Sves I49.4

Supraventricular extrasystole (SVES) refers to an extrasystole originating above the His bundle (Nicholas 2011) and triggered by the atrial myocardium (Heaton 2022).

Extrasystoles (ES) belong to the heterotopic stimulation disorders (Herold 2022).

One differentiates - depending on the origin of the excitation - between:

• ventricular ES
• supraventricular ES (Herold 2022)

SVES belong to the normo-frequency arrhythmias (Block 2006), fall prematurely into the actual basic rhythm and disturb it (Block 2006). They always arise above the His bundle (van Aken 2007) and can originate from the sinus node, atrium, or AV node (Striebel 2015).

SVES are divided according to their origin into:

• Sinus- ES: Here the excitation comes directly from the sinus node. Recognizable in the ECG by the prematurely incident P- wave. The sinus beat after the SVES occurs at the same interval that 2 sinus beats would have in succession (Haas 2011).
• Atrial ES: The excitation originates from the atrium. This results in a prematurely incident P- wave, which is often deformed or biphasic. Depending on the exact location of the excitation center, an altered P- vector occurs. The PQ- time can vary depending on the distance to the AV- node. SVES originates frequently in the lower sections of the atrium and is recognizable in the ECG by a negative P in II, III, aVF (Haas 2011).
• Nodal- ES (Block 2006): They are also called AV- nodal- ES or junctional ES and can occur with or without delayed retrograde atrial excitation. As the name implies, the excitation originates from the AV node. The former classification into upper, middle and lower AV nodes is hardly used nowadays (Herold 2022). The atrium is retrogradely excited, recognizable in the ECG by negative P waves in II, III, aVF. The P- wave itself can appear before, in or after the QRS- complex (Haas 2011).

Further classification of SVES:

• Aberrant transitioned SVES (Haas 2011): In aberrant SVES, a broadened QRS morphology occurs. The SVES runs over the AV node and meets a still refractory Tawara limb. This blockage causes an abnormal propagation of the excitation into the ventricles, which leads to a widening of the QRS morphology (Kalkreuth 2013).
• Blocked SVES: In a very early-onset SVES in which the conduction system is still refractory, the QRS- complex is absent in antegrade conduction disturbance, and the P- wave is absent in retrograde conduction disturbance (Herold 2022).
• Non-compensated pause: SVES depolarizes sinus excitation with displacement of the actual basic rhythm. This decreases the distance between pre- and postextrasystolic cardiac action. This is referred to as a non-compensated pause (Herold 2022).
• Graft wave: A graft wave may occur when a nodal ES causes simultaneous atrial and ventricular contraction against the still-closed mitral and tricuspid valves. The patient experiences this as an unpleasant bang (Greten 2010).

SVES occur very frequently, preferably in cardiac healthy individuals (Haas 2011). The prevalence increases with age (Greten 2010).

Triggers for SVES can be:

• Idiopathic:

In otherwise healthy individuals, triggers for SVES may include: overtiredness, emotional arousal, consumption of coffee, nicotine, alcohol (Herold 2022), cocaine (Haas 2011).

• Paroxysmal atrial fibrillation:

In this case, there is increased ectopic atrial activity predominantly from the pulmonary vein area

• Fever
• Infections (van Aken 2007)
• Acidosis
• Hypoxia
• In the setting of cardiac diseases such as myocarditis, CHD (Haas 2011), hypertrophic cardiomyopathy, valvular heart disease, septal defects, etc. (Heaton 2022)
• Congenital heart defects that result in atrial strain.
• In cases of atrial surgery
• Medication-induced, e.g. digitalis, antiarrhythmics, sympathomimetics
• Electrolyte disturbances, especially hypokalemia, hypercalcemia, hypomagnesemia (Haas 2011)
• Biochemical due to malformations of sodium channels, in BMP2- mutations:

The latter may be the cause of pulmonary hypertension (Heaton 2022).

SVES is an automatic center located above the His bundle (Haas 2011).

In this case, the premature contraction covers the entire heart and usually shows atrial and ventricular complexes in mutual relation on the ECG. The ventricular complexes are normal because the extra stimulus originates above the His bundle and can therefore propagate along normal conduction pathways into the ventricles of the myocardium (Roskamm 2013).

Meanwhile, the most common predilection sites of SVES are known:

- Crista terminalis

- Mouth of superior and inferior vena cava

- Ostium of the coronary sinus

- Mouth sites of pulmonary veins (Herold 2022).

Most of the time, the patient does not feel SVES. Sometimes, however, he complains of palpitations (Haas 2011). The patient notices the occurrence of a graft wave (see classification) as an unpleasant bang (Greten 2010).

The diagnosis usually consists of a resting ECG, long-term ECG, stress EC G and echocardiography (Herold 2022).

