Introduction

Most ventricular arrhythmias are associated with structural heart disease, primarily of ischemic etiology. However, a small subset occurs in patients with anatomically healthy hearts and are known as idiopathic arrhythmias.¹

Although idiopathic ventricular tachycardias (IVT) were previously considered benign and non-life-threatening, there is currently evidence that frequent premature ventricular complexes (PVC) are associated with a substantial increase in the risk of sudden cardiac death.² Also, it has been reported that between 9% and 34% of patients with IVT develop tachycardiomyopathy.³,⁴ The majority of PVC originate in the right ventricle outflow tract,⁵,⁶ however, others such as the tricuspid annulus (TA) have been identified as less frequent sites, accounting for between 8-9% of cases.⁶-⁸

Arrhythmia-induced tachycardiomyopathy (AiTCM) is defined as a reduced left ventricular ejection fraction (LVEF) ≤ 50% in the absence of any underlying heart disease, with an improvement in LVEF of ≥ 15% after effective ventricular arrhythmia treatment.⁹

Radiofrequency ablation (RFA) treatment is advised when an idiopathic ventricular arrhythmia occurs together with left ventricular dysfunction (LVD).¹⁰-¹²

The following case shows a patient that presented symptomatic PVC’s originating in the TA who underwent RFA.

Case presentation

A 75-year-old man, without relevant history, presented with mild exertion dyspnea and palpitations. The physical examination was normal, the 12-lead electrocardiogram showed premature ventricular contractions with a left bundle branch block pattern, normal axis, QS in V1, transition zone between V2-V3, R in D1 and aVL, QS in aVR, which suggested an origin in the tricuspid annulus (Figure 1). A Holter monitoring, documented a 35% arrhythmic burden and transthoracic echocardiography demonstrated an LVEF of 40%, global hypokinesia, and diastolic dysfunction type I without structural heart disease. An electrophysiological study was performed using EnSite Precision Abbott^® three-dimensional mapping software (Figure 2). The study showed fragmented and low amplitude electrograms (100 ms duration and < 1 mV) and the precocity index of the ventricular electrogram (-28 ms) in the septal region of the tricuspid annulus (Figure 3). An irrigated FlexAbility™ Abbott^® catheter was used to RFA of 30 W with a temperature limit of 25 ^oC. The PVC’s disappeared during the administration of RFA (Figure 4). Programmed ventricular stimulation was performed, with and without dobutamine infusion, without inducing contractions, neither other ventricular arrhythmias.

Figure 1: Contractions with a left bundle branch block pattern, normal axis, QRS duration 120 ms transition zone between V2-V3 and QS in V1 (TA septal region), R in DI and aVL, QS in aVR. 

Figure 2: Three-dimensional map made with the EnSite system^®, localization of the tricuspid annulus with contractions originating at the posteroseptal level (*). The red color represents the origin of the arrhythmia, the degradation towards blue and violet, are the regions where it is depolarized a later way. 

Figure 3: Intracavitary electrograms with maximum precocity of -28 ms. 

Figure 4: Disappearance of contractions after the application of radiofrequency of 30 W with a temperature limit of 25 ^oC. 

Fluoroscopy time was 26 minutes and there were no complications during the procedure. At 3 months, a 24-hour Holter monitoring was performed without evidence of ventricular arrhythmias. The AB was reduced from 35% to 0.02% with otherwise morphology from PVC’s treated and a transthoracic echocardiogram reported LVEF of 65% without mobility impairments. The ectopic focus was eliminated with the recovery of ventricular systolic function.

Discussion

Seventy to eighty percent of PVC originate in the right ventricle outflow tract.⁵,⁶ Less frequent origin sites such as the TA have been identified and accounting for between 8-9% of cases.

There is low evidence of PVCs originating from the TA due to their low incidence. To locate the site of origin of the arrhythmia, an appropriate electrocardiographic analysis must be performed. There are two studies of patients with PVC originating in the TA.⁷,⁸ Both coincide with the electrocardiographic characteristics of the PVC of this region, with LBBB patterns that have transition zones in V2-V3 and positive polarity in V6 and DI. There are two previously cases reporting of TA PVCs that were associated with tachycardiomyopathy.¹³,¹⁴

The association of fast and irregular ventricular rhythms with higher AB has been established as the main cause of tachycardiomyopathy.¹¹,¹²,¹⁵,¹⁶ There is evidence that an AB greater than 10% may result in LVD,⁸,¹⁶-¹⁸ however, PVC burden greater than 24% appears to be independently associated with a decreased ejection fraction.¹⁹ In such cases either pharmacological treatment or catheter ablation is necessary.

There are 2 types of AiTCM: type 1, in which arrhythmia is the only cause of tachycardiomyopathy, and left ventricular function returns to normal after successful treatment; type 2 refers to arrhythmic event exacerbates underlying damage, and its treatment results in partial resolution of the tachycardiomyopathy.¹¹,¹⁶

The treatment with RFA is recommended and has demonstrated high success rates when arrhythmias are associated with ventricular dysfunction or situations with AB > 10%.¹⁵ Regarding anatomy, treatment has been observed as more effective in patients with structurally healthy hearts and origin in the right ventricle,⁸-¹¹,²⁰ with a success rate between 80% and 90%.

AiTCM patients are often highly symptomatic with a significantly reduced quality of life, hence the importance of timely diagnosis and treatment given the reversibility of ventricular dysfunction.

According to the 2019 expert consensus statement of ventricular arrhythmias,²¹ catheter ablation is recommended inpatients with cardiomyopathy caused by PVC predominantly monomorphic, frequent, and for whom antiarrhythmic drugs are ineffective, not tolerated, or not preferred for long-term therapy (class I).

Different reports have shown that, after undergoing ablation treatment, patients with tachycardiomyopathy experience ejection fraction recovery within the first 12 weeks, so it is recommended to perform an echocardiogram and Holter monitor control 3 months after ablation.²¹-²³

The patient described in this report had an initial AB of 35% and an echocardiogram reported an LVEF of 40% without evidence of ischemia or structural alteration. After undergoing RFA, follow-up tests were performed at 3 months demonstrating a decrease in arrhythmic burden (0.02%) and the LVEF increased to 65%, thus complying with the criteria of AiTCM type 1.

Conclusions

Premature ventricular contractions originating from the tricuspid annulus are an uncommon cause of type 1 cardiomyopathy. High arrhythmic burden is the main determinant for ventricular dysfunction. Radiofrequency ablation is safe, effective, and indicated for patients in whom antiarrhythmic drugs are ineffective, not tolerated, or not preferred for long-tehrm therapy.