Introduction

Reentrant supraventricular tachycardia (SVT) involving the AV node, comprising either AV node reentry (AVNR) or AV reciprocating tachycardia (AVRT), readily responds to a variety of pharmacologic agents. The comments herein will be confined to pharmacologic therapy for tachycardia involving the AV node.

Intravenous Drugs

Initial measures to terminate SVT should include vagal maneuvers. If unsuccessful, termination can be achieved with antiarrhythmic drugs whose primary effects increase refractoriness and/ or decrease conduction (negative dromotropic effect) over the AV node. These drugs can have direct (e.g., verapamil blocks the slow-inward calcium current of the AV node) or indirect effects (e.g., digoxin increases vagal tone to the AV node). In most patients, the drug of choice is either adenosine or verapamil. The advantages of adenosine include its rapid onset of action (usually within 10-25 seconds via a peripheral vein), short half-life (less than 10 seconds) and high degree of efficacy.¹ Its short half-life minimizes the severity of side effects, such as facial flushing, chest tightness, dyspnea and transient sinus arrest and/or atrioventricular block. In general, adenosine has an excellent safety record, but pause-dependent torsade de pointes may infrequently occur and transient atrial fibrillation may occur due to shortening of the atrial action potential. Fortunately, atrial fibrillation usually resolves within 2 minutes of its onset, but it highlights the potential difficulties that may develop in patients with preexcitation who receive adenosine for the purpose of terminating orthodromic reciprocating tachycardia. Adenosine should be given with caution to patients with bronchospasm and is contraindicated in those with sinus node dysfunction or second- or third-degree heart block. Dipyridamole potentates adenosine's effects by blocking its cellular uptake and aminophylline blunts its effects by competitive receptor antagonism. The effective dose of adenosine is usually 6-12 mg, given as a rapid bolus. Doses up to 12 mg terminate over 90% of paroxysmal SVT episodes.² Sequential dosing can be given at 60 second intervals due to adenosine's rapid metabolism. In AV node reentry the most common site of termination is the anterograde slow pathway. Termination may also occur indirectly, i.e., due to adenosine - induced atrial or ventricular premature beats.

Calcium channel blockers such as verapamil (5-15 mg) or diltiazem (0.25 mg/ kg given over 2 minutes and, if needed, an additional dose of 0.35 mg/ kg or continuous infusion of 15 mg/ kg) are also effective drugs. Verapamil's efficacy is similar to that of adenosine's, but its negative inotropic effect, vasodilatatory effects and prolonged half-life make it unsuitable for patients with congestive heart failure or for those who are hypotensive.

Intravenous beta-blockers including propranolol (1-3 mg) and esmolol (500 mcg/ kg over 1 minute and 50 mcg / kg/ min infusion over 4 minutes) are also useful for acute termination. Digoxin (0.5-1.0 mg) is considered the least effective of the 4 categories of drugs that are available, but is a useful alternative when there is a contraindication to the other agents.

Chronic Therapy

The decision to treat SVT with oral antiarrhythmic drugs depends on the frequency and duration of the arrhythmia as well as on the severity of symptoms. For patients requiring therapy who are reluctant to undergo radiofrequency catheter ablation, antiarrhythmic therapy remains a viable alternative.

Verapamil, diltiazem and beta-blockers are the drugs of choice for AV nodal reentry. In patients who do not respond, class IC and III drugs can be considered. These drugs suppress conduction over the retrograde fast AV nodal pathway and in patients with AV reciprocating tachycardia they suppress conduction over the accessory pathway. Because the effects of class IC drugs like flecainide can be reversed by isoproterenol, a beta-blocker is often added to the regimen.

Few randomized trials have been performed to assess the efficacy of calcium channel blockers, beta-blockers and digoxin in SVT. A comparison of verapamil, propranolol and digoxin showed equivalent efficacy in a small group of patients.³ However, in general calcium channel blockers and beta-blockers are preferred to digoxin. The combination of diltiazem and propranolol has been shown to move effective than flecainide alone when administered as a single oral dose.⁴ Potential complications of using a calcium channel blocker and beta-blocker in combination include hypotension, sinus bradycardia and AV block. Class IA drugs such as procainamide, quinidine and disopycamide are seldom used.

