Atrioventricular reentrant tachycardia (AVRT) is one of the most common supraventricular tachycardias and is caused by the presence of an accessory conduction pathway between the atria and ventricles, creating a reentry circuit responsible for tachycardia. This mechanism results in regular, sudden tachycardia episodes, with a heart rate generally between 150 and 250 bpm. Onset and termination are typically paroxysmal, without a phase of progressive acceleration or slowing.
AVRT may occur in individuals without structural heart disease, often at a young-adult age, but can also be associated with congenital conditions such as Wolff-Parkinson-White (WPW) syndrome, where the accessory pathway is evident even in sinus rhythm. Patients may be completely asymptomatic or experience rapid, regular palpitations, sometimes accompanied by dyspnea, dizziness, or— in more severe cases—syncope.
Diagnosis is based on the electrocardiogram, which in patients with manifest accessory pathways can show the typical delta wave and a short PR interval, while in those with concealed pathways, the diagnosis may only be confirmed during tachycardia. Acute treatment includes vagal maneuvers, antiarrhythmic drugs, or electrical cardioversion in unstable cases. In patients with recurrent or symptomatic episodes, catheter ablation is the definitive therapy.
AVRT is caused by the presence of an accessory conduction pathway, an abnormal structure connecting the atria and ventricles directly, bypassing the atrioventricular node. These pathways may be manifest, visible on ECG in sinus rhythm as a delta wave, or concealed, undetectable until tachycardia is induced.
Under normal conditions, the electrical impulse travels from the atria to the ventricles through the AV node, with a physiological delay allowing proper ventricular filling. In AVRT, the presence of an accessory pathway creates the possibility of a reentry circuit, which can develop in two ways:
Atrioventricular reentry is usually triggered by an atrial or ventricular extrasystole, activating the accessory pathway at a time when the AV node is refractory. If conduction is unidirectional, the impulse can circulate repeatedly between atria and ventricles, generating tachycardia.
Factors such as sympathetic overactivity, stress, physical exercise, or electrolyte disturbances can modulate the refractoriness of the AV node and accessory pathway, facilitating the initiation and perpetuation of the reentry circuit.
AVRT is generally benign, but in subjects with Wolff-Parkinson-White syndrome or accessory pathways with very rapid conduction, it can increase the risk of dangerous ventricular arrhythmias. When the accessory pathway can conduct at very high rates, an episode of atrial fibrillation may degenerate into ventricular fibrillation, representing a cardiological emergency.
In patients with prolonged episodes, reduced diastolic time may result in decreased cardiac output, with possible hypotension and symptoms of acute heart failure in predisposed individuals. Furthermore, when tachycardia occurs frequently, the heart may undergo electrophysiological remodeling that increases susceptibility to recurrences and favors the development of other supraventricular arrhythmias.
AVRT can be classified according to the reentry circuit mechanism and the conduction pattern via the accessory pathway.
This is the most common form and occurs in patients with an accessory pathway with retrograde conduction, allowing the impulse to reenter the atria from the ventricles through the abnormal pathway, after anterograde conduction via the AV node. The ECG during tachycardia shows:
This is the most common form and occurs in patients with an accessory pathway with retrograde conduction, allowing the impulse to reenter the atria from the ventricles through the abnormal pathway, after anterograde conduction via the AV node. The ECG during tachycardia shows:
__STASH_2__Less common, this occurs when the accessory pathway conducts anterogradely, while retrograde conduction occurs via the AV node. In this case, the ECG shows a wide QRS, as ventricular activation does not follow the normal conduction system.
In WPW patients, the accessory pathway is active even in sinus rhythm, producing an ECG with delta wave and a short PR interval. These patients are at risk of dangerous ventricular tachycardias in case of atrial fibrillation with rapid conduction through the accessory pathway.
Atrioventricular reentrant tachycardia (AVRT) is a condition linked to the presence of an accessory conduction pathway that enables reentry of the electrical impulse between atria and ventricles. The predisposition is congenital, but clinical manifestation depends on several factors. The age of onset is variable, although AVRT occurs more frequently in young adults. Some patients discover the accessory pathway incidentally, while others develop symptomatic tachycardias even in childhood.
The main predisposing factor is the presence of an abnormal electrical connection between the atria and ventricles, which in some cases is visible on ECG during sinus rhythm, as in Wolff-Parkinson-White (WPW) syndrome. However, the mere presence of an accessory pathway does not necessarily result in tachycardia episodes. The initiation of AVRT is often influenced by stress, intense physical activity, or electrolyte imbalances, which alter the refractoriness of the AV node and accessory pathway, facilitating the establishment of the reentry circuit.
