Atrioventricular Reentrant Tachycardia

Atrioventricular reentrant tachycardia (AVRT) occurs in people with an accessory pathway that connects the atrium to the ventricle across the atrioventricular groove, a structure that separates the atria from the ventricles (Figure 1). In patients who are middle-aged or older, atrioventricular nodal reentrant tachycardia (AVNRT) is more prevalent than AVRT. However, in the adolescent population, AVRT may be more prevalent.1 The mean age for the first presentation of AVRT is younger than that for presentation of AVNRT.2 Accessory pathways can be classified by their location and by their ability to conduct anterograde, retrograde, or in both directions.Manifest accessory pathways are those that allow anterograde conduction, and in some cases both anterograde and retrograde conduction. Conversely, pathways that only conduct retrograde are called concealed pathways. Manifest pathways are present in between 0.1% and 0.3% of the population in Western countries.3 Most accessory pathways have properties similar to the myocardium and do not display decremental conduction.4When a manifest pathway allows anterograde conduction during sinus rhythm, the electrocardiogram (ECG) will show preexcitation since traveling anterograde over an accessory pathway will reach the ventricles before normal conduction through the atrioventricular node. This results in a PR interval that is shorter than normal (early ventricular activation). Conduction anterograde over an accessory pathway directly stimulates the ventricles and initiates a cell-to-cell depolarization. This depolarization is slower than His-Purkinje depolarization, and thus the width of the QRS complex will be wider than normal. In addition, with preexcitation, there is a slurring of the initial upstroke of the QRS complex called a delta wave (Figures 2 and 3). Wolff-Parkinson-White syndrome refers to the combination of a manifest pathway with preexcitation in sinus rhythm with known supraventricular tachycardia (SVT) or the presence of symptoms that suggest SVT.4 In concealed pathways that only allow retrograde conduction, there will be no evidence of preexcitation when the patient is in sinus rhythm. The presence of an accessory pathway predisposes the patient to development of tachyarrhythmias. Certain manifest accessory pathways have been shown to cause left ventricular dysynchrony due to premature septal activation. This dyssynchrony can result in left ventricular dysfunction.5,6AVRT results from an electrical circuit comprised of an accessory pathway, the atrioventricular node, the atrium, and the ventricle. There are 2 different forms of AVRT based on the direction of conduction over the accessory pathway (Figure 4).In orthodromic AVRT, conduction travels normally over the atrioventricular node, resulting in normal ventricular depolarization, and then travels retrograde up the accessory pathway. This reentrant circuit will result in a narrow complex tachycardia unless the patient has a preexisting bundle branch block or develops a rate-dependent bundle branch block. In orthodromic tachycardia, there will be a retrograde P wave that is usually seen in the early part of the ST segment (Figure 5).4 Because the P wave is located closer to the prior QRS complex, the rhythm is said to have a short RP interval. Orthodromic AVRT is the most common form of SVT in patients with accessory pathways and accounts for 90% to 95% of the SVTs in patients with manifest accessory pathways.4A unique form of orthodromic AVRT involves a concealed accessory pathway that has decremental conduction properties. This accessory pathway is usually located in the posteroseptal region, and retrograde conduction over this accessory pathway results in what is called a permanent form of junctional reciprocating tachycardia (PJRT). There will be deep inverted P waves in leads II, III, and aVF with a long RP interval.4,7 This particular orthodromic tachycardia is incessant in nature and can lead to a tachycardia-mediated cardiomyopathy, though with treatment, left ventricular ejection fraction can improve.8The remaining 5% to 10% of SVTs in patients with a manifest accessory pathway are called preexcitation AVRT because conduction occurs anterograde over the accessory pathway, thus preexciting the ventricles. Antidromic AVRT is the most common preexcitation AVRT.4 In antidromic AVRT, conduction travels anterograde over the accessory pathway and directly stimulates the ventricles, resulting in a wide complex tachycardia. Conduction then travels retrograde up the atrioventricular node and depolarizes the atria. Antidromic tachycardia will mimic ventricular tachycardia because of the direct ventricular stimulation (Figure 6). At times in antidromic tachycardia, a second accessory pathway may be used for retrograde conduction.4Another unique accessory pathway is a Mahaim fiber, an atriofascicular fiber that connects the right atrium to the distal right bundle branch. The Mahaim fiber conducts anterograde only and has decremental conduction properties. The AVRT involving this fiber travels anterograde over the Mahaim fiber and retrograde up the atrioventricular node,4 resulting in left bundle branch morphology. The pattern of an rS wave in lead III in SR in a patient with a history of palpitations or known SVT should raise suspicion for the presence of a Mahaim fiber as the etiology.9 There are other rare locations of accessory pathways, including those that connect the atrioventricular node to either a fascicle or to the ventricular myocardium. An electrophysiology study is necessary to determine the location of rare accessory pathways.The presence of a manifest accessory pathway can be dangerous if the patient develops atrial fibrillation (AF) with rapid conduction to the ventricles via anterograde conduction over the accessory pathway (preexcited AF). In patients with a manifest accessory pathway, the AVRT may trigger a sustained preexcited AF.4 Any other form of SVT may also conduct rapidly over a manifest pathway. When this occurs, the pathway is considered a bystander pathway because it is not a part of the circuit causing the SVT.4Patients with AVRT may present with syncope, though syncope is not associated with an increased risk of sudden cardiac death(SCD).10 The heart rate alone does not explain syncope in AVRT.11 However, the existence of an accessory pathway that allows anterograde conduction may place the patient at higher risk for SCD, particularly when this anterograde conduction occurs during AF. The accessory pathway may have a