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J Am Coll Cardiol, 2003; 42:1493-1531, doi:10.1016/j.jacc.2003.08.013 © 2003 by the American College of Cardiology Foundation |
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Key Words: ACC/AHA/ESC Practice Guidelines • arrhythmia • tachycardia • ablation • drugs
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Table of contents |
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 Top Table of contents PreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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Preamble |
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TopTable of contentsPreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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I. Introduction |
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TopTable of contentsPreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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Writing groups are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered, as are frequency of follow-up and cost effectiveness. In controversial areas, or with regard to issues without evidence other than usual clinical practice, a consensus was achieved by agreement of the expert panel after thorough deliberations.
This document was peer reviewed by two official external reviewers representing the American College of Cardiology Foundation, two official external reviewers representing the American Heart Association, and two official external reviewers representing the European Society of Cardiology. The North American Society for Pacing and Electrophysiology—Heart Rhythm Society assigned one organizational reviewer to the guideline. In addition, 37 external content reviewers participated in the review representing the ACC/AHA Task Force on Practice Guidelines, the ESC Committee for Practice Guidelines, the ACCF Electrophysiology Committee, the AHA ECG/Arrhythmias Committee, the ESC Working Group on Arrhythmias, and the ESC Task Force on Grown-Up Congenital Heart Disease. Please see Appendix 2 in the full-text guideline for the names of all reviewers.
The document was approved for publication by the governing bodies of the ACCF, AHA, and ESC. These guidelines will be reviewed annually by the ESC and the ACC/AHA Task Force on Practice Guidelines and will be considered current unless they are revised or withdrawn from distribution.
Recommendations are evidence-based and derived primarily from published data. The level of evidence was ranked as follows:
Level A (highest): derived from multiple randomized clinical trials;
Level B (intermediate): data are on the basis of a limited number of randomized trials, nonrandomized studies, or observational registries;
Level C (lowest): primary basis for the recommendation was expert consensus.
Recommendations follow the format of previous ACC/AHA guidelines for classifying indications, summarizing both the evidence and expert opinion.
B.. Contents of these guidelines—scope. The purpose of this joint ACC/AHA/ESC document is to provide clinicians with practical and authoritative guidelines for the management and treatment of patients with supraventricular arrhythmias (SVA). These include rhythms emanating from the sinus node, from atrial tissue (atrial flutter), and from junctional as well as reciprocating or accessory pathway-mediated tachycardia. This document does not include recommendations for patients with either atrial fibrillation (AF) (see ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation 1) or for pediatric patients with supraventricular arrhythmias. For our purposes, the term "supraventricular arrhythmia" refers to all types of supraventricular arrhythmias, excluding AF, as opposed to SVT, which includes atrioventricular nodal reciprocating tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), and atrial tachycardia (AT).
Overall, this is a consensus document that includes evidence and expert opinions from several countries. The pharmacologic and nonpharmacologic antiarrhythmic approaches discussed may, therefore, include some drugs and devices that do not have the approval of governmental regulatory agencies. Because antiarrhythmic drug dosages and drug half-lives are detailed in the ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation 1, they are not repeated in this document.
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II. Public health considerations and epidemiology |
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TopTable of contentsPreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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Failure to discriminate among AF, atrial flutter, and other supraventricular arrhythmias has complicated the precise definition of this arrhythmia in the general population. The estimated prevalence of paroxysmal supraventricular tachycardia (PSVT) in a 3.5% sample of medical records in the Marshfield (Wisconsin) Epidemiologic Study Area (MESA) was 2.25 per 1000 3. The incidence of PSVT in this survey was 35 per 100 000 person-years 3.
Age exerts an influence on the occurrence of SVT. The mean age at the time of PSVT onset in the MESA cohort was 57 years (ranging from infancy to more than 90 years old) 3. In the MESA population, compared with those with other cardiovascular disease, "lone" (no cardiac structural disease) PSVT patients were younger (mean age equals 37 versus 69 years), had faster heart rates (186 versus 155 beats per minute [bpm]), and were more likely to present first to an emergency room (69% versus 30%) 3. The age of tachycardia onset is higher for AVNRT (32 plus or minus 18 years) than for AVRT (23 plus or minus 14 years).
Gender plays a role in the epidemiology of SVT. Female residents in the MESA population had a twofold greater relative risk (RR) of PSVT (RR equals 2.0; 95% confidence interval equals 1.0 to 4.2) compared with males 3.
The only reported epidemiologic study of patients with atrial flutter 4 involved a selected sample of individuals treated in the Marshfield Clinic in predominantly white, rural mid-Wisconsin. More than 75% of the 58 820 residents and virtually all health events were included in this population database. In approximately 60% of cases, atrial flutter occurred for the first time in association with a specific precipitating event (ie, major surgery, pneumonia, or acute myocardial infarction). In the remaining patients, atrial flutter was associated with chronic comorbid conditions (ie, heart failure, hypertension, and chronic lung disease). Only 1.7% of cases had no structural cardiac disease or precipitating causes (lone atrial flutter). The overall incidence of atrial flutter was 0.088%; 58% of these patients also had AF. Atrial flutter alone was seen in 0.037%. The incidence of atrial flutter increased markedly with age, from 5 per 100 000 of those more than 50 years old to 587 per 100 000 over age 80. Atrial flutter was 2.5 times more common in men and was diagnosed twice as often as PSVT.
