Introduction

Supraventricular arrhythmias encompass tachycardias that require atrial or atrioventricular (AV) nodal tissue for initiation and maintenance (Box 39.1). The duration of symptoms may be paroxysmal or incessant. Origins include atrial musculature, AV nodal tissue, sinus node and pulmonary veins.^1–4 There are several forms which can be categorized as AV node dependent or AV node independent (Box 39.2).

Paroxysmal supraventricular tachycardia (PSVT) is generally a narrow complex tachycardia that excludes atrial flutter, atrial fibrillation and multifocal atrial tachycardia. Its incidence is 35 per 100 000 persons and higher in females.^1,2 PSVTs associated with cardiovascular disease typically occur in older males and often originate in atrial tissue.⁵ More than 50% of these patients also have associated atrial fibrillation.⁶

Typical symptoms from PSVT include palpitations, light-headedness, and chest pain. Overt syncope is rare.^1,7 However, some patients are minimally symptomatic. PSVTs are prognostically benign rhythms and often well tolerated. Hemodynamic compromise is uncommon but is more likely to occur in patients with significant structural heart disease. Incessant forms of PSVT can cause a tachycardia-mediated cardiomyopathy. Tachycardia-mediated cardiomyopathy can be reversed by either preventing the arrhythmia or control of the ventricular response either by pharmacologic or ablative treatments. Several studies have documented an improvement in left ventricular ejection fraction after catheter ablation in patients who had PSVT with rapid rates.^8,9

SVT mechanisms include re-entry, automaticity, and triggered activity.^4,10 Automaticity is a disorder of impulse initiation. It occurs when the sinus node impulse is blocked or slowed. This allows ectopic pacemakers located in the atria, coronary sinus, pulmonary veins or AV junction to reach threshold and overdrive the sinus node. Impulse formation may also occur when the sinus node is exposed to excessive adrenergic stimulation or reduced vagal input, resulting in inappropriate sinus tachycardia.¹¹

Rarely, SVTs may be secondary to triggered activity.¹⁰ Triggered activity is a disorder of impulse conduction, mainly repolarization, in which the previous action potential or summation of action potentials creates depolarizing oscillations in the membrane potential. Early afterdepolarizations (EAD) occur during phase 2 or phase 3 of the action potential. Late or delayed afterdepolarizations (DAD) occur during phase 4 of the action potential. These afterdepolarizations are capable of reaching the membrane potential threshold and initiating a new action potential. An example of a triggered arrhythmia is non-paroxysmal atrial tachycardia with block secondary to digitalis toxicity.¹² Steinbeck et al demonstrated an increase in rate secondary to a shift of the dominant pacemaker cells to a group of cells near the sinoatrial border in rabbit atrial preparations exposed to ouabain, suggesting that these triggered foci are not in the SA node but in the perisinus atrium.¹³ DAD is associated with calcium overload.

Re-entry is the most common mechanism for SVT.^1,2,4,10,14 Sixty percent of re-entry is AV nodal, 30% is atrioventricular re-entry, 10% is atrial or sinoatrial re-entry tachycardia. If the tachycardia is secondary to re-entry, initiation and termination of the tachycardia are reproducible with programmed electrical stimulation.¹⁰

History and physical examination are important and can give clues to mechanism and type of arrhythmia. If there is a gradual increase in rate with initiation or decrease with termination, automaticity is likely. Abrupt initiation and termination favor re-entry. An irregular rhythm may be more suggestive of atrial fibrillation, atrial flutter or multifocal atrial tachycardia.

A 12-lead ECG is helpful in the evaluation of PSVT. The morphology and relationship between P waves and the QRS (PR or RP) are helpful in making a more specific diagnosis and allow the diagnosis of atrioventricular nodal re entrant tachycardia (AVNRT) or atrioventricular re-entrant tachycardia (AVRT) in 80-85% of cases.¹⁵ Once the rhythm has been terminated, the tachycardia should be compared to a resting 12-lead electrocardiogram. However, 20% of ECG interpretations may incorrectly characterize PSVT. Therefore, a 12-lead ECG should not be the sole diagnostic test to determine mechanism.¹⁶

Vagal maneuvers such as Valsalva, the diving reflex, breath holding, and carotid sinus massage can be helpful in terminating tachycardia or in revealing clues to the etiology of the arrhythmia (Class I, Level B).^1,16 Intravenous adenosine can also be used to aid in the diagnosis. AVNRT and AVRT are excluded if tachycardia persists with block in the AV node. If the tachycardia is not terminated by vagal maneuvers and IV adenosine, the most likely etiology is an AV node-independent tachycardia. Intravenous AV node blocking agents, such as IV verapamil or diltiazem, may be attempted if adenosine fails to help therapeu-tically and/or clarify the mechanistic diagnosis.

