b-agonists, that cause cellular firing at multiple sites of the atrium.18 Digoxin toxicity can also produce multifocal AT, specifically with AV block. It is because of these multiple areas of the atrium firing that the criterion for this arrhythmia is met by giving 3 or more P wave morphologies on the ECG or telemetry monitoring strip.1 Atrial Flutter Atrial flutter is a reentrant circuit that occurs because of a region of tissue with slowed conduction by either anatomical constraints or tissue characteristics of regions of slowed

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include this CTI region for its circuit is called a noneCTI-dependent flutter and is termed atypical flutter. This delineation is extremely important to recognize because of the implications for catheter ablation (discussed below).

Irregular, narrow complex tachycardia (QRS width <120 ms, HR >100 beats/min)

P waves present

Absent P waves

Atrial Fibrillation Atrial fibrillation is the most common arrhythmia and is characterized by an irregularly irregular rhythm. Atrial fibrillation can lead to progressive atrial remodeling, atrial cardiomyopathy, and persistent AF. This has led to the concept of AF begets further AF. There are multiple hypotheses and layers of complexities as to the cause and natural progression of AF.3,22,23 We refer the reader to several excellent reviews, including a recent publication in Mayo Clinic Proceedings by Morin et al for a more in-depth discussion in this topical area.22,24,25 Generally, patients who initially present with paroxysms of AF are thought to have inciting triggers for AF from ectopic firing from the muscle sleeves that reside in the pulmonary veins. The rapid firing that occurs from the pulmonary vein muscle and enters the atria can lead to fibrillation.26

Atrial fibrillation II

aVL

III

aVF

II

Absence of a distinct P-wave inscription on the ECG

Sawtooth P waves

≥3 P-wave morphologies

CTI-dependent flutter with variable block

Multifocal atrial tachycardia II

III

aVF V1

II V6 VI

Negative P waves in inferior leads (II, III, and aVF) and positive P wave in lead V1

At least three different ≥3 P-wave morphologies on the ECG

FIGURE 2. Supraventricular tachycardias (SVTs) with irregular, narrow QRS complexes. SVTs with successive QRS complexes that are irregular but with a narrow QRS width (<120 ms) are separated from the regular, narrow complex tachycardias. Further subclassification involves identifying the presence and morphology of P waves. The absence of a distinct P wave with intervening isoelectric intervals is reflective of chaotic activation of the atrium underlying atrial fibrillation. The presence of continuous activity above or below the isoelectric line is characteristic of a reentry circuit reflective of continuous atrial flutter activation. Note that the characteristic flutter waves in cavotricuspid isthmus (CTI)edependent flutter are negative in leads II, III, and aVF and positive in lead V1. Note that in multifocal atrial tachycardia, there are at least 3 P wave morphologies. These are reflective of atrial activation origination at multiple sites in the atria. ECG ¼ electrocardiogram; HR ¼ heart rate.

conduction velocity. It is because of one or a combination of these that a reentrant circuit can form and continue to propagate throughout the atria with 1:1 or variable conduction to the ventricle. This type of SVT is divided into 2 types: (1) Typical flutter, which is dependent on the myocardial fibers that exist at a location in the right atrium between the inferior vena cava and the tricuspid valve called the cavotricuspid isthmus (CTI).1,19 It is because of the constraint of this muscle lying in between 2 electrically inert structures (inferior vena cava and tricuspid valve annulus) that this tachycardia can easily occur.20 It is also the reason for the high chance of successful ablation of this arrhythmia at this location.21 (2) Atrial flutter that does not 4

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SECTION II: CLASSIFICATION SCHEME OF SVTS BASED ON ECG CHARACTERISTICS Particular attention to key ECG characteristics during the tachycardia on the 12-lead ECG, ECG Holter strip, or telemetry monitoring strip may permit differentiation of SVT and thus aid in clinical management. This underscores the importance of recording the tachycardia, especially while the patient is having symptoms. We recommend that the clinicians first focus on key aspects of the ECG such as (1) narrow vs wide QRS complex, (2) regular vs irregular SVTs, (3) relationship between P waves and QRS complexes (atrial and ventricular depolarization), and (4) morphology of the P wave on the 12-lead ECG. Narrow vs Wide QRS Complex When reviewing a tachycardia on the ECG, the initial step is to classify it into a narrow or wide complex tachycardia. This is done by measuring the width of the QRS complex; these complexes are defined as narrow if the QRS width is less than 120 milliseconds and XXX 2018;nn(n):1-17

