Premature atrial contraction induced cardiomyopathy: A case report

Abstract

This case report describes the successful management of a 45-year-old female patient with incessant premature atrial complexes (PACs) leading to left ventricular dysfunction. Despite initial treatment with beta-blockers, the patient's PACs persisted, prompting catheter ablation. Mapping in the left atrium identified the site of earliest atrial activation near the right superior pulmonary vein, and radiofrequency energy successfully terminated the PACs. Follow-up assessments showed the patient remained asymptomatic, with normalized left ventricular function. This case highlights the efficacy of catheter ablation in resolving PAC-induced cardiomyopathy and emphasizes the need for further research in this area.

1. Introduction

Tachycardia cardiomyopathy (Tachy-CMP) is well known to occur in sustained atrial arrhythmia and premature ventricular complexes (PVCs), but limited data is available about the PACs causing cardiomyopathy [[1], [2], [3], [4], [5], [6], [7]]. PACs are arrhythmias characterized by premature atrial depolarizations. While usually asymptomatic, PACs can lead to significant consequences, including the development of arrhythmia-related cardiomyopathy [[8], [9], [10], [11]].

PACs are commonly identified on electrocardiogram (ECG) as premature beats with abnormal P-wave morphology. They are associated with comorbidities such as hypertension and heart failure. In some cases, PACs can be the primary cause of cardiac dysfunction.

Management strategies for PAC-induced cardiomyopathy include pharmacological therapy and catheter ablation. When medical therapy fails, catheter ablation becomes a valuable treatment option. This procedure involves identifying the source of abnormal electrical activity in the atria and ablating it using radiofrequency energy.

Limited case reports focus specifically on catheter ablation for this condition [[8], [9], [10], [11]]. The report discusses the patient's clinical presentation, diagnostic evaluation, catheter ablation procedure, and follow-up outcomes. By presenting this case, we aim to contribute to the literature on supporting the use of catheter ablation as an effective treatment for PAC-induced cardiomyopathy. It emphasizes the importance of considering this intervention in managing patients with refractory symptoms and contributes to the understanding of diagnostic and therapeutic approaches in such cases.

2. Case summary

A 45-year-old female was referred for arrhythmia management. The patient had been experiencing symptomatic PACs for several months, which eventually led to left ventricular (LV) dysfunction. Physical examination and biochemical tests yielded unremarkable results, and there was no family history of cardiac arrhythmia.

The patient had a past medical history of cholelithiasis treated by laparoscopic cholecystectomy and uterine fibroids awaiting surgical removal. The baseline ECG showed normal sinus rhythm with frequent PACs (Fig. 1). Echocardiography revealed global LV hypokinesia with severe left ventricular systolic dysfunction (left ventricular ejection fraction of 30–35 %). A 24-h Holter recorded a high burden of PACs (∼26 %), including singlets, couplets, and triplets, along with a few non-sustained and sustained runs of atrial tachycardia, despite beta-blocker treatment. Coronary angiography confirmed normal epicardial coronaries.

Fig. 1.

Illustrates a baseline electrocardiogram displaying sinus rhythm accompanied by multiple premature atrial contractions and non-sustained runs of atrial tachycardia.

Initially, the patient was managed with beta-blockers for rhythm control, but they failed to suppress her clinical PACs. Due to the symptoms and concerns of PAC-induced cardiomyopathy, the potential role of antiarrhythmic vs. catheter ablation was discussed with the patient. The patient agreed to proceed with catheter ablation. The patient arrived at the electrophysiology lab in sinus rhythm with frequent PACs.

During the electrophysiological study, the clinical PACs were mapped. Initially, an irrigated steerable ablation catheter was advanced to the right atrium (RA), and the earliest atrial activation was mapped near the SVC-RA junction with the aid of intracardiac electrograms (EGMs) and fluoroscopy. However, at this site, there was an rS configuration in the ABL-unipolar signal. Subsequently, a decision was made to perform mapping in the left atrium (LA).

After administering a heparin bolus to achieve an activated clotting time greater than 350 seconds, a single trans-septal puncture was performed. Using the same irrigated steerable ablation catheter, the LA was mapped. The earliest atrial activation was identified at the right superior pulmonary vein (RSPV). At this site, the local EGMs preceded the onset of the P-wave by −22 ms, and there was a QS configuration in the ABL-unipolar signal (Fig. 2). After confirming the absence of phrenic nerve capture, radiofrequency (RF) energy was delivered at this site, resulting in the termination of the PACs. Additional consolidation burns were performed based on impedance drop.

Fig. 2.

