Ves I49.3

The cardiologist Bernhard Lown, born in 1921, achieved the first successful cardioversion for atrial fibrillation in 1963 (Weber 2018).

The classification of ventricular extrasystoles was established by Bernhard Lown in 1971 and named after him as the "Lown Classification" (Weber 2018).

VES is the acronym for ventricular extrasystole. Ventricular extrasystole is a premature contraction of the ventricles triggered by an electrical impulse that does NOT originate from the sinus node, but rather from the Purkinje system of the ventricles (Larsen 2022).

In the ECG, VES are recognizable by the different QRS morphology and the altered QRS vector compared to the basic rhythm (Paul 2018).

VES are divided into:

• Left ventricular extrasystoles.

In left ventricular ES, the QRS complex is prolonged to > 0.11 sec. The ECG shows a right bundle branch block-like deformed QRS complex (Haas 2011).

• Right ventricular extrasystoles

Right ventricular ES also prolong the QRS complex to > 0.11 sec. The ECG shows a left bundle branch block-like deformed QRS complex (Haas 2011).

• Bundle-stem VES

The bundle-branch ES are the only ones without a widening of the QRS complex. Otherwise, however, they fulfill the characteristics of ES with undisturbed sinus rhythm and compensatory pause (Herold 2022).

• Unifocal VES / Monomorphic VES:

Unifocal ES are extrasystoles originating from the same focus. Therefore, they show the same QRS morphology in the ECG (Kasper 2015). They can occur in cardiac health as well as in organic diseases (Herold 2022).

• Multifocal VES / Polymorphic VES.

In multifocal ES, different ventricular sites are found from which the ES originate. This is recognizable in the ECG by the different QRS morphologies (Kasper 2015). Polymorphic ES occur exclusively in organic myocardial disease and indicate myocardial damage (Herold 2022).

• Full compensatory pause:

When a VES occurs, retrograde excitation of the atria occurs. This triggers discharge of the sinus node in approximately 50% of cases. If this impulse does not interfere with sinus rhythm, the next sinus stimulus follows a normal interval. This is called a full compensatory pause (Gertsch 2008).

• Non-full compensatory pause:

If retrograde excitation of the atria interferes with the impulse of sinus rhythm when a VES occurs, there will be a premature onset of the sinus beat. In this case, one speaks of a non-full compensatory pause (Gertsch 2008).

See also above "Full compensatory pause".

• Bigeminal (1:1 extrasystole):

In bigeminy, monotopic ES are found in relation to the normal rhythm: Each normal action is followed by a VES:

Normal action (N) - VES (E) - NE - NE - NE. (Herold 2022)

• Trigeminal:

Here, too, polymorphic VES are related to the normal rhythm. However, each normal action is followed by two VES (definition in Germany).

Definition of the trigeminal nerve in Germany: NEE - NEE - NEE.

Definition of trigeminal in the USA: NNE - NNE - NNE (Herold 2022).

• 2: 1- Extrasystole:

In this case, extrasystole occurs after 2 normal beats. If VES occurs after every 3rd normal beat, it is called 3: 1- extrasystole.

NNE - NNE - NNE or NNNE - NNNE - NNNE (Herold 2022)

• Couplet:

In this case, 2 VES occur in succession. NEE - N - N (Herold 2022)

• Triplet:

Denotes the occurrence of 3 VES in succession (Haas 2011) NEEE - N - N.

• Volleys:

If at least three or more VES occur consecutively in the ECG - without a normal beat in between - , this is referred to as volleys.

NEEE - N - N - (Herold 2022)

• R on T- Phenomenon:

If a VES occurs very early, there is a risk that the VES will fall in the vulnerable phase of T. This may cause ventricular fibrillation (Herold 2022).

• Classification of VES according to Lown in long-term ECG:

- Simple VES

- Grade 0: No VES

- Grade I: Monomorphic VES< 30 / h

- Grade II: Monomorphic VES > 30 / h

- Complex VES

- Grade III a: Polymorphic VES

- Grade III b: Ventricular bigeminus

- Grade IV a: Couplets

- Grade IV b: Volleys

- Grade V: R on T phenomenon (Herold 2022)

Nowadays, however, the Lown classification is no longer used (Braun 2022).