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III. General mechanisms of SVA |
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TopTable of contentsPreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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The sinoatrial node is a collection of morphologically and electrically distinct cells 5,6. The central portion of the sinus node, which houses the dominant pacemaking function, contains cells with longer action potentials and faster rates of phase 4 diastolic depolarization than other cardiac cells 6,7.
Cellular recordings support the existence of distinct populations of cells in the mammalian AV node. Differences in ion channel expression underlie the differences in the electrophysiological behavior of each of the cell types.
B. General mechanisms. All cardiac tachyarrhythmias are produced by one or more mechanisms, including disorders of impulse initiation and abnormalities of impulse conduction. The former are often referred to as automatic, and the latter as re-entrant. Tissues exhibiting abnormal automaticity that underlie SVT can reside in the atria, the AV junction, or vessels that communicate directly with the atria, such as the vena cava or pulmonary veins 8,9. The cells with enhanced automaticity exhibit enhanced diastolic phase 4 depolarization and, therefore, an increase in firing rate compared with pacemaker cells. If the firing rate of the ectopic focus exceeds that of the sinus node, then the sinus node can be overdriven and the ectopic focus will become the predominant pacemaker of the heart. The rapid firing rate may be incessant (ie, more than 50% of the day) or episodic.
Triggered activity is a tachycardia mechanism associated with disturbances of recovery or repolarization. Triggered rhythms are generated by interruptions in repolarization of a heart cell called afterdepolarizations. An afterdepolarization of sufficient magnitude may reach "threshold" and trigger an early action potential during repolarization.
The most common arrhythmia mechanism is re-entry, which may occur in different forms. In its simplest form, it occurs as repetitive excitation of a region of the heart and is a result of conduction of an electrical impulse around a fixed obstacle in a defined circuit. This is referred to as re-entrant tachycardia. There are several requirements for the initiation and maintenance of this type of re-entry. Initiation of a circus movement tachycardia requires unidirectional conduction block in one limb of a circuit. Unidirectional block may occur as a result of acceleration of the heart rate or block of a premature impulse that impinges on the refractory period of the pathway. Slow conduction is usually required for both initiation and maintenance of a circus movement tachycardia. In the case of orthodromic AV re-entry (ie, anterograde conduction across the AV node with retrograde conduction over an accessory pathway), slowed conduction through the AV node allows for recovery of, and retrograde activation over, the accessory pathway.
Re-entry is the mechanism of tachycardia in SVTs such as AVRT, AVNRT and atrial flutter; however, a fixed obstacle and predetermined circuit are not essential requirements for all forms of re-entry. In functionally determined re-entry, propagation occurs through relatively refractory tissue and there is an absence of a fully excitable gap. Specific mechanisms are considered in the following sections.
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IV. Clinical presentation, general evaluation, and management of patients with SVA |
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TopTable of contentsPreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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A history of arrhythmia-related symptoms may yield important clues to the type of arrhythmia. Premature beats are commonly described as pauses or nonconducted beats followed by a sensation of a strong heart beat, or they are described as irregularities in heart rhythm. Supraventricular tachycardias occur in all age groups and may be associated with minimal symptoms, such as palpitations, or they may present with syncope. The clinician should distinguish whether the palpitations are regular or irregular. Irregular palpitations may be due to premature depolarizations, AF, or multifocal atrial tachycardia (MAT). The latter are most commonly encountered in patients with pulmonary disease. If the arrhythmia is recurrent and has abrupt onset and termination, then it is designated paroxysmal. Sinus tachycardia is, conversely, nonparoxysmal and accelerates and terminates gradually. Patients with sinus tachycardia may require evaluation for stressors, such as infection or volume loss. Episodes of regular and paroxysmal palpitations with a sudden onset and termination (also referred to as PSVT) most commonly result from AVRT or AVNRT. Termination by vagal maneuvers further suggests a re-entrant tachycardia involving AV nodal tissue (eg, AVNRT, AVRT). Polyuria is caused by release of atrial natriuretic peptide in response to increased atrial pressures from contraction of atria against a closed AV valve, which is supportive of a sustained supraventricular arrhythmia.
With SVT, syncope is observed in approximately 15% of patients, usually just after initiation of rapid SVT or with a prolonged pause after abrupt termination of the tachycardia. Syncope may be associated with AF with rapid conduction over an accessory AV pathway or may suggest concomitant structural abnormalities, such as valvular aortic stenosis, hypertrophic cardiomyopathy, or cerebrovascular disease. Symptoms vary with the ventricular rate, underlying heart disease, duration of SVT, and individual patient perceptions. Supraventricular tachycardia that is persistent for weeks to months and associated with a fast ventricular response may lead to a tachycardia-mediated cardiomyopathy 10,11.
Of crucial importance in clinical decision making is a clinical history describing the pattern in terms of the number of episodes, duration, frequency, mode of onset, and possible triggers.
