Tachycardiomyopathy

Tachycardiomyopathy (TIC) is a form of dilated cardiomyopathy that leads to dilatation and systolic dysfunction of the left ventricle (Greten 2010).

By definition, left ventricular pump function is < 50% and improves by > 15% after catheter ablation (Rotmann 2015).

Although TIC develops only slowly, the restriction of left ventricular function can ultimately lead to the development of manifest heart failure (Rotmann 2015).

The incidence of TIC is about 8 % (Rotmann 2015). The disease can occur at any age and has already been described even in unborn children in utero. It can also be found in patients who have undergone heart transplantation (Nerheim 2004).

Tachycardiomyopathy can be caused by:

• permanent and prolonged tachycardia, such as those seen in atrial fibrillation, paroxysmal tachycardia, or ventricular tachycardia. (Greten 2010)
• clustered ventricular extrasystoles (Chugh 2000).

TIC is thought to occur when:

• approximately 22% of the total beats consist of ventricular extrasystoles (VES)
• a QRS duration of the VES of > 150 ms is present
• a retrograde P-wave occurs after the VES
• interpolated VES are present (Rotmann 2015).

The pathophysiological processes of a TIC are not fully understood. Changes of the myocardium play a role such as:

• subclinical ischemia...
• Disturbances in energy metabolism
• Disturbances of the redox reaction
• intracellular calcium overload (Martin 2017)

Often patients are free of symptoms for a long time. Otherwise they may persist:

Palpitations

or symptoms of atrial fibrillation such as:

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

In advanced stages, there may also be signs of left heart failure in systolic dysfunction with:

• Stress intolerance
• Tiredness
• Nocturia (Siegenthaler 2002)

see also Dilated Cardiomyopathy and Atrial Fibrillation

Resting ECG / Long-term ECG

In the ECG can be detectable:

• Tachycardia
• Tachyarrhythmias
• ventricular extrasystoles (VES)

and in case of atrial fibrillation:

• 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-reentry 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).

s. a. Dilated cardiomyopathy and atrial fibrillation

Transesophageal Echocardiography (TEE)

Echocardiographic may be present:

• Dilatation of the left atrium
• left-atrial volume index (LAVI) > 34 ml / m² (Pinger 2019)
• restricted LVEF (left ventricular ejection fraction; normal value 52 % - 72 % [Hagendorff 2017])
• Increase in wall thickness
• Hypokinesia of the left ventricle (Flachskampf 2006)

If extrasystoles are the cause of TIC, should be determined:

• Potassium
• Magnesium
• Digitalis level if necessary (Herold 2020)

Patients with TIC are at risk for sudden cardiac death. This has also been observed in young, asymptomatic patients who have been treated for many years. It is suspected that hidden cardiomyopathy may persist due to unknown ultrastructural changes (Nerheim 2004).

Since the underlying diseases differ, the treatment is also different:

Tachycardia: Benign forms of tachycardia can usually be controlled by medication or ablation . The success rate of a catheter ablation is - if no structural diseases of the heart are present - about 80 %.

Malignant forms of tachycardia are predominantly polymorphic and genetically determined. They always carry an increased risk of sudden cardiac death. In this case, implantation of a defibrillator (ICD) may be necessary (Rotmann 2015).

Atrial fibrillation: Atrial f ibrillation (AF) can be treated with medication, electrical cardioversion, or catheter ablation. For more detailed information, see atrial fibrillation.

Anticoagulation: Since thrombi have already been found in the left atrium when the duration of VHF is < 48 h, anticoagulation is an important therapeutic measure (Stierle 2017).

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

• Chronicheart failure or left ventricular dysfunction: 1 point
• Hypertension: 1 point
• Age≥ 75 years: 2 points
• Diabetesmellitus: 1 point
• Apoplexy/ TIA / thromboembolism: 2 points
• Priorvasculardisease: 1 point
• Age65 - 74 years: 1 point
• Sexcategory (female sex): 1 point

If the score is 0 points, the risk of apoplexy is low and anticoagulation is not required. If ≥ 2 points, oral anticoagulation should be given in any case. In between, a decision must be made on a case-by-case basis (Baenkler 2010).

Choice of anticoagulation according to ESC grade of recommendation and level of evidence:

- 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 NOAKs (Kirchof 2016).

- I A: If there is an existing indication for a vitamin K antagonist, preference should be given to a NOAK such as apixaban, dabigatran, edoxaban, or rivaroxaban, if eligible

- IIb A: Patients already pretreated with a vitamin K antagonist may be switched to NOAKs if the TTR is not stable or the patient prefers NOAKs and has no contraindications (e.g., prosthetic valve) (Kirchof 2016)

Dosage recommendation: vitamin K antagonists e.g. warfarin initially 20 mg / d, further dosage depending on INR value (target INR of 2.0 - 3.0); maintenance dose between 2.5 mg - 15 mg / d.

