Atrial fibrillation is the most common persistent arrhythmia. It affects almost 1% of the population, causing very rapid and irregular excitation of the atria, which, if left untreated, is usually transmitted rapidly and irregularly via the atrioventricular node to the ventricles. The symptoms range from palpitations and a disturbingly irregular heartbeat to breathlessness, poor performance and dizziness. A dreaded complication of atrial fibrillation is that the rapid excitation of the atria prevents an orderly pumping process. As a result, the blood flow in parts of the left atrium, especially the so-called atrial appendage, comes to a standstill and blood clots form, which can cause a stroke. For this reason, treatment with an anticoagulant such as Marcumar or new anticoagulants such as Pradaxa or Xarelto is usually necessary to protect against strokes. If anticoagulation is not possible due to an increased risk of bleeding, an atrial appendage closure can also be performed to protect against strokes.

The aim of atrial fibrillation therapy is to make the patient symptom-free. If this is achieved by simply lowering the heart rate ("rate control"), for example with a beta blocker, this is sufficient. If the symptoms persist even with optimal rate control, the aim must be to restore and stabilise the normal heart rhythm - the sinus rhythm - ("rhythm control"). Antiarrhythmic drugs and catheter ablation, i.e. pulmonary vein isolation, are available for this purpose. In pulmonary vein isolation, the pulmonary veins are electrically isolated from the left atrium. The pulmonary veins, i.e. the pulmonary veins, often contain so-called triggers that initiate atrial fibrillation. If the pulmonary veins are electrically isolated from the atrium by ablation, either by radiofrequency current or by freezing, the triggers in the pulmonary veins can no longer trigger atrial fibrillation. Pulmonary vein isolation requires a transseptal puncture, i.e. the atrial septum is punctured with a needle to place the ablation catheter in the left atrium.

AV nodal reentry tachycardia is the most common regular supraventricular tachycardia. It is based on a so-called dual AV node physiology, i.e. the AV node, normally the only structure that transmits excitations from the atrium to the ventricle, consists of two or more conduction pathways with different conduction properties. In the case of premature extra beats from the atrium or the ventricle, so-called extrasystoles, one of the conduction pathways can still be refractory, i.e. unexcitable, while the other can transmit the extra beat. This can lead to a circular excitation in the AV node, the AVNRT, which is accompanied by a high heart rate of usually 150-250/min and is then perceived as palpitations.

The treatment of choice is ablation - i.e. obliteration - of one of the conduction pathways, usually the so-called slow pathway. The chances of success are almost 100% and recurrence after successful ablation is rare (less than 5%). The most important possible complication is complete obliteration of the AV node with subsequent pacemaker dependency, although the risk is low at less than 1%.

In Wolff-Parkinson-White syndrome, or WPW syndrome for short, in addition to the AV node, which is normally the only electrical connection between the atrium and ventricle, there is another, so-called accessory pathway between the atrium and ventricle. These pathways can conduct antegrade, i.e. from the atrium into the ventricle, retrograde, i.e. from the ventricle into the atrium, or in both directions. If these pathways can conduct the excitation antegrade, the surface ECG shows pre-excitation, i.e. premature excitation of the ventricle before the excitation has passed through the AV node. This phenomenon is called a delta wave. If a premature extra beat from the atrium or ventricle hits either only the AV node or only the accessory pathway in the so-called refractory period, the time in which this structure is not electrically excitable, a circular excitation can occur between the atrium and ventricle, a so-called AV reentry tachycardia. This leads to a high heart rate, which is perceived as palpitations. The majority of accessory pathways are located between the left atrium and left ventricle, but there are also right-sided pathways and so-called paraseptal pathways, which are localised in the area of the atrial septum.

The treatment of choice is to locate and obliterate the accessory pathway using a specialised catheter via the inguinal vein or the inguinal artery. As a rule, this is possible with a high success rate of approx. 95% and a very low recurrence rate of approx. 2%. Paraseptal pathways can be problematic if they are very close to the AV node or the so-called His bundle, which are required for normal conduction from the atrium to the ventricle. If these are destroyed during ablation, this can lead to pacemaker dependency. In such cases, cryoablation, i.e. freezing, can be used instead of radiofrequency ablation.