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FIGURE 3. Classical supraventricular arrhythmias and mechanisms. Top left panel, Critical components of the atrioventricular nodal reentrant tachycardia (AVNRT) circuit. A right atrial oblique view of the heart is shown to illustrate the atria, conduction system, ventricle, and highlights of the AVNRT circuit. Note that there are 2 inputs into the atrioventricular (AV) node: the slow pathway and fast pathway inputs. Electrical activation occurs antegrade into the AV node and retrograde from the AV node back to the atrium as part of the reentry circuit. Electrical activity continues down the normal conduction system to the ventricle. Top right panel, Focal atrial tachycardia arising in the right atrium with focal origination of activation (yellow waves). This serves as the atrial impulse, which then conducts to the rest of the atria and down to the ventricles. This is different from the sinus node, which would be higher and more posterior in the right atrium. The P wave in this location would exhibit a less positive P wave in leads II, III, and aVF. This is because the focus of activation is lower in the right atrium than in the sinus node. Because the focus favors the right atrium, the P wave duration would be almost the same. Bottom panel, Accessory pathwayemediated tachycardias. In orthodromic reciprocating tachycardia (ORT) and antidromic reciprocating tachycardia (ART), the circuit includes an accessory pathway, which is comprised of muscle fibers that connect the atrium to the ventricle across the valvular annuli. In ORT, the circuit travels from the atria down through the normal conduction system down to the ventricle. The electrical activity travels from the ventricle across the accessory fibers to bypass the AV node and reach the atria. The QRS complex is therefore narrow in this tachycardia as it uses the normal conduction system to activate the ventricle. In ART, the circuit travels from the atria and bypasses the normal conduction system via the accessory pathway and activates the ventricular muscle directly and this myocardial cell-to-myocardial cell connection is slower than the normal conduction system and creates a wide QRS complex (as it takes longer to activate) on the electrocardiogram. Note that both these tachycardias involve the AV node and also require an atrioventricular connection via muscle fibers at the annulus. Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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wide if the QRS width is 120 milliseconds or more. It should be noted that wide complex tachycardias can include all the SVTs if there is concomitant aberrant ventricular conduction such as in intermittent or permanent bundle branch block (which makes the QRS complex wide) or antidromic conduction down an accessory pathway (ART). Importantly, wide complex tachycardias should alert the clinician to consider ventricular tachycardia, artifact, or a paced rhythm.27 Regular vs Irregular SVTs Once the clinician has filtered down the possible tachycardia from the ECG by triaging narrow vs wide QRS complex, the next step in characterization involves the regularity or irregularity of successive QRS complexes. The differential diagnosis of regular, narrow complex tachycardias includes sinus tachycardia, atrial flutter, AVNRT, AVRT (ORT), and focal AT1 (Figure 1). Irregular, narrow complex tachycardias include AF and multifocal AT (Figure 2). Atrial flutter can present as a regular, narrow complex tachycardia, but can be irregular because of variable AV conduction block. Relationship Between P Waves and QRS Complexes The ECG should next be scrutinized for the presence of P waves and their correlation with QRS complexes. A reasonable classification strategy is to define the SVT as a short RP tachycardia (short duration between the P wave and the QRS complex) or a long RP tachycardia (long duration between the P wave and the QRS complex)28 (Figure 1). The RP interval reflects the difference in time between activation of the ventricle and activation of the atrium. A short RP tachycardia has an RP interval that is shorter than the PR interval, and correspondingly, a long RP tachycardia has an RP interval that is longer than the PR interval. In general, AVNRT and AVRT are short RP tachycardias.29,30 In AVNRT, the RP interval can be short or even negative because there is near-simultaneous activation of the atria and ventricles from a common point near the AV node.28 In addition, AT with first-degree AV block can present as a short RP tachycardia. This is 6

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because of prolongation in the PR interval, and thus the subsequent P wave is closer to the QRS complex because of the delay. Although short, the RP interval in orthodromic AVRT (Figure 1) is almost never less than 90 milliseconds because of the necessary time it takes for electrical activation to occur in series from the ventricular tissue to the accessory pathway and from the accessory pathway to the atrium.29,30 Atrial tachycardias or sinus tachycardias are classified as long RP tachycardias. This occurs because of the short PR interval associated with these rhythms (Figure 1). SECTION III: ECG CLUES TO AID IN DIAGNOSING SUPRAVENTRICULAR ARRHYTHMIAS The characteristics of SVT based on different mechanisms are summarized in Figures 1 and 2. Electrocardiographic findings are based on narrow vs wide QRS complexes, regularity of successive QRS complexes, relationship between RP intervals (short vs long), and the morphology of the P wave. Atrioventricular Nodal Reentrant Tachycardia Typical AVNRT has nearly simultaneous or superimposed P waves and QRS complexes. This produces a relatively short PR interval, pseudo-R0 wave in lead V1, or pseudo-S0 wave in the inferior leads (leads II, III, and aVF)30 (Figure 5). The reason for P waves and QRS complexes occurring so close together is the parallel activation of the atria and ventricles from the AVNRT circuit. Accessory PathwayeRelated Tachycardias (ORT and ART) Accessory pathways with antegrade conduction to the ventricle (or ART) can manifest as a delta wave in the early portion of the QRS complex31 (Figure 6). This occurs because of early activation of the ventricle via an accessory pathway. The depolarization of the ventricle occurs in a myocardial cell-tomyocardial cell conduction manner rather than via the specialized conduction system (which itself produces a narrow QRS complex). The presence of an accessory pathway on the surface ECG is called a Wolff-Parkinson-White XXX 2018;nn(n):1-17