Supraventricular tachycardia has a heterogeneous clinical presentation, most often occurring in the absence of detectable heart disease in younger individuals. The presence of associated heart disease should nevertheless always be sought, and an echocardiogram may be helpful. While a physical examination during tachycardia is standard, it usually does not lead to a definitive diagnosis. If irregular cannon A waves and/or irregular variation in S1 intensity is present, then a ventricular origin of a regular tachycardia is strongly suggested.
2. Diagnostic investigations
A resting 12-lead echocardiogram (ECG) should be recorded. The presence of pre-excitation on the resting ECG in a patient with a history of paroxysmal regular palpitations is sufficient for the presumptive diagnosis of AVRT, and attempts to record spontaneous episodes are not required before referral to an arrhythmia specialist for therapy (Figure 1). Specific therapy is discussed in Section V. A clinical history of irregular and paroxysmal palpitations in a patient with baseline pre-excitation strongly suggests episodes of AF, which requires immediate electrophysiological evaluation because these patients are at risk for significant morbidity and possibly sudden death (see Section V-D). The diagnosis is otherwise made by careful analysis of the 12-lead ECG during tachycardia (see Section IV). Therefore, patients with a history of sustained arrhythmia should always be encouraged to have at least one 12-lead ECG taken during the arrhythmia. Automatic analysis systems of 12-lead ECGs are unreliable and commonly suggest an incorrect arrhythmia diagnosis.
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An ambulatory 24-hour Holter recording can be used in patients with frequent (ie, several episodes per week) but transient tachycardias 12. An event or wearable loop recorder is often more useful than a 24-hour recording in patients with less frequent arrhythmias. Implantable loop recorders may be helpful in selected cases with rare symptoms (ie, fewer than two episodes per month) associated with severe symptoms of hemodynamic instability 13. Exercise testing is less often useful for diagnosis unless the arrhythmia is clearly triggered by exertion.
Transesophageal atrial recordings and stimulation may be used in selected cases for diagnosis or to provoke paroxysmal tachyarrhythmias if the clinical history is insufficient or if other measures have failed to document an arrhythmia. Esophageal stimulation is not indicated if invasive electrophysiological investigation is planned. Invasive electrophysiological investigation with subsequent catheter ablation may be used for diagnoses and therapy in cases with a clear history of paroxysmal regular palpitations. It may also be used empirically in the presence of pre-excitation or disabling symptoms (Figure 1).
3. Management
The management of patients with symptoms suggestive of an arrhythmia but without ECG documentation depends on the nature of the symptoms. If the surface ECG is normal and the patient reports a history consistent with premature extra beats, then precipitating factors, such as excessive caffeine, alcohol, nicotine intake, recreational drugs, or hyperthyroidism, should be reviewed and eliminated. Benign extrasystoles are often manifest at rest and tend to become less common with exercise.
If symptoms and the clinical history indicate that the arrhythmia is paroxysmal in nature and the resting 12-lead ECG gives no clue for the arrhythmia mechanism, then further diagnostic tests for documentation may not be necessary before referral for an invasive electrophysiological study and/or catheter ablation. Patients should be taught to perform vagal maneuvers. A beta-blocking agent may be prescribed empirically provided that significant bradycardia (less than 50 bpm) have been excluded. Due to the risk of proarrhythmia, antiarrhythmic treatment with class I or class III drugs should not be initiated without a documented arrhythmia.
B. General evaluation of patients with documented arrhythmia.
1. Diagnostic evaluation
Whenever possible, a 12-lead ECG should be taken during tachycardia but should not delay immediate therapy to terminate the arrhythmia if there is hemodynamic instability. At a minimum, a monitor strip should be obtained from the defibrillator, even in cases with cardiogenic shock or cardiac arrest, before direct current (DC) cardioversion is applied to terminate the arrhythmia.
a. Differential diagnosis for narrow QRS-complex tachycardia
If ventricular action (QRS) is narrow (less than 120 ms), then the tachycardia is almost always supraventricular and the differential diagnosis relates to its mechanism (Figure 2). If no P waves or evidence of atrial activity is apparent and the RR interval is regular, then AVNRT is most commonly the mechanism. P-wave activity in AVNRT may be only partially hidden within the QRS complex and may deform the QRS to give a pseudo-R wave in lead V1 and/or a pseudo-S wave in inferior leads (Figure 3). If a P wave is present in the ST segment and separated from the QRS by 70 ms, then AVRT is most likely. In tachycardias with RP longer than PR, the most likely diagnosis is atypical AVNRT, permanent form of junctional reciprocating tachycardia (PJRT) (ie, AVRT via a slowly conducting accessory pathway), or AT (see Section V-B, D, and E). Responses of narrow QRS-complex tachycardias to adenosine or carotid massage may aid in the differential diagnosis (Figure 4) 14,15. A 12-lead ECG recording is desirable during use of adenosine or carotid massage. If P waves are not visible, then the use of esophageal pill electrodes can also be helpful.
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(2). Supraventricular tachycardia with atrioventricular conduction over an accessory pathway
Supraventricular tachycardia with AV conduction over an accessory pathway may occur during AT, atrial flutter, AF, AVNRT, or antidromic AVRT. The latter is defined as anterograde conduction over the accessory pathway and retrograde conduction over the AV node or a second accessory AV pathway. A wide-QRS complex with left bundle-branch block (LBBB) morphology may be seen with anterograde conduction over other types of accessory pathways, such as atriofascicular, nodofascicular, or nodoventricular tracts.
