Tachycardia-bradycardia syndrome I49.5

In 1973, Kaplan and colleagues proposed the term tachycardia-bradycardia syndrome, the cause of which is predominantly, but not exclusively, a disturbance in the function of the sinus node (Lüderitz 1984).

Tachycardia bradycardia syndrome (TBS) is a form of cardiac dysrhythmia in which tachycardia primarily occurs in the form of paroxysmal supraventricular tachycardia, atrial flutter or atrial fibrillation, followed by an asystolic pause before the rhythm changes to a bradycardic sinus rhythm (Herold 2020). TBS is often combined with other sinus or AV conduction disorders (Classen 2009).

Sometimes TBS is used in the literature synonymously with sick sinus syndrome (SSS) (Ferri 2014), sometimes mentioned as a complication of SSS (Tse 2017).

The tachycardia-bradycardia syndrome is part of the sick sinus syndrome (SSS) together with the following symptoms:

• Sinus Bradycardia
• Sinus arrest
• Sinuatrial blockages (SA block)
• chronotropic incompetence of the sinus node (Herold 2020 / Classen 2009)

TBS occurs in about 50 % of all cases of sick sinus syndrome and thus complicates the further course of the disease (Tse 2017).

TBS can already occur in children with a congenital heart defect or during cardiac surgery.

In adults it is more likely to be found in older age (Ferri 2014). Sometimes TBS also occurs more frequently in families (Duhme 2013).

Associated diseases:

The occurrence of TBS is accelerated by the following comorbidities:

• coronary heart disease
• arterial hypertension
• Cardiomyopathies
• Diseases of the heart valves (Kasper 2015)

TBS is caused by structural and electrophysiological changes, which can be caused primarily by the following diseases / changes:

• inflammatory changes such as:
  • cardiomyopathies
  • Pericarditis
  • Myocarditis
• Ischemias such as...
  • coronary heart disease
  • acute myocardial infarction
• certain drugs such as beta blockers, calcium channel blockers, digoxin, lithium, etc.
• genetic mutations (Tse 2017)

Pathophysiologically, TBS is a functional disorder in the ion channels responsible for the conduction and initiation of cardiac action potentials. The disorder can lead to both bradycardia and tachycardia, with tachycardia increasing the risk of bradycardia and vice versa (Tse 2017). In familial clustered TBS, a genetic dysfunction of the CHN4 channels is found (Duhme 2013).

The post-conversion pauses can cause the following symptoms in the first place:

• Dizziness
• Syncope (Stanger 2020)

In addition, symptoms of the Sick Sinus Syndrome are possible such as:

• Palpitations
• Dyspnea
• angina pectoris
• Signs of heart failure
• Formation of a so-called chronotropic incompetence (inadequate increase of the heart rate under stress) (Brandes 2019 / Kasper 2017)

Resting ECG: The ECG of TBS typically contains phases of:

• Sinus tachycardia (> 100 beats / min.)
• Sinus bradycardia (< 60 beats / min.; in young or trained patients < 40 / min [Kasper 2015])
• tachycardic supraventricular arrhythmias (mostly atrial fibrillation)
• Atrial tachycardia (Renz- pads 2008)

Exercise ECG: under ergometric stress, a maximum of up to 70 % of the age-related frequency increase can be obtained (chronotropic incompetence) (Herold 2020)

For further diagnostics see Sick- Sinus- Syndrome

• for bradycardia:
  • AV block
• for tachycardia:
  • Atrial fibrillation or atrial flutter
  • Sinus tachycardia (Ferri 2014)

The treatment of symptomatic patients consists of:

• implantation of a pacemaker
• Catheter ablation antiarrhythmic therapy (Herold 2020 / (Zhang 2019)
• Pacemaker implantation: In symptomatic patients a pacemaker should be implanted. An antiarrhythmic therapy is additionally recommended (Herold 2020).
• Antiarrhythmic drugs; dosage recommendation of antiarrhythmic drugs e.g.:

- 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

- Amiodarone e.g. 1 x 200 mg / d (Kirchhof 2016)

• Catheter ablation: In a 150 patient study conducted by Dalian Medical University between 2002 and 2013, catheter ablation was shown to eliminate both tachycardia and bradycardia in the majority of patients. The reduction of atrial fibrillation also resulted in a reduction of strokes (5.1% versus 15.4% in patients after pacemaker implantation). Of the patients treated with catheter ablation, 70.9% had a sinus rhythm without long pauses, and additional therapy with antiarrhythmic drugs was not necessary for them.

Persistent atrial fibrillation was found in 1.3 %. Patients with pacemaker implantation had 9.9% (Zhang 2019)

• Drug therapy: Good results are found in patients treated with amiodarone without simultaneous pacemaker supply (dosage recommendation: amiodarone e.g. 1 x 200 mg/d - Kirchhof 2016).
• Anticoagulation: Patients with TBS are particularly at risk of thromboembolism and should therefore be given anticoagulation in case of comorbidity (Stanger 2020).

The resulting increased risk of thromboembolism can be calculated using the CHA2 DS2 - VASc - score (Kasper 2015).

CHA2 DS2 - VASc - Score:

- 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-existing vasculardisease: 1 point

- Age 65 - 74 years: 1 point

- Sex category (female gender): 1 point (Baenkler 2010))

• Degree of recommendation/evidence level ESC 2016 of 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 with a CHA2 DS2 - VASc - score of 1 or higher, 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 (Kirchof 2016)

In Anglo-Saxon countries, patients are already treated with anticoagulants from 1 point on. For younger women, therapy with ASA can also be considered (Kasper 2015)

• 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.
  • I A:
    • if there is an indication for a vitamin K antagonist, NOAK such as Apixaban, Dabigatran, Edoxaban or Rivaroxaban should be given in preference, if it is possible
  • IIb A:
    • Patients who have already been pre-treated with a vitamin K antagonist can be switched to NOAK if the TTR is not stable or if the patient prefers NOAK and has no contraindications (e.g. valve prosthesis) (Kirchhof 2016)

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