Atrial fibrillation I48.9

In 1628 William Harvey first described an irregular pulse in humans. In 1827, Robert Adams, using the stethoscope that had been developed in the meantime, diagnosed an irregular pulse as a symptom of mitral valve stenosis. 1874, Vulpian described a connection between the arrhythmia and fibrillation of the atria, which, according to Einthoven (1900), was described as being caused by multiple atrial foci. Only after the invention of the electrocardiogram in 1909 Rothenberger and Winterberg were able to document atrial fibrillation for the first time (Doll 2008).

Atrial fibrillation (VHF / AF) is a high-frequency (between 300 - 600 / min), completely irregular and uncoordinated electromechanical activity of the atria, which by definition must be present in the long-term ECG for at least 30 seconds or in the short documentation of a 12-channel ECG for the entire time (Pinger 2019).

The VHF belongs to the group of left-atrial tachyarrhythmias (Paul 2018). The VHF differentiates between:

• Paroxysmal VHF (minutes to hours - mostly < 24 h- up to a maximum of 7 days of spontaneously terminating episodes of VHF
• Persistent VHF: The VHF exists for > 7 days to 1 year and cannot be terminated spontaneously. However, it can be brought back into sinus rhythm by cardioversion.
• Persistent VHF: The VHF exists since ≥ 1 year. Measures to restore the sinus rhythm are nevertheless successful.
• Permanent VHF: In permanent VHF, a final state is reached which cannot or should no longer be converted into a stable sinus rhythm (Stierle 2017 / Sauerbruch 2018).

In addition, a distinction is made between two different types:

• Vagotonic type: The VHF occurs preferentially when the heart rate drops, such as at night or at rest
• Sympathicotonic type: Here the VHF is mainly found during an increase in heart rate, such as during physical exertion, in the morning, after stress etc (Herold 2020):

According to EHRA 2913 and ESC 2016, a distinction is made between:

• AF as a consequence of structural heart disease
• AF for mitral valve stenosis or valve prosthesis
• Postoperative AF
• Monogenic AF
• Polygenes AF
• Focal induced AF
• AF for athletes
• Unclassified AF (Pinger 2019)

VHF is the most common cardiac arrhythmia in humans. There is an age-related incidence:

• in the 5th decade it is found in up to 1%.
• in the 6th decennium at approx. 5
• from the 7th decennium on up to 15

VHF is 1.5 times more common in men (Pinger 2019) and slightly more common in coloured people than in women and whites (Kasper 2015). However, women with VHF have a higher risk of apoplexy than men. The risk of developing VHF is twice as high among endurance athletes of middle to advanced age than among non-athletes (Herold 2020).

Patients with heart failure have a significantly higher risk of developing VHF than the general population. 37% of patients with newly developed VHF (mean age 75 years) had heart failure at the same time and 57% of patients with newly developed heart failure had VHF (Pinger 2019)

Associated diseases:

• Heart failure (Pinger 2019)
• Arterial hypertension (Kallistratos 2018)
• Coronary heart disease
• Primary myocardial diseases
• Heart valve diseases
• Hyperthyroidism
• Currently surgical interventions (preferably in the area of the cardiovascular system) (Sauerbruch 2018)

A differentiation is made between:

• primary VHF
• secondary VHF and
• extracardiac VHF

Primary VHF (so-called "idiopathic VHF" or "lone atrial defibrillation"): Primary VHF is rare and accounts for only about 15% of all cases with VHF. Occasionally a familial predisposition is found. In contrast, primary VCF is common in <50-year-olds, accounting for approximately 80% of cases (Herold 2020).

Secondary VCF: Secondary VCF is the most common form, accounting for 85% of cases. A distinction is made between cardiac and extracardiac causes.

• Cardiac-related:
  • Mitral valve stenosis, mitral valve insufficiency: These are the most common causes in younger patients.
  • coronary artery disease
  • Myocardial infarction
  • heart failure (in NYHA I, 5 % of patients have VCF, in NYHA IV, 50 %)
  • Cardiomyopathies
  • Myocarditis
  • Pericarditis
  • Sick sinus syndrome
  • Preexitation syndrome
  • Cardiac surgery (occurs postoperatively in approximately 30% of patients [Kasper 2015].
• Extracardiac VHF
  • arterial hypertension
  • pulmonary embolism
  • Cardiac trauma
  • hyperthyroidism
  • ethyltoxic (so-called holiday heart syndrome)
  • drug toxicity (e.g. due to beta-sympathomimetics, theophylline)
  • sleep apnea
  • diastolic dysfunction
  • obesity
  • subarachnoid haemorrhage
  • higher-grade renal insufficiency
  • ischemic apoplexy (Pinger 2019 / Herold 2020)
• Idiopathic VCF: In about 8% of patients, a so-called idiopathic VCF is found as a diagnosis of exclusion (Stierle 2017).