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FIGURE 4. Slow and fast pathways (SP and FP) during sinus rhythm, premature atrial contraction, and atrioventricular nodal reentrant tachycardia (AVNRT). Top left panel, In sinus rhythm, conduction travels antegrade down both the SP (red dotted) and the FP (blue dotted). The FP continues down the normal conduction system to the ventricles and also conducts retrograde back up the SP to block further conduction. This is manifested on the electrocardiogram (ECG) as a normal PR interval (bottom left panel). Top middle panel, When a premature atrial contraction (PAC) occurs (green star), it is able to conduct down toward the FP (blue dotted) and SP (green dotted). However, it is not able to conduct via the FP, as it is refractory to further electrical stimulation. This allows conduction to continue from the SP (green dotted) down to the ventricles. This is manifested on the ECG as a long PR interval (bottom right panel) compared to sinus rhythm, as the PR interval reflects SP conduction from the atria to the ventricle. Top right panel, Because the PAC conducts down the SP but not the FP, there is unidirectional block and thus a setup for a reentrant circuit (green arrows). However, retrograde conduction back to the atrial tissue can occur via the FP once it recovers from refractoriness. Electrical activity can then continue as a reentrant arrhythmia via both the SP and the FP as limbs of the AVNRT circuit. This is noted as a short RP interval with almost simultaneous P waves and QRS complexes inscribed on the ECG (bottom right panel).

pattern.32 If a patient has both an ECG pattern and a tachycardia, the diagnosis is WolffParkinson-White syndrome. Antidromic reciprocating tachycardia results in a regular tachycardia with a wide QRS complex on the surface ECG because conduction is via ventricular myocardial tissue and not through conduction system tissue. Evidence of accessory pathways may be concealed from inscription on the ECG, and Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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the QRS complex may appear to be of normal width and the delta wave may be absent.33 However, a tachycardia circuit called ORT can still occur via an accessory pathway. This can occur when the activation of the conduction system to the ventricles occurs in an antegrade fashion and returns to the atria via an accessory pathway. In ORT, the RP interval is at least 90 milliseconds because of the necessary time it takes for the impulse to

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FIGURE 5. Electrocardiographic (ECG) clues suggestive of atrioventricular nodal reentrant tachycardia (AVNRT). The ECG exhibits a regular, narrow QRS complex tachycardia. P waves are difficult to discern from the QRS complexes as these are nearly simultaneous. Close inspection of certain leads such as lead V1 reveals the presence of a sharp deflection just after the QRS complex, which is termed an R0 wave. Close inspection of the inferior leads II, III, and aVF reveals a small sharp deflection after the QRS complex, which is termed an S0 wave. These sharp deflections superimposed on the QRS complex represent activation of the P wave and are classically seen in AVNRT.

conduct in series through the ventricular tissue to reach the accessory pathway and, then via the pathway, activate the atria in a retrograde fashion.29,30

Sinus Tachycardia This arrhythmia can be noted on the ECG on the basis of the P wave morphology, which is reflective of the location of the sinus node origin. The generation of the P wave inscription reflects activation of the superior posterolateral portion of the right atrium, which then travels to the rest of the right atrium and across to the left atrium, as well as inferiorly. Thus, the P wave is noted to be wide and has a positive deflection in the inferior leads II, III, 8

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and aVF, and lead I is positive. The terminal portion of the P wave in lead V1 has a negative deflection, as the left atrium is in the chamber adjacent to that which contains the sinus node (right atrium), and the wave front is moving away from lead V1 and toward the left atrium. The P wave morphology in sinus tachycardia will therefore resemble the P wave morphology during sinus rhythm.