An echocardiogram may be useful if there is a suspicion of structural heart disease. Findings are useful in determining if patients can be treated with class IC agents or help in defining anatomy and/or congenital defects in patients prior to an ablation procedure.^1,7 Thyroid function and electrolytes should be evaluated. Electrophysiology study is helpful in patients in whom the mechanism and etiology cannot be determined with the above information and also in those patients with a history of tachycardia but no documented tachycardia on 12-lead ECG or Holter monitor. Patients with continued symptoms despite AV nodal blocking agents and those who desire to maintain normal rhythm with an antiarrhythmic agent are appropriate to refer for an electrophysiology study. Patients with hemo-dynamically unstable SVT, patients who do not wish to take medications but are interested in invasive catheter ablation, patients with evidence of pre-excitation, and those with a wide complex tachycardia requiring differentiation of SVT from VT are also candidates for an electro-physiology study.^1–3

Acute management of SVT focuses on termination or conversion of SVT to sinus rhythm or control of ventricular rate. Intravenous L-type calcium channel antagonists have proven efficacious for acute management of narrow complex hemodynamically stable SVT^1,17–20 (Class I, Level A). Verapamil and diltiazem are calcium channel antagonists which slow or depress the effects of sinus node and AVN function by inhibiting membrane transport of calcium. Sung et al studied the conversion rate of SVT to sinus rhythm in 20 patients with re-entrant SVT randomized to verapamil or placebo. Fifteen of 19 patients converted to sinus versus 1/16 patients with placebo.¹⁸ Waxman et al confirmed in a double-blind randomized trial that IV low-and high-dose verapamil were superior to placebo in slowing the ventricular rate and converting PSVT to sinus rhythm.¹⁹ The IV Diltiazem Study Group determined that the conversion rate by IV diltiazem (0.05 mg/kg) was 84%. The limitation of diltiazem and verapamil therapy is hypotension.²⁰

Adenosine is an alpha-1 receptor inhibitor in cardiac muscle cells. It prevents the influx of calcium into the cell and thus depresses conduction of the SA node and AVN.²¹ It has been proven through double-blind randomized placebo-controlled trials to be as efficacious and safe as verapamil.^22,23 Glatter et al evaluated 229 patients with SVT during an electrophysiology study and determined that the rate of conversion to sinus rhythm with adenosine was 85% for AVRT and 86% for AVNRT.²² This is comparable to the conversion rate with verapamil.²⁰ DiMarco et al evaluated the efficacy and safety of adenosine in two prospective, randomized trials. Results of this study determined that the rate of adverse events/side effects was 36%, were typically mild and lasted less than 1 minute. Also, when compared to verapamil, time to termination was much faster, occurring in 30 seconds.²³ Adenosine is an effective treatment for the acute termination of narrow complex SVT (Class I, Level A).¹ However, recurrence rate of SVT after adenosine was found to be 57% within 5 minutes of adenosine.²⁴

There are no large randomized double-blinded placebo-controlled trials evaluating the efficacy and safety of selective beta-1 adrenergic blockers, digoxin or amiodarone (Class IIb, Level C).¹ Evidence is based on small clinical trials, expert opinion and clinical experience. Intravenous esmolol and metoprolol were proven to decrease ventricular rate by 15% in patients with SVT.^25,26 Patients were also able to be switched to oral digoxin, propranolol, verapamil, metoprolol and quinidine successfully without losing therapeutic effect.²⁵ Short-term intravenous amiodarone has a high rate of conversion of SVT to sinus rhythm with low risk of toxicity.^27,28 Vietti-Ramus et al demonstrated that high-dose IV amiodarone had an 88% conversion rate and 100% conversion if atrial flutter and atrial fibrillation were excluded. Time to conversion was between 30 minutes and up to 20 hours.²⁷ Given safer and better options as noted above, intravenous amiodarone for acute symptoms of SVT is a Class IIb, Level C recommendation.¹