The VHF is based on different pathophysiological mechanisms. Despite numerous studies, the pathophysiology has not yet been sufficiently clarified. In most cases a micro-reentry excitation is found (recognizable in the ECG as a f-wave). The excitation of the atrium is transferred to the chambers only irregularly. This leads to a reduction of the cardiac output of up to 25 %. Clinically, however, this is of no relevance, as the frequency of asymptomatic recurrences proves. The atrial refractory period is shortened.

In addition there is an increase of the atrial size:

• 43 mm in the first manifested VHF
• 46 mm for paroxysmal VHF
• 51 mm for permanent VHF

The left atrium is important for the persistence of the VHF. Possibly the shorter refractory period, the proximity to the pulmonary veins and the stronger tendency to remodeling play a role (Fölsch 2000 / Pinger 2019).

There is little correlation between arrhythmia and symptoms. Up to 60% of patients are asymptomatic and 40% of patients have AF symptoms despite a sinus rhythm.

Symptoms can be:

• dyspnea
• Palpitations
• Swindle
• Decrease of physical resilience
• angina pectoris
• Occurrence of an embolism (sometimes the first symptom)
• rare occurrence of a syncope (Pinger 2019)
• Polyuria (ANP effect; atrial natriuretic peptide causes, among other things, the increased excretion of sodium and chloride by the kidneys) (Herold 2020)

With the help of the so-called EHRA classification (classification of the European Heart RythmAssociation) the severity of the symptoms can be assigned.

Modified EHRA classification:

• Class I: There are no symptoms, so-called "silent AF".
• Class II: Symptoms appear. Depending on the severity of the symptoms, one differentiates between:
  • Class II a: Only mild symptoms exist, everyday activity is not restricted, also called "not troublesome
  • Class II b: There is a moderately severe symptomatology, but this does not affect everyday activities, so-called "patient troubled by symptoms
• Class III: Severe symptoms occur. Normal everyday activity is considerably impaired.
• Class IV: At this stage, normal everyday activity is no longer possible. One speaks of so-called "disabling symptoms" (Pinger 2019 / Kirchof 2016).

The diagnostic and therapeutic procedure for atrial fibrillation corresponds to the procedure for atrial reentry tachycardia / atrial flutter (Paul 2018).

Auscultation: There is often a pulse deficit (difference between auscultable heart rate and radial pulse) (Herold 2020).

ECG: On the 12- channel ECG, there is often:

• absolute arrhythmia
• P-waves with a frequency of 300 - 600 / min are usually only visible in leads V , III and aVF (Baenkler 2010), but they can also be absent
• irregular RR- intervals
• narrow ventricular complexes
• widened ventricular complexes with additional block patterns

These can occur singly - or rarely - in volleys. They are usually a consequence of aberrant ventricular conduction (bundle branch block). Typically, they appear in the wake of a long and then short beat interval (so-called Ashman phenomenon) (Herold 2020).

• Micro- re-entrant excitations: Recognizable in the ECG as a flicker wave [so-called f-wave]; irregular frequency between 300 - 600 /min., preferentially in lead V1 (Fölsch 2000).

Long-term ECG: A long-term ECG is recommended for patients with typical symptoms but no evidence of VHF on resting ECG. If the irregular mean heart rate on the long-term ECG is > 110 beats/min, the diagnosis is tachyarrhythmia absoluta; if the rate is < 60 beats/min, the diagnosis is bradyarrhythmia absoluta (Herold 2020).

Transesophageal Echocardiography (TEE): Transesophageal echocardiography is recommended in all patients with AF to guide treatment (guideline: recommendation grade I, evidence grade B). In addition, TEE can detect or exclude atrial thrombi (before planned early cardioversion: recommendation grade I, evidence grade B )(Kirchof 2016).