(3). Ventricular tachycardia
Several ECG criteria have been described to differentiate the underlying mechanism of a wide-QRS tachycardia.
(i). Ventricular arrhythmia (VA) dissociation
VA dissociation with a ventricular rate faster than the atrial rate generally proves the diagnosis of VT (Figures 5 and 6) but is clearly discernible in only 30% of all VTs. Fusion complexes represent a merger between conducted sinus (or supraventricular complexes) impulses and ventricular depolarization occurring during AV dissociation. These complexes are pathognomonic of VT. Retrograde VA block may be present spontaneously or brought out by carotid massage. The demonstration that P waves are not necessary for tachycardia maintenance strongly suggests VT. P waves can be difficult to recognize during a wide-QRS tachycardia. Therefore, one should also look for evidence of VA dissociation on physical examination: irregular cannon A waves in the jugular venous pulse and variability in the loudness of the first heart sound and in systolic blood pressure. If P waves are not visible, then the use of esophageal pill electrodes can also be useful.
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(iii). Configurational characteristics of the QRS complex during tachycardia
Leads V1 and V6 are helpful in differentiating VT from SVT.
The width and morphological criteria are less specific for patients taking certain antiarrhythmic agents and those with hyperkalemia or severe heart failure. Despite ECG criteria, patients presenting with wide QRS-complex tachycardia are often misdiagnosed. A positive answer to two inquiries, namely the presence of a previous myocardial infarct and the first occurrence of a wide QRS-complex tachycardia after an infarct, strongly indicates a diagnosis of VT.
2. Management
When a definitive diagnosis can be made on the basis of ECG and clinical criteria, acute and chronic treatment should be initiated on the basis of the underlying mechanism (see sections on specific arrhythmias).
If the specific diagnosis of a wide QRS-complex tachycardia cannot be made despite careful evaluation, then the patient should be treated for VT. Acute management of patients with hemodynamically stable and regular tachycardia is outlined in Figure 7.
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a. Acute management of narrow QRS-complex tachycardia
In regular narrow QRS-complex tachycardia, vagal maneuvers (ie, Valsalva, carotid massage, and facial immersion in cold water) should be initiated to terminate the arrhythmia or to modify AV conduction. If this fails, then intravenous (IV) antiarrhythmic drugs should be administered for arrhythmia termination in hemodynamically stable patients. Adenosine (or adenosine triphosphate [ATP]) or nondihydropyridine calcium-channel antagonists are the drugs of choice (Figure 4). The advantage of adenosine relative to IV calcium-channel or beta blockers relates to its rapid onset and short half-life. Intravenous adenosine is, therefore, the preferred agent except for patients with severe asthma. Patients treated with theophylline may require higher doses of adenosine for effect, and adenosine effects are potentiated by dipyridamole. In addition, higher rates of heart block may be seen when adenosine is concomitantly administered with carbamazepine. Longer-acting agents (eg, IV calcium-channel blockers or beta blockers [ie, verapamil/diltiazem or metoprolol]) are of value, particularly for patients with frequent atrial premature beats or ventricular premature beats, which may serve to trigger early recurrence of PSVT. Adenosine or DC cardioversion is preferred for those with PSVT in whom a rapid therapeutic effect is essential. Potential adverse effects of adenosine include initiation of AF (1% to 15%), which is usually transient and may be particularly problematic for those with ventricular pre-excitation. Adenosine should be avoided in patients with severe bronchial asthma. It is important to use extreme care with concomitant use of IV calcium-channel blockers and beta blockers because of possible potentiation of hypotensive and/or bradycardic effects. An ECG should be recorded during vagal maneuvers or drug administration because the response may aid in the diagnosis even if the arrhythmia does not terminate (Figure 4). Termination of the tachycardia with a P wave after the last QRS complex favors a diagnosis of AVRT or AVNRT. Tachycardia termination with a QRS complex favors AT, which is often adenosine insensitive. Continuation of tachycardia with AV block is virtually diagnostic of AT or atrial flutter, excludes AVRT, and makes AVNRT very unlikely.
b. Acute management of wide QRS-complex tachycardia
Immediate DC cardioversion is the treatment for hemodynamically unstable tachycardias. If the tachycardia is hemodynamically stable and definitely supraventricular, then management is as described for narrow QRS tachycardias (Figure 4). For pharmacologic termination of a stable wide QRS-complex tachycardia, IV procainamide and/or sotalol are recommended on the basis of randomized but small studies. Amiodarone is also considered acceptable. Amiodarone is preferred compared with procainamide and sotalol for patients with impaired left ventricular (LV) function or signs of heart failure. These recommendations are in accord with the current Advanced Cardiovascular Life Support guidelines 16. Special circumstances may require alternative therapy (ie, pre-excited tachycardias and VT caused by digitalis toxicity). For termination of an irregular wide QRS-complex tachycardia (ie, pre-excited AF), DC cardioversion is recommended. Or, if the patient is hemodynamically stable, then pharmacologic conversion using IV ibutilide or flecainide is appropriate.
c. Further management
After successful termination of a wide QRS-complex tachycardia of unknown etiology, patients should be referred to an arrhythmia specialist. Patients with stable narrow QRS-complex tachycardia, normal LV function, and a normal ECG during sinus rhythm (ie, no pre-excitation) may require no specific therapy. Referral is indicated for those with drug resistance or intolerance as well as for patients desiring to be free of lifelong drug therapy. When treatment is indicated, options include catheter ablation or drug therapy. Finally, because of the potential for lethal arrhythmias, all patients with WPW syndrome (ie, pre-excitation and arrhythmias) should be referred for further evaluation. Table 1 lists recommendations for acute management of hemodynamically stable and regular tachycardia.
