Dr Oliver Segal

Atrioventricular reentrant tachycardia (AVRT) is a type of supraventricular tachycardia (SVT) that causes a rapid, racing heartbeat due to a congenital accessory pathway. This creates an electrical ‘short circuit’ between the heart's upper and lower chambers.  In most people, there’s only one route from the atria to the ventricles – via the AV node, which lies in the middle of the heart. 

The atria and ventricles usually separate during this process leaving the AV node as the only electrical connection between these chambers. However, in about 1 in every 700-1000 people, small strands of tissue are left between these chambers, and they can conduct electricity. As there are two routes between the atria and ventricles, electricity can conduct down one and back up the other, and so on, leading to a short circuit, or ‘reentry’ (see figure).

When electricity conducts down the AV node and back up the accessory pathway (as in the diagram above on the right), it is known as orthodromic reentrant tachycardia (ORT) and when it goes in the opposite direction it is called antidromic tachycardia. ORT is much more common than antidromic tachycardia. They have different ECG appearances but are otherwise treated in much the same way.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of supraventricular tachycardia. Although it’s harmless, it’s uncomfortable due to a short circuit in the heart's electrical system that causes sudden episodes of a rapid, regular heartbeat.

In 75% of the population, the AV node effectively consists of a single pathway. However, in the remaining 25%, there are 2 different pathways in the node and one conducts electricity faster than the other. Hence they are known as the fast and slow AV nodal pathways.

In a very small number of people with 2 AV nodal pathways, electricity can sometimes go down the slow pathway and then turn around and go back up the fast pathway (and even more rarely the other way around). This sets up an abnormal reentry circuit called AVNRT and causes tachycardia and palpitations. It also occurs in about 1 in every 700 people.

Atrial tachycardia is a type of SVT in which the upper chambers of the heart (the atria) fire abnormal electrical signals, causing the heart to beat faster than normal. It’s highly manageable and often curable. Atrial tachycardia can occur at any age, and medicine is often effective for treating this arrhythmia, but catheter ablation may also provide a cure.

There are broadly three different types of treatment for SVT.

1. Conservative measures – All SVTs, particularly AVRT and AVNRT, may be stopped by performing what is called a Valsalva manoeuvre. This manoeuvre is performed by bearing down (as if going to the toilet) and usually holding one’s breath at the same time. Alternative techniques include blowing into a paper bag or syringe, splashing your face with cold water, drinking ice-cold water, rubbing the side of your neck for 5 seconds or even pressing gently on your eyeballs. It is important a properly trained physician teaches the last two techniques to you. If these manoeuvres are not successful, injection of a drug called adenosine (administered in an A&E department) or verapamil is usually successful at rapidly restoring normal rhythm and is useful in confirming the diagnosis.

2. Anti-arrhythmic drugs – There are various drugs that can be taken to try to prevent episodes of SVT, although they are used infrequently for AVNRT and AVRT where ablation is the norm. Drugs include beta-blockers, verapamil, flecainide, sotalol, propafenone and sometimes amiodarone. They all have different side effect profiles and would usually need to be taken long term. If SVT attacks are rare, it is often not sensible to take a preventative medication every day, so these can be taken as a ‘pill-in-the-pocket’ instead. This means the drug is taken after an attack has started to try and limit its duration. As catheter ablation is so successful for most SVTs, it is not usually necessary for patients to take medications for long periods any more.

3. Catheter ablation for SVT – Ablation involves a procedure where fine wires are advanced from veins at the top of the leg to the heart. Pacing the heart can then induce SVT. Heat applied from the tip of one of the wires causes a tiny area of localized tissue damage (the tissue is cauterized, or more properly ‘ablated’). This destroys one limb of the abnormal circuit and so cures the arrhythmia. The abnormal limb in AVRT is the accessory pathway, in AVNRT it is the AV nodal slow pathway and in atrial tachycardia the focal spot it is arising from is the abnormality or part of a reentry circuit.

Ablation of SVT has very high success rates – >95% chance of a permanent cure with one procedure, and ablation can be repeated if necessary if it recurs.