Atrial Tachycardia This arrhythmia is recognized on the ECG with a noted change from a classical P wave that originates from the sinus node region.16,34 For example, an AT that arises from the ostium of the coronary sinus will have a XXX 2018;nn(n):1-17

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FIGURE 6. Electrocardiogram (ECG) of a patient with Wolff-Parkinson-White syndrome exhibiting preexcited QRS complexes. This ECG exhibits characteristic inscriptions noted in patients with accessory pathways that manifest on the recording strips. Note the “delta wave,” which is a deflection that occurs as the initial part of the QRS complex. This represents early activation or preexcitation of the ventricle via conduction antegrade down an accessory pathway. Another key feature on the ECG of these patients is a short PR interval, as the delta wave is occurring at the same time and thus masking the normal conduction time.

narrower P wave duration. This is because activation begins in between both atria and because activation of the right and left atria begins at a common central region.16 This is in contrast to sinus node activation, which begins in the superior and posterior aspects of the right atrium and activates the right atrium first and then the left atrium. An AT originating from the low right atrium (as opposed to the high right atrium as in sinus rhythm) along the crista terminalis would have a negative P wave axis in the inferior leads II, III, and aVF (as opposed to a positive axis that is seen in sinus).16 Sometimes it is almost impossible to distinguish between AT and sinus tachycardia. However, the clinical history and ECG monitoring are critical to the diagnosis, as findings of an abrupt onset and rate that is higher than the physiologic range can be useful in differentiation.15 Multifocal AT By definition, there should be organized atrial activity yielding P waves with 3 or more different morphologies to diagnose multifocal AT (Figure 1).1 Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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Atrial Flutter Typical atrial flutter involves the CTI.19 The key is to observe an opposite direction of P or flutter waves in the inferior leads (II, III, and aVF) and lead V1. In the more common form, counterclockwise CTI-dependent atrial flutter, P waves are positive in lead V1 and negative in leads II, III and aVF, producing a sawtooth pattern (Figure 1). In clockwise CTI-dependent atrial flutter, the opposite orientation will be observed, that is, positive flutter waves in the inferior leads and negative in lead V1.1 Atrial Fibrillation The characteristic ECG finding is the absence of a distinct P wave inscription on the ECG because of rapid oscillations (fibrillatory waves) that vary in amplitude, shape, and timing35,36 (Figure 2). Electrical activation of the atrial muscle is chaotic and signals of low amplitude may not generate sufficient voltage to manifest on the surface ECG. The QRS complexes will be irregularly irregular. Sometimes P waves in lead V1 may appear organized; however, careful inspection will find irregularity and ill-defined P waves in other leads.

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This is in contrast to atrial flutter, in which there is constant cyclical atrial activity during the flutter circuit. Lead V1 is usually over the right atrial appendage and this may have more organization than the rest of the atrium and thus confuse the clinician, especially when other leads suggest fibrillation.35 Thus, if there is evidence of AF in any lead, then the patient’s rhythm is AF.

with perturbation of the AV node, this is indicative of its necessary role in the tachycardia circuit. For example, this can include ORT, using the antegrade limb of the circuit in ORT. This can also be seen with AVNRT. In AT, AV nodal blockers may sometimes terminate the arrhythmia because of effects on abnormal atrial tissue, or alternatively it can create transient AV block with ongoing atrial activity, and thus aid in diagnosis.

SECTION IV: MANAGEMENT OF SVTS Immediate Treatment of SVT Immediate management of regular SVT is fairly standardized and aimed to stabilize the patient who presents with narrow complex tachycardia (summarized in Figure 7). The primary objective in a patient with regular and stable SVT is to slow conduction through the AV node and to terminate AVNRT or ORT.1 Vagal maneuvers can be attempted, which could include Valsalva maneuvers, carotid sinus massage, or application of a cold/wet towel to the face.8 If vagal maneuvers are ineffective, the next step is typically administration of intravenous adenosine.37,38 Other second-line treatments include AV nodeeslowing agents, such as b-blockers, diltiazem, or verapamil, and can be considered if the above are ineffective or contraindicated.1 In irregular SVT, especially AF with preexcited tachycardia, facilitation of conduction down the accessory pathway can lead to precipitation of ventricular fibrillation. Thus, AV nodal blocking agents are absolutely contraindicated in this situation as this can be fatal. Clinical Pearl 1: Perturbation of the AV Node Can Assist in Defining a Tachycardia If one cannot distinguish between atrial flutter, AF, and AT, cardiac monitoring and perturbation of the conduction system can be of great use.39 Reviewing tracings that include periods of varying AV block, which can be caused by vagal maneuvers, carotid massage, or AV node blockade, could provide the ability to see atrial activity, that is, chaotic baseline (AF) or regular sawtooth pattern (atrial flutter), and provide diagnostic insight. In this regard, adenosine, which has an extremely short half-life, can be administered to help narrow the differential diagnosis of SVT. In addition, if the tachycardia circuit breaks 10