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V. Specific arrhythmias |
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TopTable of contentsPreambleI. IntroductionII. Public health considerations...III. General mechanisms of...IV. Clinical presentation,...V. Specific arrhythmiasVI. Special circumstancesReferences |
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1. Physiological sinus tachycardia
The normally innervated sinus node generates an impulse approximately 60 to 90 times per minute and responds to autonomic influences. Nevertheless, the sinus node is a versatile structure and is influenced by many other factors, including hypoxia, acidosis, stretch, temperature, and hormones (eg, tri-iodothyronine, serotonin).
a. Definition
Sinus tachycardia is defined as an increase in sinus rate to more than 100 bpm in keeping with the level of physical, emotional, pathological, or pharmacologic stress. Pathological causes of sinus tachycardia include pyrexia, hypovolemia, or anemia, which may result from infections. Drugs that induce sinus tachycardia include stimulants (eg, caffeine, alcohol, nicotine); prescribed compounds (eg, salbutamol, aminophylline, atropine, catecholamines); and certain recreational/illicit drugs (eg, amphetamines, cocaine, "ecstasy," cannabis) 33. Anticancer treatments, in particular anthracycline compounds such as doxorubicin (or Adriamycin) and daunorubicin, can also trigger sinus tachycardia as part of the acute cardiotoxic response that is predominantly catecholamine/histamine induced 34 or part of a late cardiotoxic response. Sinus tachycardia may signal severe underlying pathologies and often requires comprehensive evaluation. Atrial and sinus tachycardias may be difficult to differentiate.
b. Mechanism
Sinus tachycardia results from physiological influences on individual pacemaker cells and from an anatomical shift in the site of origin of atrial depolarization superiorly within the sinus node.
c. Diagnosis
In normal sinus rhythm, the P wave on a 12-lead ECG is positive in leads I, II, and aVF and negative in aVR. Its axis in the frontal plane lies between 0 and +90; in the horizontal plane, it is directed anteriorly and slightly leftward and can, therefore, be negative in leads V1 and V2 but positive in leads V3 to V6. The P waves have a normal contour, but a larger amplitude may develop and the wave may become peaked 35. Sinus tachycardia is nonparoxysmal, thus differentiating it from re-entry.
d. Treatment
The mainstay in the management of sinus tachycardias primarily involves identifying the cause and either eliminating or treating it. Beta blockade, however, can be extremely useful and effective for physiological symptomatic sinus tachycardia triggered by emotional stress and other anxiety-related disorders 36–38; for prognostic benefit after myocardial infarction 39; for the symptomatic and prognostic benefits in certain other irreversible causes of sinus tachycardias, such as congestive cardiac failure 40,41; and for symptomatic thyrotoxicosis in combination with carbimazole or propylthiouracyl while these palliative agents take effect 42. Nondihydropyridine calcium-channel blockers, such as dilitiazem or verapamil, may be of benefit in patients with symptomatic thyrotoxicosis if beta blockade is contraindicated.
2. Inappropriate sinus tachycardia
a. Definition
Inappropriate sinus tachycardia is a persistent increase in resting heart rate or sinus rate unrelated to, or out of proportion with, the level of physical, emotional, pathological, or pharmacologic stress.
b. Mechanism
The underlying pathological basis for inappropriate sinus tachycardia is likely to be multifactorial, but two main mechanisms have been proposed:
c. Presentation
A high proportion of patients with inappropriate sinus tachycardia are healthcare professionals, and approximately 90% are female. The mean age of presentation is 38 plus or minus 12 years. Although the predominant symptom at presentation is that of palpitations, symptoms such as chest pain, shortness of breath, dizziness, lightheadedness, and pre-syncope have also been reported. The degree of disability can vary tremendously, from totally asymptomatic patients identified during routine medical examination to individuals who are fully incapacitated. Clinical examination and routine investigations allow elimination of a secondary cause for the tachycardia but are generally not helpful in establishing the diagnosis.
d. Diagnosis
Sinus tachycardia is diagnosed on the basis of invasive and noninvasive criteria 43:
e. Treatment
The treatment of inappropriate sinus tachycardia is predominantly symptom driven. The risk of tachycardia-induced cardiomyopathy in untreated patients is unknown but is likely to be small.
Although no randomized, double-blinded, placebo-controlled clinical trials exist, beta blockers may be useful and should be prescribed as first-line therapy in the majority of these patients. Anecdotal evidence suggests that nondihydropyridine calcium-channel blockers, such as verapamil and diltiazem, are also effective.