Prevention is based on identifying and managing triggering factors. In patients with sporadic episodes, avoiding stimulating substances such as caffeine, alcohol, and nicotine can reduce the frequency of episodes. In individuals with WPW and highly conductive accessory pathways, primary prevention involves arrhythmic risk assessment via electrophysiological study, with possible indication for catheter ablation to prevent potentially dangerous arrhythmic events.
AVRT presents with episodes of sudden and regular tachycardia, with a rate between 150 and 250 bpm. Onset is typically paroxysmal, without a phase of progressive acceleration. Patients often report a triggering event, such as physical exertion, intense emotions, or abrupt postural changes.
The main symptom is rapid and regular palpitations, often described as strong and sudden heartbeats. In patients with more prolonged episodes, reduced cardiac output may lead to dyspnea, asthenia, and exercise intolerance. In those with very rapidly conducting accessory pathways, AVRT may cause excessive ventricular acceleration, with risk of hypotension and syncope. In rare cases where tachycardia persists for long periods, tachycardiomyopathy may develop, resulting in impaired ventricular function.
In patients with WPW syndrome, anamnesis may reveal tachycardia episodes preceded by irregular heartbeats, suggesting the possible presence of atrial fibrillation with abnormal conduction. This aspect is crucial because, in WPW patients, atrial fibrillation may transform into potentially fatal ventricular tachycardia.
During an AVRT episode, the patient exhibits a regular tachycardia with a rapid, well-perceptible pulse. Blood pressure is generally preserved, but in those with prolonged episodes or reduced cardiac reserve, hypotension may occur. Cardiac auscultation reveals tachycardic, rhythmic heart sounds, without the irregularities typical of atrial arrhythmias.
In WPW patients, the physical exam may be unremarkable at baseline, but during tachycardia, signs of sympathetic overactivity such as sweating and agitation may be observed. In more severe cases, if tachycardia causes reduced cerebral perfusion, transient neurological symptoms such as confusion or near-syncope may appear.
Clinical assessment is essential for distinguishing AVRT from other supraventricular tachycardias. Rhythm regularity, absence of visible P waves or presence of retrograde P waves, and response to vagal maneuvers are useful for orienting the diagnosis before instrumental confirmation with ECG and electrophysiological study.
The diagnosis of atrioventricular reentrant tachycardia (AVRT) is based on the clinical identification of regular tachycardia episodes and the electrocardiographic confirmation of an accessory pathway. Diagnostic suspicion arises in patients reporting sudden and regular palpitations, often associated with paroxysmal high-frequency tachycardia episodes. In subjects with Wolff-Parkinson-White (WPW) syndrome, the presence of wide QRS tachycardia or episodes of atrial fibrillation with very rapid conduction may indicate a higher arrhythmic risk.
During an AVRT attack, the physical exam reveals a regular and tachycardic pulse, with rates typically between 150 and 250 bpm. In patients with prolonged episodes, reduced diastolic filling time may lead to hypotension and, rarely, signs of acute heart failure. In subjects with brief, self-limiting episodes, the clinical evaluation may be completely normal between attacks.
The electrocardiogram (ECG) is the main tool for AVRT diagnosis and enables distinction between orthodromic and antidromic forms. During a tachycardia episode, the tracing shows specific features:
In patients with WPW syndrome, the resting ECG may reveal a delta wave, characterized by early ventricular depolarization and a short PR interval. This sign indicates a manifest accessory pathway, predisposing to the risk of ventricular arrhythmias if associated with atrial fibrillation.
In patients with sporadic episodes not documented by standard ECG, prolonged monitoring can help confirm the diagnosis. Depending on episode frequency, the following may be used:
When the diagnosis is unclear, pharmacological tests may be performed to assess the nature of the tachycardia. Adenosine administration is especially useful for distinguishing AVRT from other supraventricular tachycardias. This drug transiently blocks AV node conduction, immediately interrupting tachycardia in cases of orthodromic AVRT. Lack of response to adenosine suggests a non-AV node-dependent tachycardia, such as atrial tachycardia or atrial flutter.
Vagal maneuvers, such as the Valsalva maneuver or carotid sinus massage, can slow AV conduction and interrupt the arrhythmia, providing an additional diagnostic clue.
In patients with recurrent episodes, severe symptoms, or risk of ventricular arrhythmias, electrophysiological study (EPS) is the most accurate diagnostic method. This procedure enables:
In high-risk WPW patients, EPS is essential to evaluate the need for definitive treatment before potentially fatal arrhythmias occur.
The management of atrioventricular reentrant tachycardia (AVRT) is based on three main strategies: interruption of the acute episode, prevention of recurrences, and, in patients with frequent episodes or at risk, definitive therapy with catheter ablation. Treatment choice depends on symptom severity, episode frequency, and the presence of an accessory pathway with high-risk conduction characteristics.