The left atrium is mostly dilated echocardiographically. The left atrial volume index (LAVI) is > 34 ml / m². Tachyarrhythmia-induced cardiomyopathy is often severe but reversible with adequate therapy (Pinger 2019).

Multifocal atrial tachycardia: In this case there is often an absolutely arrhythmic sequence of the QRS complex, but there are clearly distinguishable P waves, which show more than two different morphologies.

Pseudo-regularization in VHF: In this case, there are almost regular intervals of the QRS complexes with very small flicker waves of a junctional (AV nodal) rhythm.

Electrical or mechanical artifacts (Stierle 2017).

Left ventricular dysfunction and heart failure: Approximately 20 % - 30 % of patients with VHF develop ventricular dysfunction during the course of the disease. An already existing left ventricular dysfunction can be aggravated by the occurrence of VHF. However, there are also patients in whom - despite many years of VHF - the LV function remains completely intact (Kirchof 2016).

Cognitive deficits and vascular dementia: Both cognitive deficits and vascular dementia are more common in patients with VHF than in the general population, even in anticoagulated patients. Lesions of the white matter are more frequently visible on MRI (Kirchof 2016).

Tachycardiomyopathy: The occurrence of tachycardiomyopathy results in left heart enlargement with left heart failure, which belongs to dilated cardiomyopathy and is reversible (Herold 2020 / Weihrauch 2020).

The most common and important complications of VHF are:

thrombus formation in the motionless atrium

Consecutive embolisms (mostly in the brain): The risk of developing an apoplexy increases 5-fold. Atrial fibrillation is found in 25% of patients with apoplexy. The risk of dementia is also increased, as is the risk of heart failure (Kasper 2015 / Baenkler 2010).

The CHA2 DS2 - VASc - Score can be used to calculate the risk of apoplexy in VHF:

• Chronic heart failure or left ventricular dysfunction: 1 point
• Hypertension: 1 point
• Age ≥ 75 years: 2 points
• Diabetes mellitus: 1 point
• Apoplexy / TIA / Thromboembolism: 2 points
• Pre-existingvasculardisease: 1 point
• Age 65 - 74 years: 1 point
• Sex category (female sex): 1 point

With a value of 0 points, the risk of apoplexy is low and anticoagulation is not necessary.

At ≥ 2 points, oral anticoagulation should be performed in any case. A decision should be made in between in each individual case (Baenkler 2010).

The type of treatment depends on:

• the clinical appearance
• the haemodynamic effects
• the duration of the VHF
• possible risk factors for an apoplexy
• causal cardiac diseases (Kasper 2015)

The therapy goals are:

• Reduction of mortality
• Improvement of the symptoms
• Prevention of tachycardiomyopathy
• Reduction of the embolization risk (Pinger 2019)

The following therapeutic options exist for VHF:

• Drug therapy to lower the heart rate (Herold 2020)
• Administration of antiarrhythmics
• ablation
• Cardioversion (Acid Break 2018)

In the case of an acutely new VHF, conversion to sinus rhythm can occur within the first 24 hours in about 50% of cases. If this is not the case, drug treatment is recommended for haemodynamically stable patients (see "Internal therapy" for details).

In haemodynamically unstable patients (e.g. severe hypotension, acute left heart decompensation, shock), electrical cardioversion should be performed as an emergency measure (for more details, see "Internal Therapy") (Baenkler 2010).

Acute therapy: In case of an acute, newly occurring VHF with high ventricular frequencies, hemodynamic instability such as shock symptoms with hypotension, angina pectoris, pulmonary congestion as a sign of left heart failure, an electrical cardioversion should be performed immediately. Initially 200 J are administered under sedation or anaesthesia. The anterior-posterior configuration of the electrodes has proven to be the most effective. In the event of unsuccessful

• a higher energy is used, or
• the position of the electrodes can be changed (Kasper 2015)

Ablation is not indicated in acute therapy, and after cardioversion a recurrence prophylaxis should be performed in any case (see below) (Stierle 2017).