Sinus node modification by catheter ablation remains a potentially important therapeutic option in the most refractory cases of inappropriate sinus tachycardia. Potential adverse effects include pericarditis, phrenic nerve injury, superior vena cava (SVC) syndrome, or need for permanent pacing. A number of case reports have recorded successful surgical excision or radiofrequency (RF) ablation of the sinus node 44,45. The diagnosis of POTS (see Section V-A-3) must be excluded before considering ablation. In a retrospective analysis of 29 cases undergoing sinus node modification for inappropriate sinus tachycardia 46, a 76% acute success rate (22 out of 29 cases) was reported. The long-term success rate has been reported to be around 66%. Table 2 lists recommendations for treatment of inappropriate sinus tachycardia.
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4. Sinus node re-entry tachycardia
a. Definition
Sinus node re-entry tachycardias arise from re-entrant circuits involving the sinus node’s production of paroxysmal, often nonsustained bursts of tachycardia with P waves that are similar, if not identical, to those in sinus rhythm. They are usually triggered and terminated abruptly by an atrial premature beat.
b. Mechanism
Heterogeneity of conduction within the sinus node provides a substrate for re-entry, but it is still not known whether the re-entry circuit is isolated within the sinus node itself, whether perisinus atrial tissue is necessary, or whether re-entry around a portion of the crista terminalis is responsible. The fact that this arrhythmia, like AVNRT, responds to vagal maneuvers and adenosine, however, suggests that sinus node tissue is involved in the re-entrant circuit.
c. Presentation
The incidence of sinus node re-entry tachycardia in patients undergoing electrophysiological study for SVT ranges between 1.8% and 16.9% and up to 27% for those with focal AT. Contrary to popular belief, there is a high incidence of underlying organic heart disease in patients with sinus node re-entry tachycardia. Patients present with symptoms of palpitations, lightheadedness, and presyncope. Syncope is extremely rare, as the rates of the tachycardia are rarely higher than 180 bpm. An important clue for diagnosis is the paroxysmal nature of the attacks.
d. Diagnosis
Sinus node re-entry tachycardia is diagnosed on the basis of invasive and noninvasive criteria 43. Clinically, the following features are highly suggestive of this arrhythmia:
e. Treatment
There have been no controlled trials of drug prophylaxis involving patients with sinus node re-entrant tachycardia. Clinically suspected cases of symptomatic sinus node re-entrant tachycardia may respond to vagal maneuvers, adenosine, amiodarone, beta blockers, nondihydropyridine calcium-channel blockers, or even digoxin. Patients whose tachyarrhythmias are well tolerated and easily controlled by vagal maneuvers and/or drug therapy should not be considered for electrophysiological studies. Electrophysiological studies are indicated for patients with frequent or poorly tolerated episodes of tachycardia that do not adequately respond to drug therapy and for patients in whom the exact nature of the tachycardia is uncertain and for whom electrophysiological studies would aid appropriate therapy. Radiofrequency catheter ablation of persistent sinus node re-entry tachycardias identified through electrophysiological study is generally successful 52.
B. Atrioventricular nodal reciprocating tachycardia.
1. Definitions and clinical features
Atrioventricular nodal reciprocating tachycardia is the most common form of PSVT. It is more prevalent in females; is associated with palpitations, dizziness, and neck pulsations; and is not usually associated with structural heart disease. Rates of tachycardia are often between 140 and 250 per minute.
Although the re-entrant circuit was initially thought to be confined to the compact AV node, a more contemporary view recognizes the usual participation of perinodal atrial tissue as the most common component of the re-entrant circuit. It has been shown convincingly, however, that AVNRT may persist without participation of atrial tissue. Atrioventricular nodal reciprocating tachycardia involves reciprocation between two functionally and anatomically distinct pathways. In most cases, the fast pathway appears to be located near the apex of Koch’s triangle. The slow pathway extends inferoposterior to the compact AV-node tissue and stretches along the septal margin of the tricuspid annulus at the level of, or slightly superior to, the coronary sinus.
During typical AVNRT, the fast pathway serves as the retrograde limb of the circuit, whereas the slow pathway is the anterograde limb (ie, slow-fast AV-node re-entry). After conduction through the slow pathway to the His bundle and ventricle, brisk conduction back to the atrium over the fast pathway results in inscription of the shorter duration (40 ms) P wave during or close to the QRS complex (less than or equal to 70 ms) often with a pseudo-r' in V1 (see Figure 3). Less commonly (approximately 5% to 10%), the tachycardia circuit is reversed such that conduction proceeds anterogradely over the fast pathway and retrogradely over the slow pathway (ie, fast-slow AV-node re-entry, or atypical AVNRT) producing a long R-P tachycardia (ie, atypical AVNRT) but other circuits may also be involved. The P wave, negative in leads III and aVF, is inscribed prior to the QRS. Infrequently, both limbs of the tachycardia circuit are composed of slowly conducting tissue (ie, slow-slow AV-node re-entry), and the P wave is inscribed after the QRS (ie, RP interval more than or equal to 70 ms).
2. Acute treatment
Acute evaluation and treatment of the patient with PSVT are discussed in Sections IV-A and IV-B.