The goals of long-term management of PSVT are arrhythmia suppression or significant decrease in frequency and duration of symptomatic episodes. If PSVT recurrence rates are high, long-term management with an antiarrhythmic or catheter-based ablation should be considered. Fle-cainide is a class IC antiarrhythmic that is proven efficacious and safe in the treatment of PSVT (Class IIa, Level B). Henthorn et al performed a double-blind placebo-controlled trial evaluating time to first recurrence in 34 patients with PSVT.²⁹ The time to first recurrence in the flecainide group was 55 days compared to 11 days with placebo. Freedom from symptoms during 60 days was 70% of the flecainide group and 15% of the placebo group. Anderson et al performed a similar double-blind placebo-controlled trial evaluating chronic therapy with flecainide to increase the time to recurrent SVT.³⁰ Of patients on flecainide, 82% were symptom free versus 24% on placebo. There were no proarrhythmic events or deaths during treatment with fle-cainide. In a multicenter trial evaluating the safety and efficacy of oral flecainide (100–200 mg bid), 87% of patients improved symptomatically.³¹ Minor subjective side effects such as headache, dizziness and abnormal vision occurred but these were rarely severe enough to necessitate discontinuation of flecainide.

Propafenone, a class IC agent with beta-adrenergic blocker properties, has also been proven efficacious and safe in the long-term management of PSVT^1,32 (Class IIa, Level B). A 6-month randomized placebo-controlled trial evaluating recurrence rates after treatment with 300 mg tid, 300 mg bid, and 150 mg bid of propafenone compared with placebo revealed that the recurrence rate in the propafenone group was one-fifth of that seen in the placebo group.³³ In the UK Propafenone PSVT Study Group, 100 patients with PSVT, paroxysmal atrial fibrillation or atrial flutter were evaluated comparing propafenone 300 mg bid or tid and placebo. This therapy was proven efficacious and safe for the prophylaxis of recurrent PSVT. Patients who could tolerate higher doses of propafenone had a trend towards fewer episodes compared to when treated with lower doses.³⁴

Multiple class III antiarrhythmics have been evaluated in the long-term treatment of PSVT. A multicenter randomized, double-blind placebo-controlled trial has been performed with sotalol to evaluate its efficacy and safety (Class IIa, Level C). Recurrent SVT was less frequent in the sotalol group versus placebo. There were no adverse events of cardiac death, heart failure or proarrhythmia in patients receiving either 160 mg or 80 mg bid.³⁵

Amiodarone was assessed in 121 patients with atrial tachyarrhythmias refractory to digoxin, beta-blockers, and other antiarrhythmics over 27 months and 81% did not have recurrent episodes.³⁶ Amiodarone was discontinued in 6% because of adverse side effects.³⁶ Therefore, amiodarone can be used as long-term management of PSVT for pharmacologic control but is generally not used due to long-term end-organ toxicity (Class IIa, Level C).

The efficacy of dofetilide was compared to propafenone and placebo in 122 patients over 6 months. The endpoints were episode-free periods and reduction in the frequency of symptomatic PSVT, assessed using diaries and event recorders. Episode-free rates were 50% in the dofetilide group, 54% in the propafenone group and 6% in the placebo group.³⁷ The results of this study confirmed that dofetilide, a class III antiarrhythmic agent, was as efficacious as propafenone in preventing recurrence and in decreasing frequency of PSVT (Class IIa, Level C). Although an effective alternative, the use of dofetilide is usually limited to the treatment of AF/atrial flutter due to its proarrhythmia potential (Class IIa, Level C).

The pill-in-the-pocket method has been evaluated in the management of PSVT that occurs infrequently.³⁸ This approach can effectively terminate SVT and reduce hospitalizations and cost of care. Alboni et al evaluated the conversion rate within 2 hours and the safety profile of a single oral dose of flecainide, diltiazem and propranolol, and placebo in 33 patients with inducible SVT during electro-physiology studies.³⁹ The conversion rate was 52% for placebo, 61% with flecainide and 94% with combination diltiazem and propranolol.³⁹ Patients were discharged on the most effective medication for conversion based on results of electrophysiology study. At 1 year, the rate of emergency room consultation decreased from 100% at baseline to 9%. Adverse events included hypotension, bradycardia and an episode of syncope.³⁹

Catheter ablation for the treatment of PSVT is a first-line acceptable alternative to pharmacologic therapy in very symptomatic patients or in patients with high-risk professions seeking a definitive cure (Class I, Level B).^1,40 Cure rates for AVNRT and AVRT are greater than 95% with low risks of heart block, tamponade, and vascular complications.⁷ Catheter ablation improves quality of life and reduces healthcare costs in symptomatic patients compared to pharmacologic management.⁴⁰

Sinus tachycardia

Atrial tachycardia

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