Dosage recommendation NOAK: e.g. apixaban 2 x 2.5 mg - 5 mg / d p.o. (Stierle 2017).

Paroxysmaltachycardias: Paroxysmal tachycardias include the AV- nodal- reentry- tachycardia and AV- reentry- tachycardia.

For AV nodal re entry tachycardia, slow pathway ablation is recommended, whereas fast pathway ablation is no longer recommended because the success rate is equally high, but the risk of complete AV blockis significantly increased (Kuck 2007). The success rate is >95%, the recurrence rate is 5%-10%, and the risk of 3rd degree AV blockis <0.5%.

Ablation is the treatment of choice for atrioventricular reentrant tachycardia . The success rate is 95%-98.5%, and the recurrence rate is 5% (Pinger 2019).

Extrasystoles: If organic heart disease is present (such as CHD), it should be treated appropriately (Herold 2020).

Furthermore, it is recommended to check the potassium and magnesium balance and, if necessary, the digitalis level. Potassium and magnesium levels should be adjusted to high-normal values, and digitalis levels should be in the lower therapeutic range (the more damaged a heart is, the less digitalis it can tolerate) (Herold 2020).

Patients with post-myocardial infarction or impaired pumping ability should be treated with class II antiarrhythmic agents such as beta-blockers. These reduce the risk of ventricular fibrillation due to the lack of intrinsic sympathomimetic activity. Dosage recommendation: e.g., metoprolol 50 mg - 200 mg / d orally (Herold 2020).

Class- I- antiarrhythmic drugs are contraindicated in patients with structural heart disease, as they lead to worsening of prognosis. Amiodarone and sotalol also do not improve prognosis. From NYHA III, these even lead to a worsening of prognosis.

If there is an increased risk of ventricular fibrillation or sudden cardiac death, implantation of an ICD should be performed (Herold 2020).

If the origin of the extrasystoles is at the right ventricular outflow tract (RVOT), catheter ablation can be performed (Stierle 2017).

Supportive therapy:

Medications such as beta-blockers, calcium antagonists, and class I and II antiarrhythmic drugs can assist in reversibility of TIC in the period after the cause of TIC has been eliminated (Rotmann 2015).

Dosage recommendation beta blocker: - e.g. metoprolol 50 mg - 200 mg / d.

Dosage recommendation calcium channel blockers: - e.g. verapamil 120 mg - 480 mg / d

Dosage recommendation antiarrhythmic drugs class I and II: flecainide 200 mg - 300 mg orally, alternatively: propafenone 450 mg - 600 mg orally (Kirchof 2016).

TIC is a reversible form of cardiomyopathy - in most cases after the causes have been eliminated. The myocardium usually needs days to weeks to recover completely (Greten 2010).

Regeneration can be supported by medications such as beta blockers, calcium antagonists, class I and II antiarrhythmics (for dosage recommendations, see "Therapy"). (Rotmann 2015)

However, deaths are also described that occurred under long-term treatment (see "Complication") - (Nerheim 2004).

1. Baenkler H W et al (2010) Short textbook on internal medicine. Georg Thieme Publisher 72 - 75
2. Chugh S S et al (2000) First Evidence of Premature Ventricular Complex-Induced Cardiomyopathy: A Potentially Reversible Cause of Heart Failure. J Cardiovasc Electrophysiol. 11 (3) 328 - 329
3. Flachskampf F A (2006) Coursebook Echocardiography: In consideration of the guidelines of the German Society of Cardiology and the KBV Georg Thieme Verlag 88
4. Fölsch U R et al (2000) Pathophysiology. Springer Publishing House 78
5. Greten H et al (2010) Internal Medicine. Georg Thieme Publisher 142
6. Hagendorff A et al. (2017) Basic knowledge echocardiography: "Ars echocardiographica" - step by step to correct diagnosis. Elsevier 231
7. Herold G et al (2020) Internal medicine. Herold Publisher 225
8. Kirchhof P et al (2016) ESC Pocket Guidelines: Management of Atrial Fibrillation. DGK Börm Bruckmeier Publisher 164
9. Kuck K H et al (2007) Guidelines for catheter ablation. Clin Res Cardiol (96) 833 - 849
10. Martin C A et al (2017) Pathophysiology, diagnosis and treatment of tachycardiomyopathy. Heart Jnl (103) 1543 - 1552
11. Nerheim P et al (2004) Heart Failure and Sudden Death in Patients WithTachycardia-Induced Cardiomyopathy andRecurrent Tachycardia. Circulation (110) 247 - 252
12. Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German medical publisher. 680 – 686
13. Rotmann B (2015) Ventricular extrasystole in patients without structural heart disease. J Cardiol Austrian 22 (3 - 4) 70 - 75
14. Siegenthaler W et al (2002) Siegenthaler's differential diagnosis: Internal diseases - from symptom to diagnosis. Georg Thieme Publisher 618
15. Stierle U et al (2014) Clinical Guide to Cardiology. Elsevier Urban and Fischer 583, 586