3. Long-term pharmacologic therapy
For patients with frequent, recurrent sustained episodes of AVNRT who prefer long-term oral therapy instead of catheter ablation, a spectrum of antiarrhythmic agents is available. Standard therapy includes nondihydropyridine calcium-channel blockers, beta blockers, and digoxin. In patients without structural heart disease who do not respond to AV-nodal-blocking agents, the class Ic drugs flecainide and propafenone have become the preferred choice. In most cases, class III drugs, such as sotalol or amiodarone, are unnecessary 53. Class Ia drugs, such as quinidine, procainamide, and disopyramide, have limited appeal due to their multidosing regimens, modest efficacy, and adverse and proarrhythmic effects.
A major limitation in evaluating antiarrhythmic agents for treating AVNRT is the general absence of large multicenter, randomized, placebo-controlled studies.
a. Prophylactic pharmacologic therapy
(1). Calcium-channel blockers, beta blockers, and digoxin
Comments regarding the long-term efficacy of calcium-channel blockers, beta blockers, and digoxin taken orally for management of AVNRT are limited by the small number of randomized patients studied. A small randomized (11 patients), double-blinded, placebo-controlled trial showed that verapamil taken orally decreases the number and duration of both patient-reported and electrophysiologically-recorded episodes. A similar finding was demonstrated with doses of 360 to 480 mg/d with a trend toward greater effect with higher doses; however, the study was underpowered to detect a modest difference. Oral digoxin (0.375 mg/d), verapamil (480 mg/d), and propranolol (240 mg/d) showed similar efficacy in 11 patients in a randomized, double-blinded, crossover study. There was no difference among the drugs with respect to frequency or duration of PSVT.
(2). Class I drugs
The data showing efficacy of procainamide, quinidine, and disopyramide are from the older literature and are derived from small studies. These drugs are rarely used for treating AVNRT today. Long-term benefits of oral flecainide in AVNRT were initially shown in an open-labeled study. At doses between 200 and 300 mg/d, flecainide completely suppressed episodes in 65% of patients. Several double-blinded, placebo-controlled trials have confirmed the efficacy of flecainide for prevention of recurrences. Events are reduced when compared with placebo, with an increase in the median time to the first recurrence and a greater interval between attacks. Open-labeled, long-term studies suggest excellent chronic tolerance and safety. In patients without structural heart disease, 7.6% discontinued the drug due to a suboptimal clinical response, and 5% discontinued it because of noncardiac (usually central nervous system) side effects. Class Ic agents (ie, flecainide and propafenone) are contraindicated for patients with structural heart disease. Moreover, class Ic drugs are often combined with beta-blocking agents to enhance efficacy and reduce the risk of one-to-one conduction over the AV node if atrial flutter occurs. Flecainide appears to have greater long-term efficacy than verapamil. Although both drugs (median doses 200 mg/d and 240 mg/d, respectively) have an equivalent reduction in the frequency of episodes, 30% of patients had complete suppression of all symptomatic episodes with flecainide, whereas 13% had complete suppression with verapamil. Discontinuation rates due to adverse effects were equivalent, 19% and 24%, respectively. Propafenone is also an effective drug for prophylaxis of AVNRT. In a double-blinded, placebo-controlled trial, in which time to treatment failure was analyzed, the RR of treatment failure for placebo versus propafenone was 6.8. A single-center, randomized, double-blinded, placebo-controlled study showed that propafenone (300 mg taken three times per day) reduced the recurrence rate to one-fifth of that of placebo.
(3). Class III drugs
Limited prospective data are available for use of class III drugs (eg, amiodarone, sotalol, dofetilide). Although many have been used effectively to prevent recurrences, routine use should be avoided due to their toxicities, including proarrhythmia (ie, torsades de pointes). A placebo-controlled trial found sotalol to be superior to placebo in prolonging time to recurrence of PSVT. With regard to dofetilide, a multicenter, randomized, placebo-controlled study showed that patients with PSVT had a 50% probability of complete symptomatic suppression with dofetilide over a 6-month follow-up (500 µg taken twice per day), whereas the probability of suppression in the control group was 6% (p less than 0.001). There were no proarrhythmic events 53. In this study, dofetilide was shown to be as effective as propafenone (150 mg taken three times per day). Little data exists regarding the effects of amiodarone on AVNRT. In one open-labeled study in the electrophysiology laboratory, IV amiodarone (5 mg · kg–1 · 5 minutes–1) terminated tachycardia in seven out of nine patients. Treatment with oral amiodarone (maintenance dose 200 to 400 mg/d) for 66 plus or minus 24 days prevented recurrence and inducibility in all patients, with its predominant effect being the depression of conduction in the retrograde fast pathway. Of note, amiodarone has been shown to be safe in structural heart disease, particularly LV dysfunction.
b. Single-dose oral therapy (Pill-in-the-Pocket)
Single-dose therapy refers to administration of a drug only during an episode of tachycardia for the purpose of termination of the arrhythmia when vagal maneuvers alone are not effective. This approach is appropriate to consider for patients with infrequent episodes of AVNRT that are prolonged (ie, lasting hours) but yet well tolerated 54, and obviates exposure of patients to chronic and unnecessary therapy between their rare arrhythmic events. This approach necessitates the use of a drug that has a short time to take effect (ie, immediate-release preparations). Candidate patients should be free of significant LV dysfunction, sinus bradycardia, or pre-excitation.