Depicts the intra-cardiac electrograms captured from various electrodes positioned inside the heart. The right panel inset showcases fluoroscopic images of different catheters observed from the right anterior oblique (RAO) and left anterior oblique (LAO) views. Notably, an ablation catheter is placed near the right superior pulmonary vein (RSPV), where a fractionated signal preceding the surface P wave by 22 milliseconds is visible. Ablation performed at this site successfully terminated the clinical premature atrial contractions (PACs).

Afterwards, isoproterenol was initiated and gradually increased to a maximum dose of 20mcg. Aggressive programmed stimulation was performed, but no tachycardia/clinical PAC was induced (Fig. 3).

Fig. 3.

The upper panel illustrates the lead V1 recording prior to the initiation of ablation, demonstrating salvos of premature atrial contractions (PACs). However, in the lower panel, following a successful ablation procedure, all clinical PACs were suppressed, and no PACs were recorded during maximum isoproterenol stimulation.

During follow-up appointments, the patient remained asymptomatic, and a repeat echocardiogram showed normalized LV function (Fig. 4).

Fig. 4.

Illustrates a series of key images from a follow-up echocardiogram that capture the cardiac cycle in both systolic and diastolic frames. These images highlight significant improvements in left ventricular function. Notably, the left ventricular end-diastolic diameter (LVEDD) measured as 5.0 cm, and the left atrium diameter as 2.7 cm, signifying a positive trend in cardiac performance.

3. Discussion

In this case report, catheter ablation was successfully employed to manage symptomatic PACs in a patient with associated LV dysfunction. The targeted ablation of the RSPV site, identified through precise mapping within the left atrium, resulted in the termination of PACs and subsequent improvement in LV function confirmed by follow-up echocardiogram.

The efficacy of catheter ablation for symptomatic PACs has been supported by previous studies. While catheter ablation has shown promising outcomes, it is essential to consider potential risks and complications associated with the procedure. Further studies are warranted to validate these findings and refine the selection criteria for catheter ablation in patients with PAC-induced cardiomyopathy.

3.1. Literature review

PACs are a common arrhythmia encountered in clinical practice. While PACs are often benign and asymptomatic, they can have significant clinical implications, including the development of tachy-CMP. This literature review aims to provide an overview of the current understanding of PAC-induced cardiomyopathy, its pathophysiology, diagnostic evaluation, and therapeutic approaches, with a particular focus on catheter ablation as a management strategy.

3.2. Pathophysiology

The exact mechanisms by which PACs contribute to the development of cardiomyopathy are not fully understood. Unlike PVCs, where Tachy-CMP is caused by both dyssynchrony and irregularity, the predominant mechanism in PAC is irregularity. It is believed that repetitive atrial premature depolarizations can lead to atrial remodeling, including electrical and structural changes, ultimately resulting in impaired atrial and ventricular function. The remodeling process may involve alterations in intracellular calcium handling, activation of neurohormonal systems, and fibrotic changes within the atrial and ventricular myocardium [[12], [13], [14], [15]].

3.3. Diagnostic evaluation

The diagnosis of PAC-induced cardiomyopathy is primarily based on clinical presentation, electrocardiographic findings, and echocardiographic assessment. Patients typically present with symptoms such as palpitations, dyspnoea, and fatigue. Electrocardiograms often reveal premature atrial beats with abnormal P-wave morphology. Echocardiography plays a crucial role in assessing ventricular function and ruling out other causes of cardiomyopathy.

3.4. Management strategies

The management of PAC-induced cardiomyopathy involves both pharmacological therapy and interventional approaches. Pharmacological therapy aims to control symptoms and reduce the burden of PACs. Beta blockers are commonly used as first-line agents, targeting the adrenergic stimulation associated with PACs. Antiarrhythmic medications may be considered in cases of refractory symptoms or high PAC burden.

3.5. Catheter ablation

Catheter ablation has emerged as a promising therapeutic option for patients with symptomatic PACs that are refractory to medical therapy. The procedure involves mapping the site of origin of the ectopic foci within the atria and delivering radiofrequency energy to ablate the focal source. Successful ablation leads to the elimination or significant reduction of PACs, subsequently improving atrial and ventricular function.

Few case reports have reported the efficacy of catheter ablation in managing PAC-induced cardiomyopathy. These reports highlight the potential benefits of catheter ablation as a definitive treatment option in selected patients.

4. Conclusion

PAC-induced cardiomyopathy is a less common but clinically significant condition that can lead to impaired cardiac function. Catheter ablation has shown to be an effective and durable treatment option for refractory cases when medical therapy fails. Early recognition, patient selection, comprehensive evaluation, and close follow-up are crucial for optimal outcomes. Further research is needed to validate these findings, establish management guidelines, and assess long-term outcomes and patient prognosis.

Conflict of interest

No conflict of interest.

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Declaration of competing interest

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:nothing to disclose