**7. Conclusion**

cardioversion, NT-pro BNP has decreased in virtually all patients, but the decrease has been quicker in tachycardia-induced cardiopmyopathy patients. Therefore, the ratio between the baseline NT-pro BNP and NT-pro BNP after one week following cardioversion ≥ 2.3 has had 90% sensitivity, 95% specificity and 90% accuracy to predict tachycardia-induced origin of

Therapeutic approach to the tachycardia-induced cardiomyopathy includes two steps: 1. tachyarrhythmia correction as it represents causal therapeutic intervention and 2. heart

Due to the potential reversibility of hemodynamic and structural changes in tachycardiainduced cardiomyopathy, all efforts should be made to achieve **heart rate correction or appropriate rate control.** Rhythm or rate control may be achieved using both pharmacological and non-pharmacological tools. Depending on the type of arrhythmia and presence/absence of concomitant structural heart disease, various antiarrhytmic drugs may be used to terminate the arrhythmia or to achieve adequate rate control. Especially, betablockers and class III antiarrhythmics play an irreplaceable role regarding this treatment. It is very important to avoid drugs with higher pro-arrhythmic effect (e.g. flecainide) in the presence of systolic dysfunction or drugs that may contribute to further progression of systolic dysfunction (e.g. disopyramide). Most arrhythmias that lead to tachycardia-induced cardiomyopathy are currently treatable using catheterization ablation, success rate of which reaches 60–90% depending on the type of arrhythmia. This therapeutic approach should be therefore consid‐

In atrial fibrillation, rate and rhythm control strategy have been shown to be comparable with respect to quality of life, mortality or stroke rate [64, 69]. The decision to favor rhythm control over rate control should thus be made on an individual basis, and discussed with the patient [70]. In case rate control strategy is chosen, repeated long-term ECG monitoring is instrumental to decide whether the selected treatment is appropriate and ensures acceptable rate control (strict rate control requires 60–80 bpm at rest and 90–115 bpm at moderate exercise; lenient rate control requests resting rate < 110 bpm). Atrial arrhythmias are often refractory to antiarrhythmic drugs and an acceptable rate control may be then achieved only with higher doses of AV nodal blocking agent. In such cases, catheter ablation is an option. By other supraventricular tachyarrhythmias, which lead to tachycardia-induced cardiomyopathy, restoration of sinus rhythm is usually preferred. Rhythm correction may be achieved through either pharmacological or electrical cardioversion or (preferably) via catheter ablation of the

In rare cases, failing to restore sinus rhythm (even using catheter ablation) and to achieve adequate ventricular control, an ablation of AV node with insertion of a permanent pacemaker may be considered. Because of the present ventricular dysfunction prior to pacemaker

ventricular dysfunction based on these authors.

ered as a first-line treatment in the absence of contraindication.

insertion, biventricular systems are usually favored [71].

**5. Therapy**

86 Abnormal Heart Rhythms

failure treatment.

arrhythmia in these patients.

The difficulties to differentiate reliably between tachycardia-induced cardiomyopathy and other forms of dilated cardiomyopathy, and the fact that the correct diagnosis is often estab‐ lished only retrospectively based on the improved systolic function after heart rate correction are the two most important reasons why the real prevalence of tachycardia-induced cardio‐ myopathy may be much higher than it is currently reported. Since it is a potentially reversible cause of heart failure, it is very important to always consider this option in the concomitant presence of dilated cardiomyopathy pattern and persistent tachycardia. An early heart rate intervention may then have substantial clinical impact.

Although experimental studies helped us to understand the basic pathophysiologic process behind the tachycardia-induced cardiomyopathy development, there is still a number of questions that need to be answered. For example, it is not clear why the tachycardia-induced cardiomyopathy does not occur in all patients with persistent tachycardia of the same type and heart rate. Furthermore, it is not clear whether or not are the patients who once developed tachycardia-induced cardiomyopathy in their life more susceptible to heart failure of another origin in the long-term perspective, similarly as are women with gestational diabetes more prone to develop the second type of diabetes in their future life. In addition, the exact patho‐ physiology behind tachycardia-induced cardiomyopathy is still not well understood. All these and other questions should therefore become the subjects of future research.