Heparin: In addition, anticoagulation should be started immediately, since cardioversion increases the risk of thromboembolic complications. Dosage recommendation: Heparin initial 5,000 IU i. v., then 10,000 IU / 50 ml, 5 ml / h by heparin perfusor with daily PTT control (PTT should be extended to 2 times the normal value). After successful rhythmization, anticoagulation should be maintained for at least 4 weeks if appropriate risk factors (see also CHA2 DS2 - VASc - score under "Complications") are present, permanently (Stierle 2017)

Beta blockers or calcium channel blockers: If left ventricular function is good, both beta blockers and calcium antagonists can be used. Recommended dosage of beta-blockers: e.g. metoprolol 5 mg - 15 mg i. v., orally 50 mg - 200 mg / day. Recommended dosage of calcium channel blocker: e.g. verapamil 5 mg - 10 mg i. v., orally 120 mg - 480 mg / day

Digitalis: see below under "Chronic therapy". If left ventricular function is limited, rapid digitization is recommended (Stierle 2017). Dosage recommendation: e.g. digoxin 3 x 0.4 mg i. v. in 24 h, followed by daily administration of the maintenance dose of 0.25 mg - 0.375 mg / d depending on the serum level (therapeutic level 0.8 - 2 ng / ml) (Luippold 2012).

Chronic therapy: The chronic treatment of a VHF can be done by frequency control or rhythm control. These are two equivalent strategies (Herold 2020).

1st frequency control: Frequency control should be used for:

- VHF known for > 1 year (can prevent clinically relevant tachyarrhythmias and bradycardias [Herold 2020])

- high risk of treatment with antiarrhythmics

- LA- Diameter > 55 mm (Stierle 2017)

The aim of treatment for tachyarrhythmia absoluta is a reduction of the frequency to < 110 / min.

The frequency can be controlled with drugs that influence the AV transition, such as beta blockers, calcium antagonists and cardiac glycosides (Hadjamu 2020):

• beta-receptor blockers: these are used in particular in tachyarrhythmia caused by hyperthyroidism and heart failure. They are effective on their own in 58% of cases and reduce the resting frequency in 68% and the exercise frequency in 72% (Pinger 2019). It should be noted, however, that they should not be combined with verapamil, otherwise there is a risk of AV block (Herold 2020). Dosage recommendation: e.g. Atenolol 25 mg - 100 mg / d (Woolliscroft 1999)
• Non-dihydropyridine calcium antagonists: Verapamil-type calcium antagonists should be used preferably in patients without heart failure. Recommended dosage of non-dihydropyridine calcium antagonists: e.g. Diltiazem ret. 2 x 90 mg / d (Machraoui 2006)
• Digitalis: In patients with concomitant heart failure, the ventricular rate can be lowered by Digitalis at rest, but not under physical exertion. However, it has been shown that patients with VHF have increased mortality under treatment with digitalis. Digitalis should therefore be used only with caution and in low doses under constant blood level monitoring. Dosage recommendation: Digoxin 0.25 mg - 0.375 mg / d depending on serum level (therapeutic level 0.8 - 2 ng / ml) (Luippold 2012)
• AV- nodal ablation / VVI- pacemaker implantation: In rare cases, the above-mentioned drug treatment does not succeed in reducing the frequency sufficiently. In this case, there is the possibility of an AV nodule ablation plus the implantation of a VVI pacemaker. It should be noted, however, that a worsening of the heart failure is possible with VVI stimulation.

Bradyarrhythmia absoluta: If the bradyarrhythmia absoluta caused by an AV conduction disorder is symptomatic of chronotropic incompetence under stress and regulation by frequency control is not possible, implantation of a VVI (R) pacemaker with frequency-adaptive stimulation is also recommended.

Rhythm control (RK) = conversion of VHF: The goal of rhythm control is to stabilize the sinus rhythm (Pinger 2019). This can be achieved with antiarrhythmic drugs or by electrical cardioversion (Stierle 2017). Rhythm control can be used for:

• - symptomatic paroxysmal VHF
• - a symptomatic, persistent VHF that has occurred for the first time
• - difficult to achieve frequency control
• - left ventricular dysfunction
• - worsening of heart failure (Kasper 2015)

Drug conversion: Antiarrhythmic drugs have the potential for drug-induced cardioversion (Hadjamu 2020). According to ESC 2016, there is a recommendation or evidence level I B for rhythm maintenance therapy (Kirchof 2016). However, the effectiveness is lower than that of electric cardioversion. Drug-induced cardioversion is indicated in patients without a relevant structural heart disease (with the exception of amiodarone). Drug conversion should be performed under continuous ECG monitoring and the possibility of emergency defibrillation. The drugs used are class IC antiarrhythmics such as flecainide, propafenone, amiodarone (Sauerbruch 2018). Recommended dosage:

• - Flecainide 200 mg - 300 mg orally or 1,5 mg - 2 mg / kg KW i. v. over 10 min.
• - Propafenone 450 mg - 600 mg orally or 1,5 mg - 2 mg / kg KW i. v. over 10 min (Kirchof 2016)

Usually, conversion to sinus rhythm occurs within the first 2 - 5 h after application (Sauerbruch 2018). In patients with structural heart disease, conversion should be performed with the class III antiarrhythmic agent amiodarone (Sauerbruch 2018). Since amiodarone often causes extracardiac side effects, catheter ablation is the first choice therapy for patients with structural heart disease. Recommended dosage: Amiodarone 5 mg - 7 mg / kg KW over 2 h i. v. (Kirchof 2016).

Long-term therapy with antiarrhythmic drugs: A long-term use of antiarrhythmic drugs aims at:

- to reduce the symptoms

- to maintain the sinus rhythm (but only moderate effect by antiarrhythmic drugs)

According to ESC 2016, the following drugs have an I / A recommendation or evidence level for long-term therapy with antiarrhythmics in patients with no or minimal signs of structural heart disease:

• - Dronedarone e.g. 2 x 400 mg / d
• - Flecainide e.g. 2 x 100 mg - 150 mg / d
• - Propafenone e.g. 3 x 150 mg - 300 mg / d
• - Sotalol e.g. 2 x 80 mg - 160 mg / d

A IIa / B recommendation or evidence level exists for catheter ablation. For patients with CHD, abnormal hypertrophy of the left ventricle or relevant heart valve disease, there is an I / A level of recommendation or evidence for the following drugs:

• Dronedarone e.g. 2 x 400 mg / d
• Sotalol e.g. 2 x 80 mg - 160 mg / d
• Amiodaran e.g. 1 x 200 mg / d

A IIa / B recommendation or evidence level exists for catheter ablation. For patients with heart failure, there is an I / A recommendation or evidence level for amiodarone, e.g. 1 x 200 mg / d

A IIa / B recommendation or evidence level exists for catheter ablation (Kirchof 2016)

Electrical cardioversion: According to ESC 2016, acutely hemodynamically unstable patients have a recommendation or evidence level I / B for electrical cardioversion. Indications for electrical cardioversion may be:

• unsuccessful drug-induced cardioversion
• haemodynamic instability (Sauerbruch 2018)

In cardioversion there is a high risk of thromboembolic complications. Therefore, in patients with VHF lasting longer than 48 h or if the duration of the VHF is unknown - according to the guideline - it should only be carried out after at least 3 weeks of effective anticoagulation (see below for details) and a current INR between 2 and 3 using a vit. K antagonist (Sauerbruch 2018).

Contraindication of cardioversion:

• Hypokalemia
• Digitalis overdose
• Existence of an acute infection
• detected thrombus in the left atrium (TEE)
• Hyperthyroidism
• Decompensated heart failure (except emergencies) (Pinger 2019)
• In elective cardioversion, pre-treatment with antiarrhythmic drugs such as:

amiodarone e.g. 1 x 200 mg/d

Flecainide e.g. 2 x 100 mg - 150 mg / d

Propafenone e.g. 3 x 150 mg - 300 mg / d

the success of cardioversion and simultaneously prevents the occurrence of recurrences (IIa / B recommendation or evidence level) (Kirchof 2016)

Electrical cardioversion is performed under monitoring of ECG, blood pressure and O2 saturation under short anaesthesia monophasically with 100 - 360 J or biphasically with 50 - 150 J (Baenkler 2010).

The success rate of biphasic cardioversion is clearly superior to monophasic cardioversion with a success rate of > 90%, but the study evidence is poor (Trappe 2012).

Catheter ablation: In patients with paroxysmal VHF or a short history of persistent VHF, sclerotherapy of the trigger areas (these are mainly located in the area of the pulmonary veins) can be performed using cold or heat (Baenkler 2010). Because of the procedural risk, the procedure should be performed in experienced centres. In 60 % of patients a sinus rhythm can be achieved after one session and in 70 % - 80 % after several interventions. However, ablation is less effective with persistent VHF (Kasper 2015)

Anticoagulation: As thrombi in the left atrium have already been found with a duration of the VHF of < 48 h, a TEE should be performed before cardioversion and followed by a 4-week anticoagulation (Stierle 2017). If the VHF has already lasted longer or if the duration of the VHF is unclear, an anticoagulation with a vitamin K antagonist should be performed for 3 weeks with a target INR of 2.0 - 3.0 prior to electrical cardioversion. As an alternative to the administration of the vitamin K antagonist, a TEE can also be performed prior to cardioversion to ensure the exclusion of thrombi.