In atrial tachycardia (AT), there are one or more circumscribed areas in the right or left atrium that lead to a high heart rate due to regular discharges or small circular excitations and thus to the perception of palpitations.

The therapy consists of locating and obliterating the areas in the atrium from which the AT originates. Depending on the localisation, the chances of success are 70 to over 90%. Recurrences, i.e. recurrent atrial tachycardia after successful ablation, are rare. Unfortunately, some atrial tachycardias cannot be triggered in the EPU and therefore cannot be treated by ablation.

Typical atrial flutter is a relatively common arrhythmia in which the excitation in the right atrium circles around the tricuspid valve - the heart valve between the right atrium and the right ventricle. This circular excitation results in a high heart rate in the atrium of 200-300/min and is then transmitted to the ventricles via the AV node, usually with a 2:1 to 3:1 conduction. So-called flutter waves are recognisable on the ECG. In addition to the discomfort caused by the usually high heart rate, atrial flutter harbours the risk of a stroke. Treatment with anticoagulants, such as Marcumar, is therefore usually necessary.

The treatment of choice for typical atrial flutter is usually catheter ablation, known as cavotricuspid isthmus ablation. In the circular excitation around the tricuspid valve, the excitation must pass through a relatively narrow muscle bridge, the cavotricuspid isthmus, which lies between the inferior vena cava and the lower part of the tricuspid valve ring. A conduction block is created at this point by the catheter ablation, which means that the circular excitation and therefore the atrial flutter can no longer occur.

Atypical atrial flutter is any atrial fibrillation that is not "isthmus-dependent", i.e. does not pass through the cavotricuspid isthmus in the right atrium between the tricuspid valve ring and the inferior vena cava. These are circular excitations ("macro re-entry") in the right or left atrium, whereby the circular excitation circles around a specific structure (e.g. scar, pulmonary veins, mitral valve, etc.). The usually rapid atrial excitation with frequencies usually between 200 and 350/min is usually transmitted to the ventricle through the AV node in a 2:1 to 3:1 ratio.

Catheter ablation is possible, but much more difficult compared to typical atrial flutter. As a rule, a 3D mapping procedure is necessary; often the atrial septum must be punctured by a transseptal puncture in order to reach the left atrium with the catheter.

Ventricular extrasystoles are additional beats from the ventricle. These are usually harmless, but can be very disturbing if they occur frequently. Only if they occur very frequently can they lead to a deterioration in the heart's pumping capacity in rare cases. One treatment option is to suppress the extra beats with medication, although the chances of success are limited. In the case of very frequent extra beats, there is also the option of catheter ablation. This involves using a catheter to locate the site of origin of the extra beats in the right or left ventricle and sclerosing this site using radiofrequency current. Depending on the localisation, the chances of success of catheter ablation are up to 90%.

Ventricular tachycardias are generally dangerous arrhythmias from the ventricle that harbour the risk of sudden cardiac death. If ventricular tachycardia is detected, secondary prophylactic implantation of a defibrillator (ICD) is often the treatment of choice in order to prevent death from the arrhythmia in the future. Regularly occurring, so-called monomorphic ventricular tachycardias, i.e. those that always originate from the same site, can also be treated by catheter ablation under certain circumstances. To do this, it must first be determined whether there is an underlying heart disease. Sometimes the arrhythmia can also be treated by treating the underlying disease. Catheter ablation requires so-called 3D mapping procedures to create a three-dimensional image of the right and/or left ventricle and to record the electrical activation during the arrhythmia. If the mechanism of the ventricular tachycardia can be clarified, the development of the tachycardia can be prevented by radiofrequency ablation. There are also rare cases of so-called idiopathic ventricular tachycardia, which occur without other heart disease and are usually relatively accessible to catheter ablation.