The efficacy of flecainide in SVT has been confirmed in double-blind, placebo controlled trials.^5,6 Flecainide should be reserved for patients who have no evidence of structural heart disease. In this group of patients flecainide is well tolerated. Propafenone has also been shown to be effective in SVT. The recurrence rate of tachycardia with propafenone is 20% of that which occurs with placebo.⁷

Class III drugs, although rarely used for AV node reentry, can suppress the arrhythmia. Placebo -controlled trials show that sotalol and dofetilide are superior to placebo.^8,9 Dofetilide has a favorable safety profile in these patients when the dose is appropriately calibrated for decreased creatinine clearance and QT interval.

Amiodarone has also been shown to be effective in SVT, although is used rarely.

Summary

The drugs of choice for the acute termination of SVT are adenosine and verapamil. In patients with hypotension, myocardial dysfunction or preexcitation, adenosine should be given. For chronic oral therapy in AV node reentry, calcium channel blockers and beta-blockers are preferred. These drugs are also effective in AV reciprocating tachycardia as are class IC drugs.

References

1. Lerman BB, Belardinelli L. Cardiac electrophysiology of adenosine. Basic and clinical concepts. Circulation 83:1499-1509, 1991.

2. DiMarco JP, Miles W, Akhtat M, Milstein S, Sharma AD, Platia E, McGovern B, Scheinman MM, Govier WC. Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group. Ann Intern Med 113:104-110, 1990.

3. Winniford MD, Fulton KL, Hillis LD. Long-term therapy of paroxysmal supraventricular tachycardia: A randomized, double-blind comparison of digoxin, propranolol and verapamil. Am J Cardiol 54:1138-1139, 1984.

4. Alboni P, Tomasi C, Menozzi C, Bolton N, Paparella N, Fuca G, Brignole M, Cappato R. Efficacy and safety of out-of-hospital self-administered single-dose oral drug treatment in the management of infrequent, well-tolerated paroxysmal supraventricular tachycardia. J Am Coll Cardiol 37:548-553, 2001.

5. Anderson JL, Platt ML, Guarnieri T, Fox TL, Maser MJ, Pritchett EL. Flecainide acetate for paroxysmal supraventricular tachyarrhythmias. The Flecainide Supraventricular Tachycardia Study Group. Am J Cardiol 578-584, 1994.

6. Henthorn RW, Waldo AL, Anderson JL, Gilbert EM, Alpert BL, Bhandari AK, Hawkinson RW, Pritchett EL. Flecainde acetate prevents recurrence of symptomatic paroxysmal supraventricular tachycardia. The Flecainide Supraventricular Tachycardia Study Group. Circulation 86:119-125, 1991.

7. Pritchett EL, McCarthy EA, Wilkinson WE. Propafenone treatment of symptomatic paroxysmal supraventricular arrhythmias: A randomized, placeb-controlled, crossover trial in patients tolerating oral therapy. Ann Intern Med 114:539-544, 1991.

8. Wanless RS, Anderson K, Joy M, Joseph SP. Multicenter comparative study of the efficacy and safety of sotalol in the prophylactic treatment of patients with paroxysmal supraventricular tachyarrhythmias. Am Heart J 133:441-446, 1997.

9. Tendera M, Wnuk-Wojnar AM, Kulakowski P, Malolepszy J, Kozlowski JW, Krzeminska-Pakula M, Szechinski J, Droszcz W, Kawecka-Jaszczk, Swiatecka G, Ruzyllo W, Graffo. Efficacy and safety of dofetilide in the prevention of symptomatic episodes of paroxysmal supraventricular tachycardia: 6-month double-blind comparison with propafenone and placebo. Am Heart J 142:93-98, 2001.