In patients with an acute AVRT episode, the first therapeutic approach involves vagal maneuvers, which increase parasympathetic tone and slow conduction through the AV node. The Valsalva maneuver and carotid sinus massage can be attempted in stable patients, with variable success rates. If vagal maneuvers do not interrupt tachycardia, intravenous adenosine is administered, temporarily blocking AV conduction and interrupting AVRT in most cases.
In patients in whom adenosine is ineffective or contraindicated, beta-blockers or non-dihydropyridine calcium channel blockers (verapamil, diltiazem) may be used to reduce AV conduction and favor tachycardia termination. Electrical cardioversion is reserved for hemodynamically unstable patients or tachycardias refractory to drug therapy.
In patients with sporadic, well-tolerated episodes, management involves avoiding triggers and monitoring clinical progression. However, in those with frequent or symptomatic tachycardias, long-term pharmacological therapy may be necessary. The most commonly used drugs for episode prevention are beta-blockers and non-dihydropyridine calcium channel blockers, which reduce AV node conduction and decrease the likelihood of tachycardia initiation.
If these drugs are ineffective, class IC antiarrhythmics such as flecainide and propafenone may be considered. However, these drugs should be avoided in patients with structural heart disease due to the risk of proarrhythmic effects. In patients with Wolff-Parkinson-White (WPW) syndrome and rapidly conducting accessory pathways, pharmacological therapy may not sufficiently reduce the risk of rapid ventricular arrhythmias, making catheter ablation evaluation necessary.
In patients with recurrent episodes, disabling symptoms, or high arrhythmic risk, catheter ablation with radiofrequency is the treatment of choice. This procedure, performed during electrophysiological study, allows elimination of the accessory pathway responsible for reentry, with a success rate above 95%. Ablation is particularly indicated in patients with anterograde-conducting WPW, in whom the accessory pathway may facilitate chaotic atrial rhythm conduction to the ventricles, increasing the risk of ventricular fibrillation.
The risk of ablation complications is low, but in rare cases, injury to the normal conduction pathway may occur, requiring permanent pacemaker implantation. For this reason, the procedure must be performed by experienced operators, with careful pre-procedural assessment of accessory pathway characteristics.
The prognosis of AVRT is generally favorable, especially in patients without structural heart disease. In those responding well to vagal maneuvers or drugs, episodes can be managed effectively without further intervention. However, in patients with very frequent episodes or severe symptoms, quality of life can be significantly compromised, necessitating a more aggressive therapeutic strategy.
In patients treated with catheter ablation, the rate of complete arrhythmia resolution is very high, and most no longer require drug therapy. The risk of recurrence is low and occurs mainly in the first months after the procedure. In WPW patients with rapidly conducting accessory pathways, ablation drastically reduces the risk of potentially fatal ventricular arrhythmias, significantly improving long-term prognosis.
In patients with very frequent, untreated episodes, there is a risk of tachycardiomyopathy, a condition in which sustained high heart rate over time may cause reversible ventricular dysfunction. Therefore, in patients with recurrent tachycardias, early assessment is advisable to determine the most appropriate therapeutic strategy.
Atrioventricular reentrant tachycardia (AVRT) is generally considered a benign arrhythmia, but in some cases, it may cause complications affecting the patient's quality of life and, in rare situations, represent a risk for hemodynamic stability. The severity of complications depends on episode duration and frequency, the presence of a rapidly conducting accessory pathway, and underlying heart disease.
In patients with very frequent episodes or sustained tachycardias over long periods, chronic heart rate elevation can lead to left ventricular overload and progressive contractile dysfunction. This condition, known as tachycardiomyopathy, is potentially reversible with arrhythmia control, but in advanced cases may require specific management to recover myocardial function.
In patients with structural heart disease or reduced cardiac reserve, prolonged AVRT episodes may decrease ventricular filling and result in hypotension, leading to syncope or near-syncope. This risk is higher in those with very rapidly conducting accessory pathways, where high-frequency tachycardia may impair coronary perfusion and cardiac output.
In some patients, especially those with very frequent AVRT episodes, repetitive atrial stimulation may promote the development of atrial fibrillation. In those with Wolff-Parkinson-White syndrome, the presence of an anterograde-conducting accessory pathway increases the risk of atrial fibrillation with very rapid ventricular conduction, a potentially dangerous condition that may degenerate into ventricular fibrillation.
Catheter ablation is considered the definitive treatment for AVRT, with a high success rate and low complication risk. However, in a small percentage of patients, injury to the normal conduction pathway may occur, resulting in complete atrioventricular block and requiring permanent pacemaker implantation. This event is rare (<1%) but represents the main complication of the procedure.