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Clinical Pearl 2: Unstable SVT May Require Cardioversion Although SVT is usually hemodynamically tolerated, certain patients, particularly when already ill and hospitalized, may quickly decompensate in tachycardia. In these situations, synchronized electrical cardioversion should be performed. However, even in this scenario, vagal maneuvers and adenosine can be attempted first while preparation for cardioversion is ongoing. Intravenous adenosine is short acting and works on the AV node to create slowing or block in conduction. If the tachycardia involves the AV node, adenosine can serve to break the tachycardia circuit. Specific Treatment Options for SVT Based on the Tachycardia Mechanism Atrioventricular Nodal Reentrant Tachycardia. Long-term treatment is focused on symptomatic management, which is dictated by severity, frequency, and patient preference. The treatment of this arrhythmia can be noninvasively done by performing vagal maneuvers or with the use of AV nodal blockers such as b-blockers, which can interrupt this circuit.40 These are sometimes effective, though sometimes these medications are not well tolerated.41 Catheter ablation typically involving ablation of the slow pathway offers a potential for curing AVNRT with an almost 95% success rate.42,43 Accessory PathwayeRelated Tachycardia (ORT and ART). The treatment of these pathway-related tachycardias is typically ablation,44 although in those averse to invasive procedures, AV nodal blocking agents or antiarrhythmic agents that slow conduction in the atria as well as accessory pathway tissue, such as class 1C antiarrhythmic agents, for example, flecainide, can be trialed.1 However, XXX 2018;nn(n):1-17

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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST

Regular, narrow complex tachycardia (QRS width <120 ms, HR >100 beats/min)

Hemodynamically unstable

Irregular, narrow complex tachycardia (QRS width <120 ms, HR >100 beats/min)

Hemodynamically stable

1. Electrical cardioversion 2. Adenosine can be tried but should not delay cardioversion

Hemodynamically unstable

Hemodynamically stable

Electrical cardioversion

Atrial fibrillation

RP interval

Long RP interval

Short RP interval

Treat the underlying cause

Sinus tachycardia

AVNRT ORT

1. β-Blockers/ calcium channel blockers 2. Catheter ablation

Focal atrial tachycardia

Treat like AF

Atrial flutter

1. Vagal maneuvers 2. Intravenous adenosine 3. β-Blockers/ calcium channel blockers 4. Catheter ablation

Anticoagulationa Rate or rhythm controlb Risk factor modification

Multifocal atrial tachycardia

Treat underlying lung disease

Atrial flutter with variable block

Treat like AF

score ≥2, AF >48 h, not actively bleeding If >48 hours, not receiving anticoagulation and/or unsure of anticoagulation compliance use TEE guidance before cardioversion Anticoagulation required for a minimum of 4–6 wk after cardioversion

aCHA DS VASc 2 2

bCan

be accomplished by rate control (β-blocker/calcium channel blocker, and digoxin) or rhythm control (amiodaron, flecainide, propafenone, sotalol, and dofetilide) and/or catheter ablation

FIGURE 7. Treatment algorithm for supraventricular arrhythmias. Treatment schema for supraventricular tachycardias (SVTs) is delineated according to the classification schema used in this review. The first decision step depends on the hemodynamic stability of the patient. If the patient is hemodynamically unstable, electrical cardioversion is recommended for regular, narrow as well as irregular, narrow complex tachycardias. Of note, in regular, narrow complex tachycardias, adenosine can be tried for diagnostic and therapeutic purposes during preparation for cardioversion but should not delay therapy. With regular, narrow complex SVTs and hemodynamic stability, the RP interval is treated on the basis of subclassifications. Note that antidromic reentrant tachycardia/orthodromic reciprocating tachycardia, which involve the atrioventricular node, include therapies to perturb this structure, such as intravenous adenosine or vagal maneuvers. Atrial flutter is generally treated like atrial fibrillation (AF) in terms of rate/rhythm control and importantly anticoagulation. Please note that atrial flutter is difficult to treat with rate controlling agents. Thus, especially if it is CTI-dependent flutter, catheter ablation is a viable strategy. AVNRT ¼ atrioventricular nodal reentrant tachycardia; HR ¼ heart rate; ORT ¼ orthodromic reciprocating tachycardia; TEE ¼ transesophageal echocardiogram.

