Arrhythmia-Induced Cardiomyopathy

Huizar JF, Ellenbogen KA, Tan AY, Kaszala K.
Arrhythmia-Induced Cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol 2019;73:2328-2344.

The term arrhythmia-induced cardiomyopathy (AiCM) refers to a reversible type of cardiomyopathy and includes distinct entities of tachycardia-induced cardiomyopathy (T-CM), atrial fibrillation-induced cardiomyopathy (AF-CM), and premature ventricular contraction-induced cardiomyopathy (PVC-CM). The following are key points to remember from this review about AiCM:

Tachycardia-induced cardiomyopathy (T-CM):

  1. T-CM refers to the presence of a reversible left ventricular (LV) dysfunction solely due to increase in ventricular rates, regardless of tachycardia origin.
  2. Animal models of T-CM show that rapid atrial or ventricular pacing causes structural and electrical remodeling. Cessation of tachy-pacing results in significant recovery of LV ejection fraction (LVEF) or its normalization. Importantly, however, fibrosis appears to persist despite elimination of the tachycardia and normalization of LV function.
  3. An ambulatory electrocardiogram (ECG) monitor for ≥2 weeks should be considered to confirm or exclude T-CM. The final diagnosis of T-CM can only be confirmed after recovery or improvement of LV systolic function within 1 to 6 months after elimination of the tachyarrhythmia.
  4. In addition to treating tachycardia with antiarrhythmic drugs or radiofrequency ablation, the initial treatment of T-CM should include initiation and optimization of medical therapy for heart failure and LV systolic dysfunction (beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers, diuretic agents, and aldosterone blockers) to optimize reverse remodeling.

Atrial fibrillation-induced cardiomyopathy (AF-CM):

  1. AF-CM is defined as LV systolic dysfunction in patients with paroxysmal or persistent AF despite appropriate rate control. AF-CM may be due to: 1) heart rate irregularity with calcium mishandling; and 2) loss of atrial contraction associated with sympathetic activation contributing to limited ventricular filling and increased filling pressures, functional mitral regurgitation, and diastolic dysfunction.
  2. Landmark AF trials with antiarrhythmic drugs have failed to demonstrate outcome benefits including HF admissions in patients with and without HF or CM. This is in contrast to randomized clinical studies comparing AF ablation as a rhythm control versus rate control strategy, which reported an 8-18% absolute increase in LVEF in 60-70% of patients with AF and CM randomized to ablation.
  3. The only trial comparing rhythm control strategies (ablation vs. amiodarone) in patients with AF and CM demonstrated ablation to be superior by improving freedom of AF (70% vs. 34%), quality of life, HF admissions (31% vs. 57%), and mortality (8% vs. 18%) after 2-year follow-up.
  4. Absence of ventricular scar on cardiac magnetic resonance imaging or scar burden <10% may predict reversibility of AF-CM.

Premature ventricular contraction-induced cardiomyopathy (PVC-CM):

  1. PVC-CM is a diagnosis of exclusion when PVC burden is >10%; however, improvement in LV function may occur with treatment of PVC burden as low as 6%. A prolonged ambulatory ECG monitor (≥6 days), rather than 24-hour Holter monitor, is essential to improve the diagnostic yield of high PVC burden.
  2. The primary cause of contractile dysfunction in PVC-CM appears to be disorders of the calcium-induced calcium release mechanism, with alterations of L-type Ca channel and Ryanodine receptor. There is minimal or no fibrosis on histological examination and on cardiac magnetic resonance imaging.
  3. Independent predictors of PVC-CM are: male sex, lack of symptoms, duration of palpitations >30 months, variability of PVC coupling interval (dispersion), interpolation of PVCs, coupling interval <450 ms, QRS duration of PVC >150 ms, and epicardial origin.
  4. The optimal approach to frequent PVCs (>10% burden) without LV dysfunction, symptoms, or idiopathic ventricular fibrillation is unclear, but patients should probably be monitored every 6-12 months with echocardiography and PVC burden assessment.
  5. There are no randomized prospective studies comparing the efficacy and outcomes between radiofrequency ablation and antiarrhythmic drug therapy, but a retrospective study showed that PVC reduction was greater with radiofrequency ablation than antiarrhythmic drug therapy.

Clinical Topics: Arrhythmias and Clinical EP, Dyslipidemia, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Valvular Heart Disease, Implantable Devices, EP Basic Science, Genetic Arrhythmic Conditions, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Lipid Metabolism, Acute Heart Failure, Magnetic Resonance Imaging, Mitral Regurgitation

Keywords: Arrhythmias, Cardiac, Aldosterone, Amiodarone, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Anti-Arrhythmia Agents, Atrial Fibrillation, Atrial Remodeling, Cardiomyopathies, Catheter Ablation, Diuretics, Electrocardiography, Ambulatory, Heart Failure, Magnetic Resonance Imaging, Mitral Valve Insufficiency, Quality of Life, Ryanodine Receptor Calcium Release Channel, Stroke Volume, Tachycardia, Ventricular Fibrillation, Ventricular Premature Complexes, Ventricular Dysfunction, Left

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