Ventricular extrasystoles are the most common form of arrhythmia (Gertsch 2008). They occur in 3-20% of the general population. It is not uncommon for them to be detected incidentally during routine testing (Klewer 2022).

The proportion of idiopathic VES is about 10%. The incidence increases with age, with an age-adjusted incidence of symptomatic VES being higher in women than in men (46.2 vs. 20.5 per 100,000). Approximately 1 / 3 of these patients experience non-sustained ventricular tachycardia (NSVT) and / or supraventricular reentry tachycardia (SVT). (Muser 2021)

The most common site of origin of idiopathic VES is the right ventricular outflow tract with left bundle-branch block-like configuration of the QRS complex (see also "Localization"), accounting for approximately 80% (Muser 2021).

(Kasper 2015)

The incidence of sudden cardiac death due to the occurrence of VES is <0.1%/year (Ector 2021).

- Myocardial ischemia

- hypoxia

- abnormalities of electrolytes (especially hypokalemia)

- increased sympathetic tone (Kasper 2015)

- Digitalis intoxication (in this case, bigeminal and trigeminal symptoms occur in particular [Herold 2022])

- hyperthyroidism (Haas 2011)

- congenital heart defects

- inflammatory heart diseases

- cardiac tumors (Paul 2018)

- Certain medications such as catecholamines, quinidine, atropine, antiarrhythmics, theophylline

- Intoxication with alcohol, barbiturates (Wolff 2012).

- idiopathic (Ip 2017)

Risk factors for VES are:

- increasing age

- arterial hypertension

- little physical activity

- smoking

- obesity (Marcus 2020)

In VES, premature contraction of the chambers occurs. Depolarization occurs first in the chamber in which the VES originated and only then in the other chamber (Kasper 2015). Premature excitation can be triggered by:

- an increased automaticity

- a triggered automaticity

- a reentry mechanism (Haas 2011).

The ECG shows a dissociated and deformed ventricular complex (Roskamm 2013), as excitation propagation away from the ventricular focus through the ventricular myocardium is slower. This results in a QRS- complex that is typically broadened to > 0.12 s (Kasper 2015). The broadening and deformation are more pronounced the more distal the origin of the VES (Haas 2011).

VES arise below the bifurcation of the His- bundle (Herold 2022), predominantly in the peripheral or proximal His- Purkinje system (Wolff 2012).

VES can originate from:

- a focus of the myocardial or Purkinje cells, which is capable of automatism

- a triggered automaticity

- from a re-entry through areas with scars

- a diseased Purkinje system (Kasper 2015)

• Left bundle branch block-like configuration

The sequence of ventricular ES depends on the initial site of ventricular excitation. Therefore, QRS morphology can be used to infer the site of origin within the ventricles. In arrhythmias originating in the right ventricle or septum, much of the left ventricle is activated late. Recognizable in the ECG by a prominent S-wave in V1 and the left bundle-branch block-like configuration of the QRS complex (Kasper 2015).

• Right bundle-branch block-like configuration

Arrhythmias originating in the wall of the left ventricle show a prominent positive deflection in V1 and a right bundle branch block-like configuration of the QRS complex (Kasper 2015).

• Downward axis

This is found when the first to be excited is the cranial ventricle. In the ECG, dominant R waves are found in leads II, III, and AVF (Kasper 2015).

• Upward axis

The upward axis with dominant S- waves in II, III, and AVF indicates the onset of activation in the inferior wall (Kasper 2015).

• Ectopy

Evidence of ectopy includes smooth, uninterrupted contours of the VES with sharp QRS deviations detectable on the ECG. Wide notches, on the other hand, and indistinct QRS- deviations indicate myocardial disease (Kasper 2015).

• Discordant T-wave

In this case, the deflection of the T-wave is opposite to the deflection of the QRS complex (Haas 2011).

• Combination systole / fusion beat

The QRS complex appears as a mixture between a VES and a sinus beat. Thus, depolarization of the ventricles occurs partly from the VES and partly from the sinus beat (Haas 2011).

