EF, the concern exists that at least some component is related to arrhythmia-induced cardiomyopathy. This is particularly suspected in younger patients with severe symptoms from the AF. A trial of early cardioversion is warranted in these patients with subsequent monitoring for improvement in cardiac function [99]. Patients with another SVT For supraventricular tachyarrhythmias (SVTs) other than AF or atrial flutter that result in arrhythmia-induced cardiomyopathy, restoration of sinus rhythm is the usual goal. Options for the restoration of sinus rhythm include electrical cardioversion, antiarrhythmic drugs, and catheter ablation of the arrhythmia. The initial choice of modality will vary depending upon the underlying SVT as well as the local expertise and availability of options (ie, some centers do not perform catheter ablation) but should be made in conjunction with an electrophysiologist experienced in the treatment of sustained tachyarrhythmias. Certain SVTs are more amenable to electrical cardioversion (eg, atrioventricular nodal reentrant tachycardia), while others are often refractory or recurrent following cardioversion (eg, atrial tachycardia). Often, atrial arrhythmias can be refractory to antiarrhythmics, and AV nodal blocking agents may be required in high doses to achieve appropriate heart rates. In patients with depressed LVEF, it is important to avoid agents that have a higher likelihood of proarrhythmia (eg, flecainide) or that could further depress LVEF (eg, disopyramide). If an ablation is performed, close follow-up is required even after successful ablation because of the tendency for cardiomyopathy to recur if tachycardia recurs. (See "Focal atrial tachycardia", https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy/print 12/29 7/6/23, 11:10 AM Arrhythmia-induced cardiomyopathy - UpToDate section on 'Catheter ablation' and "Treatment of arrhythmias associated with the Wolff- Parkinson-White syndrome", section on 'Catheter ablation' and "Atrial tachyarrhythmias in children", section on 'Management' and "Atrioventricular nodal reentrant tachycardia", section on 'Catheter ablation'.) Patients with frequent ectopy For patients presenting with a high burden of premature ventricular complexes/contractions (PVCs) and newly recognized cardiomyopathy, initial management is to look for underlying causes (such as CAD, valvular heart disease, arrhythmogenic right ventricular dysplasia [ARVD], etc) and initiation of guideline-based optimal medical therapy for HF [100]. Correction of electrolytes and initiation of beta blockers are typical first therapies. (See "Overview of the management of heart failure with reduced ejection fraction in adults".) Given the possibility of arrhythmia-induced cardiomyopathy in patients with a high PVC burden (eg, >15 to 20 percent of total beats on a 24-hour ambulatory monitor) and associated with LV dysfunction, we generally pursue radiofrequency catheter ablation [100-102]. Catheter ablation of high-frequency PVCs has emerged as a safe and effective therapy and may be considered if medical management is ineffective or poorly tolerated and depending on patient preference [59,74,103-105]. While it is not possible to specify an exact percentage (PVC burden) for which a patient might benefit from ablation of frequent PVCs as studies have had a wide range in their inclusion criteria, consideration may be given with a burden of above 10 percent, but our approach is typically to offer ablation at a higher burden (eg, >15 to 20 percent PVCs). The approach to catheter ablation in patients with a high PVC burden is discussed in greater detail separately. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy" and "Premature ventricular complexes: Treatment and prognosis", section on 'Catheter ablation'.) Patients with refractory tachyarrhythmias In the event that a supraventricular arrhythmia is likely the cause of cardiomyopathy and cannot be primarily ablated, AV node ablation with either biventricular pacing or conduction system pacing is a reasonable approach to management. While there are no studies that specifically address the strategy of AV nodal ablation and biventricular pacemaker placement in patients with arrhythmia-induced cardiomyopathy, there is indirect evidence to support this approach. In a trial that included patients with HF, a narrow QRS, and permanent AF but who did not explicitly have arrhythmia-induced cardiomyopathy, patients assigned to medical rate control had a higher risk of death or rehospitalization due to HF or worsening of HF when compared with patients assigned to AV node ablation and cardiac https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy/print 13/29 7/6/23, 11:10 AM Arrhythmia-induced cardiomyopathy - UpToDate resynchronization therapy (38 versus 10 percent; hazard ratio 0.28, 95% CI 0.11-0.72) [106]. The effect of this approach on recovery of LVEF was not reported. Other trials and studies of patients with preexisting AV node block, HF, and various causes of LV systolic dysfunction are discussed elsewhere. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system".) FOLLOW-UP Whereas the initial cardiomyopathy may have taken months to develop, recurrent tachycardia can lead to an abrupt decline in LVEF. Diastolic dysfunction can persist even after systolic function has normalized and can lead to decreased coronary flow reserve. In patients who develop a recurrence of the arrhythmia, the increased myocardial oxygen demand in the face of the decreased reserve can lead to redevelopment of cardiomyopathy [107,108]. As such, close ongoing monitoring with clinic visits, ambulatory (Holter) monitoring, and echocardiography are essential. Although there are minimal data and no society guidelines regarding the frequency of monitoring in these patients, we follow up with patients using a combination of clinic visits, echocardiography, and ambulatory monitoring every three to six months for one to two years following the initial clinical improvement. The following is a typical follow-up schedule: Four to six weeks after initial presentation Clinical follow-up, ECG. Three months after initial presentation Clinical follow-up, ECG, echocardiogram, outpatient ambulatory monitor. Six months after initial presentation Clinical follow-up, ECG. Twelve months after initial presentation Clinical follow-up, ECG, echocardiogram, ECG, outpatient ambulatory monitor if symptoms suggest recurrence. Eighteen to 24 months after initial presentation Clinical follow-up, ECG. If complete recovery of EF is noted and angiotensin converting enzyme (ACE) inhibitors and beta blockers are tapered off, additional monitoring is required to be sure that EF remains normal [4]. PROGNOSIS https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy/print 14/29 7/6/23, 11:10 AM Arrhythmia-induced cardiomyopathy - UpToDate Following the restoration of sinus rhythm or ventricular rate control of the presenting tachycardia, most patients will have significant improvement and/or normalization of LVEF over a period of months. As such, patients who have not experienced sudden cardiac arrest or a sustained ventricular arrhythmia, and whose LVEF has improved to 40 percent or greater, usually do not require implantation of an implantable cardioverter-defibrillator (ICD). (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".) In some patients whose LVEF has normalized, the LV chamber may remain somewhat enlarged. Despite the apparent normalization of cardiac function when a tachycardia has been terminated or rate controlled, ultrastructural abnormalities of the myocardium may persist [60]. Additional evidence for persistent myocardial abnormality despite normalization of systolic function was seen in a study of successfully ablated patients with atrial tachycardia. These patients demonstrated LV structure and function changes including diffuse fibrosis on contrast-enhanced CMR imaging long after successful ablation (64 36 months) [90]. As noted previously, late- gadolinium enhancement on CMR suggests the presence of fibrosis and identifies irreversible structural changes that may predict incomplete recovery of LV function. For any patient whose LVEF fails to normalize with correction of the tachyarrhythmia, other underlying pathology should be considered including permanent structural changes [90,109]. If arrhythmia-induced cardiomyopathy recurs, these patients are at substantial risk for sudden death, and ICD implantation should be contemplated [107]. SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Ventricular arrhythmias" and "Society guideline links: Cardiac implantable electronic devices" and "Society guideline links: Supraventricular arrhythmias".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy/print 15/29 7/6/23, 11:10 AM Arrhythmia-induced cardiomyopathy - UpToDate level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Beyond the Basics topics (see "Patient education: Atrial fibrillation (Beyond the Basics)" and "Patient education: Catheter ablation for abnormal heartbeats (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS Definition Arrhythmia-induced cardiomyopathy is a relatively rare cause of a dilated cardiomyopathy resulting from prolonged periods of rapid ventricular heart rates. Arrhythmia-induced cardiomyopathy often improves or resolves following treatment and is associated with a good prognosis in most patients. (See 'Introduction' above.) Pathophysiology Chronic tachycardia ultimately produces significant structural changes in the heart, with impressive left ventricular (LV) dilation and cellular morphologic changes leading to a cardiomyopathy. The precise mechanism(s) by which a chronic tachycardia produces these changes remain incompletely described. (See 'Pathophysiology' above.) Association with specific arrhythmias Virtually all tachyarrhythmias have been reported to cause arrhythmia-induced cardiomyopathy, and frequent ectopic beats have also been associated with this condition. In most cases, the myocardial dysfunction improves or normalizes following therapy to control the ventricular heart rate or to restore normal sinus rhythm. (See 'Arrhythmias associated with arrhythmia-induced cardiomyopathy' above.) Clinical