The principal risk of ablation in SVT is damage to the normal wiring of the heart (the AV node). If this does not resolve, a pacemaker needs to be implanted to stop the heart from beating too slowly. This is a risk in ablation of AVNRT (the AV nodal slow pathway is always somewhere near the AV node itself) and of accessory pathways or atrial tachycardias that lie close to the AV node. Fortunately, most accessory pathways and atrial tachycardias are not located close to the AV node. The usually quoted risk of AV node damage requiring a pacemaker for SVT ablation is <1% or 1 in 200. Ablation in areas very close to the node may have a risk as high as 2-5%.

Accessory pathways are most often located on the left side of the heart – somewhere along the mitral valve, which lies between the left atrium and left ventricle. A procedure called transseptal puncture is required to access this region with catheters (see figure below). A long metal needle is introduced from the top of the leg into the heart. It is advanced through the wall between the right and left atria (the inter-atrial septum). The hole created allows passage of a long plastic sheath over the needle, which can then be used to introduce an ablation catheter. Risks include making a hole in an outer wall of the heart, leading to blood leaking out into the cavity around the heart, a complication called pericardial tamponade. The risk of this happening is less than 1%. If it occurs, it can usually be successfully treated with temporary insertion of a small tube under the ribs. If this doesn’t work, surgery can be required, but this is very rare. Another theoretical risk of ablating on the left side of the heart is causing a stroke, although this would be exceptionally rare. The hole created in the inter-atrial septum by transseptal puncture usually heals itself. Even if it does not, it does not cause any further problems.

Wolff-Parkinson-White (WPW) syndrome is a congenital heart defect, meaning it’s present at birth. An extra electrical pathway between the heart's upper and lower chambers causes the heart to beat abnormally fast (tachycardia) and symptoms often emerge in adulthood. 

Dr Segal can help you to successfully manage symptoms with medication or with a minor surgical procedure.

People born with an accessory pathway which conducts electricity from the atria to the ventricles have an abnormal ECG appearance called pre-excitation. This is because the area of the ventricle connected to the accessory pathway is activated earlier than normal. People with a pre-excited ECG and who also have AVRT are said to have the Wolff-Parkinson-White Syndrome (or WPW for short). People with a pre-excited ECG are often said to have a ‘WPW’ ECG, although this is technically incorrect, as the ECG alone is insufficient to make this diagnosis.

In addition to causing palpitations (the abnormal reentry circuit of AVRT), Wolff-Parkinson-White Syndrome has another important implication. People with accessory pathways are known to occasionally get another rhythm called atrial fibrillation (AF). This is a rapid, chaotic rhythm confined to the atria causing rapid, irregular palpitations. Unlike the AV node, some accessory pathway can conduct electricity very rapidly. This type of pathway will allow lots of the abnormal signals from the atria during an episode of atrial fibrillation to conduct to the ventricles. This is known as pre-excited AF. This rhythm is potentially dangerous as it can degenerate into a lethal heart rhythm called ventricular fibrillation, which causes cardiac arrest and death. This risk is very small, but nevertheless clearly very important. It sometimes means ablation is performed to destroy the pathway even if a patient has never had palpitations or AVRT. This is known as asymptomatic pre-excitation.

The distinction is important as it is known that people with WPW have a slightly higher risk of dying suddenly due to pre-excited AF than people with asymptomatic pre-excitation. For this reason, all people with WPW Syndrome (i.e. patients with pre-excitation and symptoms due to AVRT) are typically offered ablation as first line treatment. If you have asymptomatic pre-excitation, the risk of dying suddenly is thought to be very small indeed, perhaps 1 in every 10,000 people with this condition. An electrophysiology study can be performed to calculate the speed electricity conduct down an accessory pathway in order to determine the future risk of sudden death, although this is not routine. If it conducts very rapidly, ablation may still be performed to prevent pre-excited AF from occurring but it is quite reasonable not to perform an EP study in this setting as the risk of dying is so small.