• His-bundle extrasystole.

The VES appears as a prematurely dipping QRS- complex that is narrowed and followed by a compensatory pause (Haas 2011).

The majority of those affected do not perceive any symptoms. Otherwise, the following symptoms may exist:

- Palpitations:

Extrasystoles are noticed as palpitations by about 30% of affected persons. These give heart stumbles or dropouts as symptoms. Only a proportion of them feel ill due to the extrasystoles (Herold 2022).

- Feeling of weakness, dizziness:

These result from prolonged periods of bigeminy with a drop in cardiac output (Braun 2022).

- Dyspnea:

Since extrasystoles cause an unconscious reaction of the autonomic nervous system, palpitations can trigger an anxiety reaction up to a panic attack in affected persons. They may then complain of dyspnea, chest tightness, etc. (Meismann 2021).

- (Cardiac) syncope:

If syncope or presyncope occurs in patients with VES, it may indicate orthostatic hypotension, reflex-mediated neurocardiogenic syncope, or cardiac disease or a genetic syndrome. If the V. a. latter exists, the risk of sudden cardiac death is increased. In this case, hospitalization with monitoring and detailed diagnostics should be performed (Kasper 2015).

Syncope or presyncope can be caused by volleys or by triggering ventricular tachycardia in VES (Haas 2011).

The diagnosis of a VES is usually initially determined on a resting ECG. For further localization, recording with a 12-lead ECG is recommended (Kasper 2015).

In the family history, in particular, any cardiomyopathies or sudden deaths should be inquired about (Kasper 2015).

This should be followed by a long-term ECG for further verification. Further diagnostics consist of ergometry, echocardiography (Herold 2022) and, if necessary, cardiac MRI (Braun 2019).

12- channel ECG

The ECG typically shows:

- P- wave is absent (in the majority of cases)

- widening of the QRS complexes deformed like a leg block (Haas 2011)

- prematurely dipping QRS complexes (Braun 2022)

- discordant T-wave

- combination systole / fusion beat (Haas 2011) see also "localization".

- subsequent compensatory pause (Braun 2022)

Long-term ECG

The frequency of VES can be clarified in the long-term ECG (Haas 2011). Usually, more VES are found during the day than at night (Braun 2022).

Detection or exclusion of possible volleys and ventricular tachycardia can be performed, as well as monitoring the success of antiarrhythmic therapy (Haas 2011).

Exercise ECG

This should be performed in patients with a history of exercise-induced VES and a history of coronary artery disease (Kasper 2015). In general, VES that increase with exercise or during the recovery phase should be considered more severe (Haas 2011).

Echocardiography

Echocardiography should assess in particular:

- ventricular function

- evidence of cardiomyopathy

- evidence of ventricular hypertrophy

- Evidence of disease of the heart valves (Kasper 2015).

Cardiac magnetic resonance imaging

MRI is used to assess cardiac structure, cardiac function, and characterize myocardial tissue (Muser 2021).

The examination should be performed with late gadolinium enhancement to visualize any ventricular scars that may be present. In addition, artherosclerotic coronary artery disease should be excluded (Kasper 2015).

If VES is clustered, the following blood tests are useful:

- Serum electrolytes

- CK / CK- MB

- Troponin I

- TSH

- Drug levels especially if taking digitalis and theophylline

- Drug screening (Haas 2011)

- Aberrant SV ES (Haas 2011)

Aberrant SVES is characterized by a widened QRS morphology. Here, 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 widened QRS morphology (Kalkreuth 2013).

- (Reversible) cardiomyopathy (Latchamsetty 2019).

In idiopathic VES, the occurrence of cardiomyopathy is possible if > than 15% of cardiac actions are VES on long-term ECG. Cardiomyopathy is reversible if a substantial reduction in VES is achieved (Braun 2022).

However, if this is not the case, progressive left ventricular dysfunction and heart failure may occur (Muser 2021).

- Decrease in ventricular function

- Ventricular dilatation (Latchamsetty 2019).

- Risk factor for developing heart failure increases with increasing incidence of VES

- sudden cardiac death (Marcus 2020).