there are a few issues that merit additional consideration. First, AV nodal agents should not be used in patients with documented preexcited tachycardias, which conduct antegrade across an accessory pathway, such as those who experience ART or AF with preexcitation Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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(Figure 8). This could be life-threatening because of 1:1 atrial to ventricular conduction and degeneration to ventricular fibrillation.1 In the immediate setting, electrical cardioversion, intravenous procainamide, or intravenous ibutilide can be

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FIGURE 8. Electrocardiographic (ECG) characteristics in a patient with preexcited atrial fibrillation. Notable ECG findings in a patient with preexcited atrial fibrillation are annotated on the ECG. A delta wave is present at the onset of the QRS complex. In addition, the QRS complex is wide because of myocardial cell-to-myocardial cell conduction, which is slower than if it travels via conduction tissue. In atrial fibrillation, which is an irregular chaotic atrial rhythm, conduction to the ventricle is also irregular. With ECG findings such as these, atrioventricular nodal blockers are completely contraindicated.

administered. Procainamide and ibutilide have a short half-life, slow conduction down the accessory pathway, and have the additional benefit of potential AF termination.45 Second, it is important to ensure that the pathway is not a high-risk pathway for the patient, that is, one with rapid antegrade accessory pathway conduction that predisposes the patient to the risk of sudden cardiac death.46 In a population-based study in Olmsted County, Minnesota, the incidence of sudden cardiac death was found to be approximately 0.15% per year.47 In addition, in a parallel cohort of patients who underwent radiofrequency ablation vs those who did not, an incidence of sudden cardiac death/ventricular fibrillation of 2.4 cases per 1000 person-years was reported for those who did not undergo catheter ablation.48 Risk stratification can be either observed on the resting or exercise ECG or at the time of electrophysiology study. Clues for low-risk pathways include intermittent loss of 12

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preexcitation during resting or ambulatory monitoring as well as abrupt loss of conduction of preexcitation during exercise.1 During electrophysiology study, the antegrade and retrograde conduction characteristics of the pathway can be defined. In addition, the patient can be put into AF to evaluate how fast the pathway conducts to the ventricles if future AF were to occur.1 If the pathway is weakly conducting, it is safe to avoid ablation. If the pathway is of high risk, ablation can be performed during the same procedure. It is also safe to use AV nodal blockers if the pathway is weakly conducting. Clinical Pearl 3: Do Not Use AV Node Blocker Agents for Tachycardia With Preexcitation and an Irregular Rhythm In the case of a conducting antegrade pathway with preexcitation on the ECG and irregular QRS complexes, Valsalva maneuvers, adenosine, b-blockers, or calcium channel blockers, that is, those that block the AV node and XXX 2018;nn(n):1-17

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facilitate pathway conduction, should not be attempted.1 The concern is that conduction would be preferentially shifted from down the AV node to the pathway, which may not have any decremental properties, and thus conduct rapidly. Thus, if the AV node is blocked but atrial activity occurs rapidly (eg, in AF), it is possible for 1:1 atrial to ventricular conduction via an accessory pathway to occur.1 This could degenerate into ventricular fibrillation. The clinician will note AF because of the lack of P waves and irregularly irregular rate of subsequent QRS complexes. Of note, QRS morphologies will have various degrees of preexcitation and fusion between ventricular excitation from the normal conduction system and preexcitation from the antegrade pathway. Clinical Pearl 4: Electrical Cardioversion or Procainamide for Tachycardia With Preexcitation and Irregular Rhythm As stated above, if the preexcited rhythm looks irregular, this is particularly a dire circumstance and most likely AF with rapid ventricular conduction via an accessory pathway. Atrioventricular nodal blockers such as adenosine, b-blockers, and calcium channel blockers should not be administered.1 In these cases, intravenous procainamide can be given or, if hemodynamically unstable, electrical cardioversion is warranted.45 It is particularly these situations that we want to identify early and these patients should be referred for electrophysiologic consultation for further laboratory study and possible ablation. Specific pacing maneuvers are performed in a controlled setting to see how fast the pathway conducts to risk stratify the patient. High-risk patients are to undergo catheter ablation of these pathways during the same study.1 Similarly, weakly conducting pathwaysd those in which preexcitation is intermittent, or not present, especially at heart rates below 100 beats/mindare unlikely to be of concern and AV nodal blockers can still be used. Atrial Tachycardia. The approach to longterm management is dictated by the frequency and severity of symptoms. A medical approach may include oral b-blockers, diltiazem, verapamil, or antiarrhythmic agents. Catheter ablation is also an appropriate initial treatment.1 Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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For sinus tachycardia and multifocal AT, treatment is aimed at treating the underlying cause.49 In the case of sinus tachycardia, this can be of multiple stressors such as anemia, hypoxia, fever, or infection. In multifocal AT, in general, the goal is to treat the underlying lung disease. Atrial Flutter. Cavotricuspid isthmuse dependent atrial flutter can be targeted with a relatively high success rate of more than 90% via catheter ablation21,50 (Figure 9). Thus, catheter ablation for this arrhythmia is typically recommended. Rate-controlling agents can be used to decrease the ventricular rate, which may improve symptoms, although these are not always effective.50 Atrial flutters that are noneCTI-dependent are typically much more difficult to ablate, and antiarrhythmic agents may be trialed initially before engaging in a more complex ablation procedure. Clinical Pearl 5: Relationship Between AF and Atrial Flutter The trigger for AF as well as AF itself can be the trigger for atrial flutter. Thus, it is common to observe both arrhythmias together. In patients with both arrhythmias recorded, catheter ablation for atrial flutter can be undertaken at the same time as that for AF.22 Atrial Fibrillation. The goal of therapies for these patients are multitiered and include lifestyle modifications to remove or reduce triggers such as alcohol, caffeine, obstructive sleep apnea treatment,51 weight loss in those with obesity,52 and exercise in those with a sedentary lifestyle.24,52-54 In addition, modification of hypertension is essential and treatment of heart failure is critical to lower the pressure seen in the left atrium, which leads to stretch and remodeling, and potentially scar formation, all of which could be a setup for AF.22 These strategies should be the basis for every patient regardless of further therapies. Clinical Pearl 6: Rate vs Rhythm Control Strategy Landmark trials including Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) and Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) observed no clinical

