Successful Reversal of Tachycardia Induced Cardiomyopathy After Flecainide Therapy in an Infant With Focal Atrial Tachycardia

Technical Summary: Successful Reversal of Tachycardia Induced Cardiomyopathy After Flecainide Therapy in an Infant With Focal Atrial Tachycardia

Problem Statement
Focal atrial tachycardia (FAT) is an uncommon but clinically significant cause of persistent supraventricular tachycardia (SVT) in infants. Unlike reentrant SVTs, FAT is driven by abnormal automaticity, rendering it less responsive to conventional antiarrhythmic strategies that primarily target ventricular rate reduction. Infants are uniquely vulnerable to the hemodynamic consequences of sustained tachycardia due to limited myocardial reserve and immature ventricular compliance. Prolonged arrhythmia can rapidly precipitate tachycardia-induced cardiomyopathy (TIC), characterized by ventricular dysfunction, chamber dilatation, and secondary atrioventricular valve regurgitation. A critical clinical challenge identified in this case is that partial rate control may mask ongoing myocardial injury, leading to progressive deterioration even when heart rates appear managed.

Methodology and Case Presentation
This study presents a single case report of a 4.5-month-old former preterm infant (born at 33+4 weeks) with a structurally normal heart (except for a small 3 mm secundum atrial septal defect) who presented with persistent narrow QRS atrial tachycardia. The patient exhibited a high arrhythmic burden with heart rates fluctuating between 100 and 210 bpm.

The management strategy followed a stepwise escalation:

1. Initial Therapy: Treatment began with propranolol, which failed to restore sinus rhythm.
2. Escalation: Due to persistent arrhythmia, the patient was transferred to the pediatric intensive care unit for continuous intravenous amiodarone (loading dose 5 mg/kg, followed by 5–7 mg/kg/day). While this achieved partial ventricular rate control, it failed to restore sinus rhythm.
3. Monitoring of Deterioration: Serial echocardiograms during the amiodarone phase revealed progressive myocardial dysfunction. Left ventricular ejection fraction (LVEF) declined from 66% to 58%, accompanied by left ventricular dilatation and worsening tricuspid regurgitation, confirming evolving TIC.
4. Intervention: Amiodarone was discontinued, and oral flecainide (100 mg/m²/day in two divided doses) was initiated in combination with propranolol. This required special acquisition arrangements due to limited regional availability of the drug.
5. Follow-up: The patient was monitored via electrocardiography, Holter monitoring, and serial echocardiography. Long-term follow-up included clinical assessment and planning for potential future electrophysiological study and catheter ablation.

Key Results

• Rhythm Restoration: Following the initiation of flecainide, the patient experienced rapid restoration of sinus rhythm. Subsequent Holter monitoring confirmed complete normalization with uninterrupted sinus rhythm and no recurrence of atrial tachycardia.
• Safety Profile: No QRS widening was observed under flecainide therapy. While transient QTc prolongation (up to 0.50 seconds) occurred during prior amiodarone infusion, QTc intervals normalized after discontinuation and remained stable under flecainide.
• Cardiac Recovery: Echocardiographic follow-up demonstrated marked improvement in ventricular systolic function and a significant regression of valvular insufficiency. Mitral regurgitation returned to trivial levels, and tricuspid regurgitation improved to mild severity.
• Clinical Improvement: The infant showed substantial recovery in feeding tolerance, activity levels, and overall functional status, allowing for transfer from the intensive care unit to the general ward and eventual discharge.

Key Contributions
This case report contributes to the pediatric cardiology literature by:

• Highlighting the Limitations of Rate Control: It demonstrates that in infantile FAT, partial rate control is insufficient to prevent myocardial injury. The cumulative burden of tachyarrhythmia, rather than the ventricular rate alone, drives the progression of TIC.
• Validating Rhythm Control: The case supports the efficacy of early rhythm control strategies, specifically the use of Class IC agents like flecainide, in refractory infantile FAT where first-line therapies fail.
• Documenting Reversibility: It provides evidence that TIC and secondary valvular insufficiency in infants are reversible upon the prompt restoration of sinus rhythm, distinguishing functional remodeling from primary structural pathology.
• Identifying Systemic Barriers: The report notes the significant therapeutic challenge posed by the limited regional availability of flecainide, which can delay effective treatment and prolong exposure to tachyarrhythmia.

Significance and Claims
The authors assert that this case underscores the critical importance of early rhythm control in persistent infantile FAT. They claim that while rate control may offer temporary hemodynamic stabilization, it does not prevent progressive myocardial dysfunction. Instead, the restoration of sinus rhythm is presented as the key determinant for myocardial recovery and the reversal of TIC. The paper concludes that flecainide is a highly effective agent for refractory infantile FAT, though its utility in certain regions is currently constrained by supply limitations. The authors maintain a modest scope, acknowledging that as a single case report, the findings cannot be generalized to all infants with FAT, but the clinical message regarding the inadequacy of rate control alone remains significant.