In organic heart disease such as acute myocardial infarction, VES can be harbingers of life-threatening arrhythmias, including ventricular fibrillation. Harbingers include:

- clustered polytopic and polymorphic VES

- bigeminy

- couplets

- volleys

- R on T phenomenon (Herold 2022)

see also "Classification

• - VES in organically healthy individuals:

Organically healthy individuals do not usually require therapy for VES. However, if there is an increasing limitation of cardiac function, as is the case in the rare tachycardia-induced cardiomyopathy, or if the patient complains of subjective complaints, therapeutic measures are advisable (see below).

(Herold 2022)

• - VES in organically proven heart disease:

Here, one differentiates between causal and symptomatic therapy (Herold 2022).

Causal therapy is the most important and, with regard to prognosis, the most decisive form of treatment. In the case of CHD , for example, it is revascularization (Herold 2022).

See also "Internal therapy".

Symptomatic therapy consists of:

- Checking the potassium and magnesium balance.

In case of deficiencies, substitution to high-normal serum levels is recommended (Herold 2022).

• Antiarrhythmic therapy:

- Indications for antiarrhythmic drugs are:

- increased risk of sudden cardiac death due to e.g. ventricular fibrillation

- complex VES in patients with limitation of left ventricular pump function or severe underlying myocardial disease (Herold 2022)

- symptomatic idiopathic VES (Muser 2021).

In patients with idiopathic VES, the indication for antiarrhythmic therapy is in the case of

- frequently occurring VES, i.e., > 15% of cardiac actions are VES

- echocardiographic evidence of left ventricular dysfunction

- Occurrence of warning arrhythmias, ie:

- Occurrence of volley-like VES with limitations in exercise capacity.

- occurrence of syncope (Braun 2022)

When these warning arrhythmias occur, there is always a risk of sudden cardiac death due to the onset of ventricular fibrillation (Braun 2022).

In these patients, the use of class I antiarrhythmic drugs or beta-blockers is indicated as a basic measure (Braun 2022).

• Beta-blockers:

Antiarrhythmics of 1st choice are beta-blockers without intrinsic sympathomimetic activity for patients with impaired pumping capacity and Z. n. myocardial infarction (Herold 2022).

• Calcium channel blockers:

If beta-blockers do not produce the desired outcome, therapy with non- dihydropyridine calcium channel blockers is indicated. Dosing should be at the lowest effective dose, except in patients with recent myocardial infarction or existing heart failure. Here, the maximum tolerated dose should be titrated (Muser 2021).

• Sodium Channel Blockers:

If therapeutic success cannot be achieved with both beta blockers and calcium channel blockers, therapy with sodium channel blockers such as flecainide or propafenone is recommended. However, sodium channel blockers are contraindicated in the presence of existing coronary artery disease, heart failure, or severe left ventricular hypertrophy (Muser 2021).

• Amiodarone:

In patients with VES-induced cardiomyopathy , amiodarone has been shown to improve symptoms and left ventricular function (Muser 2021)

Class I antiarrhythmic drugs are contraindicated in patients with structural heart disease, e.g., heart failure, CHD, because they may worsen prognosis. Similarly, amiodarone and sotalol show no prognostic advantage, even leading to worsening of prognosis in patients with NYHA III . In all these cases, an implantable cardioverter- defibrillator (ICD) is recommended (Herold 2022).

• Checking digitalis levels:

Digitalis levels should be checked in digitized patients. The therapeutic serum level is

- Digoxin: generally 0.8 - 2.0 ng / ml, in heart failure 0.5 - 0.8 ng / ml

- Digitoxin: generally 9 - 30 ng / ml, in heart failure no data (Karow 2021).

- Calcium: Ca2+ enhances the effect of digitalis and thus promotes toxicity (Karow 2021)

- Potassium: Hyperkalemia increases the risk of AV block (Lemmer 2007).

Any digitalis intoxication can be treated as follows:

Immediate cessation of digitalis intake.

Promote elimination of digitalis by:

Antidote treatment with Fab antibody fragments such as DigiFab (Böhm 2000). Dosage:

- if the amount of digitalis is known: 80 mg of antidigoxin- Fab binds 1 mg of digoxin, so that the digoxin- level decreases by 1ng / ml and for digitoxin by 10 ng / ml (Flake 2021).