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isolation was common and only limited antiarrhythmic drugs (ie, amiodarone and sotalol) were used.41,54 Subsequent trials, however, are more supportive of a catheter-based approach. In patients with a left ventricular ejection fraction of 35% or less who already had an implantable cardioverter-defibrillator, catheter ablation improved outcomes (death or hospitalization for heart failure) and left ventricular dysfunction, compared with conventional drug treatment in the Catheter Ablation for Atrial Fibrillation with Heart Failure (CASTLE-AF) trial.56 The recently reported Catheter Ablation versus Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABABA) trial, which randomized approximately 2200 patients with AF to either catheter ablation or drug therapy, reported that ablation is not superior to drugs for a composite of cardiovascular outcomes during 5-year follow-up. However, its preliminary results suggest a reduction in cardiovascular hospitalization and AF recurrence with a catheter ablation approach.57 Further analysis and reports on quality of life and cost-effectiveness are underway. Conclusively, the decisions to use a rate or rhythm control strategy depend largely on symptoms, as well as notable comorbidities such as heart failure/cardiomyopathy, and on patient preference for ablation over drug therapy.22 It is therefore reasonable to refer patients with AF to an electrophysiologist for a detailed discussion about rate vs rhythm control strategy (antiarrhythmic drugs and catheterbased ablation). Finally, it is important to emphasize that the cornerstone of management of AF (and atrial flutter) is stroke prevention and the need of anticoagulation is not modified with any treatment modalities (including ablation).

FIGURE 9. Catheter ablation of the cavotricuspid isthmus line for atrial flutter treatment. Because of the anatomical constraint of typical atrial flutter circuits from the electrically inert structures of the tricuspid valve (TCV) annulus and inferior vena cava (ICV), not only is there a region for flutter to occur but also a practical location to create a line of block with radiofrequency catheter ablation. During catheter ablation for typical atrial flutter, radiofrequency energy is used to create a line of tissue destruction that creates a line of electrical block between the TCV and the ICV and thus eliminates a necessary region for the flutter circuit.

benefits (survival or stroke prevention) regardless of a rhythm or rate control strategy.41,54 In addition, both strict rate control (resting heart rate, <80 beats/min; heart rate during moderate exercise, <110 beats/min) and lenient rate control (resting heart rate, <110 beats/min) offer similar clinical outcomes as noted in the RACE II trial.55 However, the results did not account for tachycardia-induced cardiomyopathy (see discussion below). There are considerable limitations of trial data evaluating rate and rhythm control. Mainly, the AFFIRM and RACE trials were largely conducted before catheter-based pulmonary vein 14

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Clinical Pearl 7: Anticoagulation for Atrial Flutter and AF A mainstay of AF is that of stroke prophylaxis with the use of anticoagulation. This is also necessary in patients with atrial flutter. The decision to initiate anticoagulation should be based on the CHADS2-VASc risk score, and not dependent on the duration of arrhythmias, or treatment strategy (ie, rate, rhythm, or ablation).58 Tachycardia-Induced Cardiomyopathy Atrial arrhythmiaemediated cardiomyopathy is not uncommonly seen and can have severe XXX 2018;nn(n):1-17