very short refractory period, contributing to a rapid ventricular response (Figure 7) that can result in ventricular fibrillation or even SCD.4 The 10-year risk of SCD ranges from 0.15% to 0.24%.12 Sudden cariac death may be the first presentation in patients who have not yet been diagnosed. The risk of SCD in AVRT patients seems to be greatest in the first 2 decades of life.4 Risk factors for SCD include multiple accessory pathways, history of symptomatic tachycardia, and a preexcited R-R interval of <250 ms during AF.12 In one study, risk factors for malignant arrhythmias included (1) a short accessory pathway effective refractory period and (2) AVRT triggering sustained preexcited AF.13 It is difficult to stratify patients at risk for SCD because of the overall low event rate.14 Because of the relatively low risk for SCD in asymptomatic patients, routine invasive testing is often not performed in asymptomatic patients with evidence of preexcitation in sinus rhythm.15Pharmacologic treatment for AVRT can be directed at either the atrioventricular node or the accessory pathway, since both are involved in the reentrant circuit. However, medications that slow conduction through the atrioventricular node are contraindicated in patients at risk for rapid anterograde conduction over the accessory pathway during AF.4 Specific treatment considerations are outlined in this section.Acute treatment for orthodromic AVRT includes use of a vagal maneuver or administration of adenosine. Adenosine will convert orthodromic AVRT 90% to 95% of the time.16 The use of adenosine may result in the development of AF, and the patient may experience rapid conduction over the accessory pathway causing a rapid ventricular response. Equipment should be readily available for cardioversion.4 Intravenous diltiazem, verapamil, or beta-blockers may be used to terminate an orthodromic AVRT only in those patients with no evidence of preexcitation on their resting ECG.4 Synchronized electrical cardioversion should be performed on any patient who is not hemodynamically stable.4Synchronized electrical cardioversion should be a first-line strategy in preexcited AF because of the risk for a rapid and unstable rhythm with the potential to deteriorate into ventricular fibrillation.4 Premature atrial and ventricular contractions may occur after cardioversion (with adenosine or electrical cardioversion) and can precipitate a further episode of AVRT. This is also true if cardioversion is used to treat an orthodromic tachycardia. In this situation, antiarrhythmic agents may be needed to suppress the premature beats.4Two antiarrhythmic agents can be considered in hemodynamically stable patients with AF. Ibutilide or intravenous procainamide may be considered because they both slow conduction over the accessory pathway and have the potential to convert the AF.4 In patients with preexcitation AF, the following medications should not be used: diltiazem, verapamil, beta-blockers, digoxin, and amiodarone. Whereas these medications slow conduction across the atrioventricular node, they enhance conduction over the accessory pathway. Digoxin shortens the refractory period of the accessory pathway, and the other medications enhance accessory pathway conduction by inducing hypotension and causing release of catecholamines.4 Increased conduction over the accessory pathway will accelerate the ventricular rate, thus increasing the risk for ventricular fibrillation.Amiodarone has properties that slow conduction over the accessory pathway and was once a recommended treatment option for patients with AF and anterograde conduction over the accessory pathway. However, amiodarone also slows conduction through the atrioventricular node, and there have been reports of ventricular fibrillation induced by amiodarone administration in patients with accessory pathways.17Catheter ablation is a nonpharmacologic treatment that directly targets the accessory pathway and eliminates its ability to conduct. Catheter ablation is used as a first-line strategy in patients with AVRT or preexcitation AF. The success rate for ablation is between 93% and 95%.12,18,19 In younger patients with preexcitation AF, the AF does not typically recur after ablation of the accessory pathway. However, in older patients, AF is more likely to recur for the same reasons it occurs in the general population.4 Catheter ablation is also used for treatment of PJRT20 and Mahaim pathways.21Long-term Medical Management For patients with AVRT or preexcitation AF who do not want or are not candidates for ablation, class IC antiarrhythmic agents such as propafenone or flecainide can be used if the patient has a structurally normal heart and is free of ischemic heart disease.4 These medications work by slowing conduction over the accessory pathway. Dofetilide or sotalol can be considered in patients with structural or ischemic heart disease. Because of the risk for QT prolongation, these agents are typically initiated in the hospital setting, where serial ECGs are performed.4 Oral digoxin is not used with patients with AVRT or preexcitation AF because it shortens the refractory period of the accessory pathway.4 An oral beta-blocker, diltiazem, or verapamil may be used to suppress AVRT in patients without evidence of preexcitation on a resting ECG.AVRT occurs as a result of an accessory pathway; the mean onset age is younger than those presenting with AVNRT. The type of accessory pathway determines conduction during supraventricular arrhythmias. A manifest accessory pathway may be evident on a resting ECG; however, there may be no evidence of a concealed pathway. The most common form of AVRT is orthodromic tachycardia involving retrograde conduction up the accessory pathway. A manifest accessory pathway allows antegrade conduction and can result in antidromic AVRT, a preexcitation AVRT, or AF with a very rapid ventricular response, preexcitation AF.The type of accessory pathway present (ie, manifest or concealed) must be determined since the type of conduction will dictate the most appropriate intervention and the patient’s risk over time for SCD or other decompensating conditions (eg, ventricular failure, preexcitation AF). Pharmacologic treatments are available to slow conduction across the atrioventricular node or the accessory pathway. Pharmacologic agents that slow conduction across the atrioventricular node must be used cautiously in patients with a manifest accessory pathway. Cardiac ablation is the treatment of choice to give patients with manifest accessory pathways and symptomatic tachycardias.