- If the amount of digitalis is unknown: bolus 160 mg as a short infusion in 5% glucose over 20 min, then 20 mg / h over 12 h (Flake 2021)

In case of recent intoxication e.g. suicidal intent:

- Detoxification measures in the form of:

- Gastric lavage for a time interval < 1 h.

- administration of activated charcoal

- in case of intoxication with digitoxin:

- additional use of exchange resins such as colestipol or colestyramine

- Hemoperfusion:

- however, does not work in case of intoxication with digoxin

- Hemodialysis and peritoneal dialysis are not suitable for glycoside elimination (Böhm 2000).

- Symptomatic therapy of digitalisin intoxication in the form of:

- temporary pacemaker

- Atropine for bradycardia (Herold 2022) Dosage: 1mg atropine i. v. (Böhm 2000)

- For ventricular extrasystoles, tachycardia and ventricular flutter use of:

- Magnesium 20 mval i. v. (2 mval = 1 mmol / l (Hartig 2004).

- Phenytoin 100 mg i. v.

- Lidocaine 100 mg i. v.

- defibrillation

- Cardioversion (Böhm 2000)

• Radiofrequency catheter ablation (CA) (Muser 2021).

CA is usually more effective than treatment with antiarrhythmic drugs (Ene 2019).

Indications are:

- idiopathic VES, in which

- monomorphic VES consist of a singular arrhythmic focus (Braun 2022)

- antiarrhythmic therapy is ineffective, not tolerated, or long-term treatment is not preferred, and in addition, there is V. a. cardiomyopathy triggered by VES

- frequent and symptomatic VES (Cronin 2020)

- In focally triggered atrial fibrillation due to VES that has been shown to be refractory to antiarrhythmic drugs (Cronin 2020).

The best results can be achieved with CA when there is a singular arrhythmic focus and it can be easily reached with the ablation catheter as is the case, for example, when located in the right or left ventricular outflow tract (Braun 2022).

• Implantation of a defibrillator

The implantation of a defibrillator serves to prevent sudden cardiac death (Braun 2022).

Indications are:

- Presence of multiple extrasystolic foci.

- Foci in the vicinity of conduction systems

- Foci in the area of the cardiac apex (Braun 2022)

- idiopathic malignant VES (Ip 2017).

Until the 1980s (Ip 2017), ventricular extrasystoles without evidence of structural heart disease were believed to have a good prognosis, even when they were clustered (Rath 2005).

Meanwhile, this view regarding idiopathic VES has changed, as it has been shown that susceptible patients:

- can develop a malignant potential that can trigger ventricular fibrillation via polymorphic ventricular tachycardia and end in sudden cardiac death

- Can induce cardiomyopathy (Ip 2017).

Muser (2021) considers the occurrence of syncope in patients with idiopathic VES to be a warning signal regarding polymorphic ventricular tachycardia or ventricular fibrillation. Otherwise, he considers the long-term prognosis of idiopathic VES without structural heart disease to be good.

Two recent meta-analyses involving nearly 150,000 healthy subjects reported a 1.7-fold risk of major cardiac events and a 2.64-fold risk of sudden cardiac death. However, Muser (2021) recommends that these results be interpreted carefully because only a single study in this meta-analysis considered history, physical examination, and resting ECG (Muser 2021).

Patients with preexisting heart failure show increased mortality when VES occurs (Kasper 2015).

Patients with recent myocardial infarction are at increased risk for ventricular fibrillation when VES occurs (Herold 2022).

Antiarrhythmic drug therapy does not improve life expectancy in patients with heart disease (Kasper 2015).

Patients with frequent VES should be monitored regularly for VES load and left ventricular function (Cronin 2020).

General Information

Idiopathic VES used to be considered a benign phenomenon. It has since been shown that in susceptible patients, idiopathic VES:

- can develop a malignant potential, causing ventricular fibrillation that can end in sudden cardiac death

- Can induce cardiomyopathy caused by the VES (Ip 2017).

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