A single oral dose of flecainide (approximately 3 mg/kg) has been reported to terminate acute episodes of AVNRT in adolescents and young adults without structural heart disease, although it offered no benefit compared with placebo in other studies 54.
Single-dose oral therapy with diltiazem (120 mg) plus propranolol (80 mg) has been shown to be superior to both placebo and flecainide in sequential testing in 33 patients with PSVT in terms of conversion to sinus rhythm 54. Favorable results comparing diltiazem plus propranolol with placebo have also been reported by others. Hypotension and sinus bradycardia are rare complications. Single-dose therapy with diltiazem plus propranolol is associated with a significant reduction in emergency room visits in appropriately selected patients 54.
4. Catheter ablation
Targeting the slow pathway along the posteroseptal region of the tricuspid annulus markedly reduces the risk of heart block and is the preferable approach. A prospective, randomized comparison of the fast- and slow-pathway approaches demonstrates equivalent success rates. Advantages of slow-pathway ablation include a lower incidence of complete AV block (1% versus 8%) and the absence of the hemodynamic consequences of marked prolongation of the PR interval. Hence, slow pathway ablation is always used initially and fast pathway ablation is considered only when slow pathway ablation fails.
The NASPE Prospective Catheter Ablation Registry included 1197 patients who underwent AV-nodal modification for AVNRT. Success was achieved in 96.1%, and the only significant complication was a 1% incidence of second-degree or third-degree AV block 55. These data have been confirmed by others 56. Atrioventricular block may complicate slow-pathway ablation caused by posterior displacement of the fast pathway, superior displacement of the slow pathway (and coronary sinus), or inadvertent anterior displacement of the catheter during RF application. Pre-existing first-degree AV block does not appear to increase appreciably the risk of developing complete AV block, although caution is advised. The recurrence rate after ablation is approximately 3% to 7% 56,57.
Ablation of the slow pathway may be performed in patients with documented SVT (which is morphologically consistent with AVNRT) but in whom only dual AV-nodal physiology (but not tachycardia) is demonstrated during electrophysiological study. Because arrhythmia induction is not an available endpoint for successful ablation in this circumstance, the surrogate endpoint of an accelerated junctional rhythm during ablation is a good indication of slow-pathway ablation.
Slow-pathway ablation may be considered at the discretion of the physician when sustained (more than 30 seconds) AVNRT is induced incidentally during an ablation procedure directed at a different clinical tachycardia.
Indications for ablation depend on clinical judgment and patient preference. Factors that contribute to the therapeutic decision include the frequency and duration of tachycardia, tolerance of symptoms, effectiveness and tolerance of antiarrhythmic drugs, the need for lifelong drug therapy, and the presence of concomitant structural heart disease. Catheter ablation has become the preferred therapy, over long-term pharmacologic therapy, for management of patients with AVNRT. The decision to ablate or proceed with drug therapy as initial therapy is, however, often patient specific, related to lifestyle issues (eg, planned pregnancy, competitive athlete, recreational pilot), affected by individual inclinations or aversions with regard to an invasive procedure or the chronicity of drug therapy, and influenced by the availability of an experienced center for ablation. Because drug efficacy is in the range of 30% to 50%, catheter ablation may be offered as first-line therapy for patients with frequent episodes of tachycardia. Patients considering RF ablation must be willing to accept the risk, albeit low, of AV block and pacemaker implantation. Table 3 lists recommendations for long-term treatment of patients with recurrent AVNRT.
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b. Diagnoses
The unifying feature of focal junctional tachycardias is their origin from the AV node or His bundle. This site of arrhythmia origin results in varied ECG manifestations because the arrhythmia requires participation of neither the atrium nor the ventricle for its propagation. The ECG features of focal junctional tachycardia include heart rates of 110 to 250 bpm and a narrow complex or typical BBB conduction pattern. Atrioventricular dissociation is often present (Figure 8), although one-to-one retrograde conduction may be transiently observed. On occasion, the junctional rhythm is quite erratic, suggesting AF. Finally, isolated, concealed junctional extrasystoles that fail to conduct to the ventricles may produce episodic AV block by rendering the AV node intermittently refractory.
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c. Clinical features
Focal junctional tachycardia, also known as automatic or paroxysmal junctional tachycardia, is a very uncommon arrhythmia. It is rare in the pediatric population and even less common in adults. Under the common umbrella of "focal junctional tachycardia" are several distinct clinical syndromes. The most prevalent among these, so-called "congenital junctional ectopic tachycardia" and "postoperative junctional ectopic tachycardia," occur exclusively in pediatric patients and are, therefore, outside of the scope of this document.
Focal junctional tachycardia usually presents in young adulthood. It has been speculated that this form of arrhythmia is an adult extension of the pediatric disorder commonly termed
In pre-excited tachycardias, the QRS is generally wider (ie, more pre-excited) compared with sinus rhythm. A indicates atrial; AP, accessory pathway; AT, atrial tachycardia; AV, atrioventricular; AVRT, atrioventricular reciprocating tachycardia; BBB, bundle-branch block; LBBB, left bundle-branch block; ms, milliseconds; QRS, ventricular activation on ECG; RBBB, right bundle-branch block; SR, sinus rhythm; SVT, supraventricular tachycardias; V, ventricular; VF, ventricular fibrillation; VT, ventricular tachycardia.