presentation The clinical presentation of arrhythmia-induced cardiomyopathy is variable but usually involves signs and/or symptoms related to the tachyarrhythmia (eg, palpitations, dyspnea, chest discomfort, etc), heart failure (HF; eg, dyspnea, edema, weight gain, orthopnea, etc), or both. In our experience, HF symptoms are more common since patients with symptomatic tachyarrhythmias will frequently seek medical attention earlier in the course of their care and prior to the development of a cardiomyopathy. (See 'Clinical presentation' above.) ECG findings All patients should have an ECG to document the cardiac rhythm and ventricular heart rate, with comparison to prior ECGs when available. There are no specific https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy/print 16/29 7/6/23, 11:10 AM Arrhythmia-induced cardiomyopathy - UpToDate ECG findings that distinguish patients with and without arrhythmia-induced cardiomyopathy, and the ECG findings will vary depending upon the underlying tachyarrhythmia. (See 'ECG findings' above.) Approach to diagnosis Arrhythmia-induced cardiomyopathy is defined by the presence of a sustained tachycardia (or frequent episodes of tachycardia or very frequent ectopy) that results in with LV systolic dysfunction. Usually the diagnosis of arrhythmia-induced cardiomyopathy can only be made following a successful trial of therapy to slow the ventricular rate or to restore sinus rhythm along with the exclusion of other potential causes of cardiomyopathy. Patients in whom arrhythmia-induced cardiomyopathy is suspected should undergo continuous cardiac monitoring for 24 to 48 hours and have non- invasive imaging to assess cardiac structure and function. For most patients, a transthoracic echocardiogram is the preferred test for assessing cardiac structure and function, although cardiovascular magnetic resonance (CMR) imaging is a reasonable alternative. (See 'Approach to the diagnosis' above and 'Diagnostic testing' above.) Treatment The initial treatments for a patient with HF and suspected arrhythmia-induced cardiomyopathy are the same as those used in most other patients with HF (eg, angiotensin converting enzyme [ACE] inhibitors or angiotensin II receptor blockers [ARBs], beta blockers, diuretics) and tachyarrhythmias (eg, rate-control medications, consideration of antiarrhythmic drugs and/or cardioversion). However, because of the potential reversible nature of arrhythmia-induced cardiomyopathy, aggressive efforts should be made to achieve excellent ventricular heart rate control or to restore sinus rhythm. (See 'Treatment' above.) For minimally symptomatic patients with atrial fibrillation (AF) in whom adequate rate control is achieved, we continue medical therapy. For patients with AF who remain significantly symptomatic, or patients in whom adequate rate control is not achieved with medical therapy alone, we pursue a rhythm control strategy. (See "Management of atrial fibrillation: Rhythm control versus rate control" and "Atrial fibrillation: Cardioversion".) For patients with atrial flutter, rapid ventricular rates, and newly recognized depressed LV ejection fraction (LVEF), rate control may be difficult to achieve with medication. Because of this, we perform early electrical cardioversion in these patients. (See "Restoration of sinus rhythm in atrial flutter".) For supraventricular tachyarrhythmias (SVTs) other than AF or atrial flutter that result in arrhythmia-induced cardiomyopathy, restoration of sinus rhythm is the usual goal. The https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy/print 17/29 7/6/23, 11:10 AM Arrhythmia-induced cardiomyopathy - UpToDate initial choice of modality (ie, electrical cardioversion, antiarrhythmic drugs, or catheter ablation of the arrhythmia) will vary depending upon the underlying SVT as well as the local expertise and availability of options. For patients presenting with a high burden of premature ventricular complexes/contractions (PVCs) and associated with LV dysfunction, we generally pursue radiofrequency catheter ablation. On rare occasions when all efforts at ventricular rate control, restoration of sinus rhythm, and catheter ablation of the arrhythmia have been unsuccessful for the treatment of SVTs, ablation of the AV node with insertion of a permanent pacemaker may be considered. Long-term monitoring Close ongoing monitoring with clinic visits, ambulatory (Holter) monitoring, and echocardiography is essential to assess for any recurrence. We follow up with patients using a combination of clinic visits, echocardiography, and ambulatory monitoring every three to six months for one to two years following the initial clinical improvement. (See 'Follow-up' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Westphal JG, Rigopoulos AG, Bakogiannis C, et al. The MOGE(S) classification for cardiomyopathies: current status and future outlook. Heart Fail Rev 2017; 22:743. 2. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. J Card Fail 2017; 23:628. 3. Shinbane JS, Wood MA, Jensen DN, et al. 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