• 12- channel ECG

SVES are characterized in the ECG by:

- Change of the PQ- time (Herold 2022)

- Premature collapse of the P-wave

- Slight deformation of the P-wave

- The cardiac action following the ES shows no compensatory pause (Block 2006).

- Negative P in II, III, aVF:

Arises from SVES originating in the inferior segment of the atrium and leading to caudo- cranial excitation of the atrium. Found in atrial ES and nodal ES (Haas 2011).

- Negative P in I and aVL:

Occurs in nodal ES (Haas 2011).

This is an SVES with a left atrial origin (Schuster 2005).

- Negative P waves before, in or after the QRS complex:

These can occur in nodal SVES (Haas 2011).

- QRS- complex of SVES is normal in shape and width in most cases (Block 2006), QRS- duration is < 120 ms (Kasper 2015).

The only exception is early-onset SVES - also known as aberrant SVES (Herold 2022). In this case, the excitation runs over the AV node and encounters a still refractory Tawara limb. Due to this blockage, an abnormal propagation of the excitation into the ventricles takes place, resulting in a widened QRS morphology (Kalkreuth 2013).

- PR interval: This can be shortened, normal, or prolonged (Heaton 2022).

• Long-term ECG: Long-term ECG should focus particularly on the occurrence of paroxysmal supraventricular tachycardia or intermittent atrial fibrillation (Herold 2022). Often SVES occur in patients with paroxysmal atrial fibrillation due to increased atrial activity from the pulmonary vein area in a salvo-like fashion (Greten 2010).
• Exercise ECG: Used to assess exercise-related symptoms (Kasper 2015).
• Echocardiography: In patients with clustered SVES, echocardiography should always be performed to rule out structural heart disease in terms of need for therapy and prognostic significance (Heaton 2022).

- Checking the electrolytes (Heaton 2022) especially K, Mg, Ca

- CK / CK- MB

- Troponin I

- TSH

- drug levels

- Drug screening (Haas 2011)

Arrhythmic etiologies such as:

- VES

Here, as in aberrant SVES, there is a widening of the QRS complex. However, SVES is recognizable by the preceding P-wave (Herold 2022).

- Junctional contractions

- Narrow or wide complex tachycardias (Heaton 2022).

Non-arrhythmic etiologies such as:

- Acute coronary syndrome

- Diseases of the heart valves (especially mitral valve prolapse)

- pericarditis

- heart failure

- Complications after pacemaker implantation (Heaton 2022)

Non-cardiac causes:

- Panic attacks

- Side effects of prescribed drugs

- Consumption of (illegal) drugs

- pulmonary embolism

- hyperthyroidism

- Anemia (Heaton 2022)

• Heart failure:

Signs of heart failure may occur with consistent SVES (Heaton 2022).

• Supraventricular tachycardia:

With an appropriate disposition such as dual AV nodal physiology or accessory pathways, SVES can trigger supraventricular tachycardias (Haas 2011).

• Ischemic Apoplexy (Heaton 2022).
• Sudden cardiac death:

Sudden cardiac death may occur exclusively and only in rare cases in patients with severe cardiac disease such as hypertrophic cardiomyopathy or Wolff- Parkinson-White syndrome (Kasper 2015).

Healthy patients do not require any therapy if SVES occurs. Only the occurrence of paroxysmal supraventricular tachycardia or intermittent atrial fibrillation should be treated (Herold 2022), as it has been shown that patients suffering from symptoms due to atrial ectopy are more likely to develop subclinical atrial fibrillation, which may subsequently lead to apoplexy (Larsen 2015).

If cardiac disease is present, it should be treated appropriately (Herold 2022).

Healthy patients should be made aware that SVES can be avoided by avoiding certain triggers such as alcohol, nicotine, coffee, overtiredness, emotional arousal. However, if symptoms and SVES persist, Heaton (2022) recommends pharmacologic treatment with low-dose beta-blockers .

In patients with cardiomyopathy, heart failure, and atrial fibrillation associated withSVES, further interventional therapy is indicated. These may include atrial pacing, catheter ablation, thoracoscopic ablation (Heaton 2022).

In earlier years, supraventricular extrasystoles - in the absence of structural heart disease - were thought to be harmless, requiring no therapy (Rath 2005). Meanwhile, increasing evidence implicates the role of symptomatic (clustered) SVES with atrial fibrillation and apoplexy. However, further research is needed in this area (Marcus 2015).

In contrast, in patients with underlying diseases, the occurrence of SVES may herald early mortality (Heaton 2022).

In addition, the clustered occurrence of SVES is associated with the development of atrial fibrillation or atrial flutter and an increased risk of cardiac - or all-cause - mortality (Heaton 2022). Eckart (2021) points out that SVES from the left atrium in particular play a central role in the development of AF and atrial flutter.

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