After cardioversion, anticoagulation should be maintained in both cases for at least another 4 weeks (Stierle 2017). However, if corresponding risk factors are present (see CHA2 DS2 - VASc - Score), permanent anticoagulation is recommended (Stierle 2017).

The risk of a thromboembolism per year with a CHA2 DS2 - VASc - Score (see complications below) of:

• 0: 0 %
• 1: 1,3 %
• 2: 2,2 %
• 3: 3,2 %
• 4: 4,0 %
• 5: 6,7 %
• 6: 9,8 %
• The risk of intracranial bleeding under therapy with Marcumar (INR between 2.0 - 3.0) is 0.3% / year. The benefit of antithrombotic treatment is significantly higher than the risk of intracranial bleeding. This also applies to therapy with NOAK. The risk of severe bleeding can be calculated with the HAS- BLED- Score (Herold 2020). Degree of recommendation / evidence level ESC 2016 of a permanent oral anticoagulation:
• I A:
  • for all male patients with a CHA2 DS2 - VASc - score of 2 or higher
  • for all female patients with a CHA2 DS2 - VASc - score of 3 or higher
• IIa B:
  • for all male patients from a CHA2 DS2 - VASc - Score from 1 taking into account individual characteristics and preferences
  • for all female patients with a CHA2 DS2 - VASc - score of 2 or higher, taking into account individual characteristics and preferences

Choice of anticoagulation:

• I B:
  • Vitamin K antagonists such as warfarin, phenprocoumon (INR 2.0 - 3.0 or higher) in patients with moderately severe mitral valve stenosis or after implantation of mechanical heart valves. These patients should not receive NOAK (Kirchof 2016).
• I A:
  • if there is an indication for a vitamin K antagonist, NOAK such as Apixaban, Dabigatran, Edoxaban or Rivaroxaban should be given preference, if it is possible
• IIb A:
  • in patients already pre-treated with a vitamin K antagonist, a switch to NOAK can be made if the TTR is not stable or the patient prefers NOAK and has no contraindications (e.g. valve prosthesis) (Kirchof 2016).

The prognosis depends on the underlying cardiac or extracardiac disease (Herold 2020). The risk of an apoplexy is 5 times higher (also applies to patients with subclinical VHF or with > 5 min. lasting VHF) and the risk of heart failure is 3 times higher (Pinger 2019).

Overall, the survival probability of a patient with sinus rhythm is better than that of a patient with VHF (Kasper 2015).

The most frequent causes of death are:

• sudden cardiac death
• Heart Failure
• Apoplexy

(Kirchof 2016)

The AFFIRM study published in 2002, which included 4,060 patients, showed that the prognosis of patients with sinus rhythm maintenance therapy and those with drug frequency control showed no difference with persistent VHF.

The only exception were patients with heart failure plus atrial fibrillation. Mortality is twice as high in these patients as in patients with preserved sinus rhythm.

(Herold 2020 / Wyse 2002)

The recurrence rate in patients with initial paroxysmal VHF is 25 % after 5 years and after > more than 10 years more than 50 % of patients with paroxysmal VHF develop chronic VHF.

(pinger 2019)

Various antiarrhythmic drugs are available to prevent the recurrence of VHF:

• Class Ic: such as propafenone 3 x 150 mg - 300 mg / d in patients without structural heart disease
• Class II: beta-blockers such as metoprolol 1 x 100 mg - 200 mg / d (Kirchof 2016)
• Class III: such as amiodarone 1 x 200 mg/d

(Baenkler 2010)

Anticoagulants reduce the risk of stroke by about 60% in primary prevention and by almost 70% in secondary prevention.

(Herold 2020)

For the first time, the ESC guidelines 2016 mentioned a screening for the possible existence of VHF for patients > 65 years of age with recommendation class I (Pinger 2019).

These patients should receive a 24-hour ECG to exclude VHF - even if they are free of symptoms.

(Herold 2020)

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