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consequences because of severe decline in ventricular function.59 These patients tend to have slower tachycardia (and without much symptoms), but incessant or frequent paroxysmal tachycardia.60 Aggressive management of this arrhythmia is recommended. Atrial fibrillation or flutter with poor rate control can also cause cardiomyopathy. The general recommendation in this scenario is to ensure adequacy of rate control or offer a rhythm control strategy.22 When frequent enough, any SVT can cause cardiomyopathy. In particular, an arrhythmia that classically causes cardiomyopathy is a permanent form of junctional reciprocating tachycardia. This is an uncommon subtype of AVRT that involves a concealed accessory pathway with retrograde decremental conduction properties. Patients often present with slow and incessant AVRT. Catheter ablation can often successfully restore cardiac function.61,62

CONCLUSION Supraventricular arrhythmias can cause distress and comorbidity to patients. These arrhythmias are not uncommon, and the internist requires a fundamental knowledge of the mechanisms and management of these arrhythmias. With an approach to reviewing the ECG and clues to arrive at a differential SVT diagnosis, the proper triage in patient management will be augmented. This may require rate or rhythm control, electrical cardioversion, or even catheter ablation. With an understanding of downstream therapies used, the internist will be equipped to provide initial counseling to the patient and recognize the importance of referral to cardiac electrophysiology for advanced measures including catheter ablation. These essential tenets are all the more important as these can involve younger patients with life-threatening ramifications as well as older patients who may be at risk of heart failure progression. Abbreviations and Acronyms: AF = atrial fibrillation; ART = antidromic reciprocating tachycardia; AT = atrial tachycardia; AV = atrioventricular; AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; CTI = cavotricuspid isthmus; ECG = electrocardiographic/electrocardiogram; ORT = orthodromic reciprocating tachycardia; SVT = supraventricular tachycardia Mayo Clin Proc. n XXX 2018;nn(n):1-17 www.mayoclinicproceedings.org

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Potential Competing Interests: Dr Asirvatham serves as a consultant to Aegis, ATP, Nevro, Sanovas, Sorin Medical, and FocusStart. Correspondence: Address to Samuel J. Asirvatham, MD, Department of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (asirvatham.samuel@ mayo.edu).

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52. Lavie CJ, Pandey A, Lau DH, Alpert MA, Sanders P. Obesity and atrial fibrillation prevalence, pathogenesis, and prognosis: effects of weight loss and exercise. J Am Coll Cardiol. 2017;70(16): 2022-2035. 53. Pathak RK, Middeldorp ME, Meredith M, et al. Long-term effect of goal-directed weight management in an atrial fibrillation cohort: a long-term follow-up study (LEGACY). J Am Coll Cardiol. 2015;65(20):2159-2169. 54. Van Gelder IC, Hagens VE, Bosker HA, et al; Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study Group. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002;347(23):1834-1840. 55. Van Gelder IC, Groenveld HF, Crijns HJ, et al; RACE II Investigators. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010;362(15):1363-1373. 56. Marrouche NF, Brachmann J, Andresen D, et al; CASTLE-AF Investigators. Catheter ablation for atrial fibrillation with heart failure. N Engl J Med. 2018;378(5):417-427. 57. Packer DL, Mark DB, Robb RA, et al; CABANA Investigators. Catheter Ablation versus Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial: study rationale and design. Am Heart J. 2018;199:192-199.

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58. January CT, Wann LS, Alpert JS, et al; ACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2014;130(23):e270-e271]. Circulation. 2014;130(23): 2071-2104. 59. Gillette PC, Smith RT, Garson A Jr, et al. Chronic supraventricular tachycardia: a curable cause of congestive cardiomyopathy. JAMA. 1985;253(3):391-392. 60. Medi C, Kalman JM, Haqqani H, et al. Tachycardia-mediated cardiomyopathy secondary to focal atrial tachycardia: long-term outcome after catheter ablation. J Am Coll Cardiol. 2009;53(19):1791-1797. 61. Noë P, Van Driel V, Wittkampf F, Sreeram N. Rapid recovery of cardiac function after catheter ablation of persistent junctional reciprocating tachycardia in children. Pacing Clin Electrophysiol. 2002;25(2):191-194. 62. Sanchez C, Benito F, Moreno F. Reversibility of tachycardiainduced cardiomyopathy after radiofrequency ablation of incessant supraventricular tachycardia in infants. Br Heart J. 1995;74(3):332-333.

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