ClinicalAblationSinus rhythm electrocardiographic abnormalities, sites of origin, and ablation outcomes of ventricular premature depolarizations initiating ventricular fibrillation
Graphical abstract
Introduction
Ventricular fibrillation (VF) can be initiated by ventricular premature depolarizations (VPDs) in the absence of gross cardiac structural abnormalites.1,2 The distal Purkinje network, particularly within papillary muscles (PAPs), seems to be a common source of these VPDs initiating “idiopathic” VF.1,3, 4, 5
Clinical evidence supports an association between the electrocardiographic (ECG) pattern of early repolarization (ER), inferior epicardial substrate with abnormal electrograms (EGMs) in some patients, and VF.6 However, there are limited data describing 12-lead ECG sinus rhythm depolarization abnormalities such as QRS fractionation (QRSf) and reduced QRS amplitude in patients with VPDs initiating VF.
We sought to evaluate the prevalence and distribution of sinus rhythm ECG abnormalities reflected on the 12-lead ECG as reduced QRS amplitude, QRSf, and the presence of an ER pattern and to describe the observations made during, and the outcome of, catheter ablation of VPDs initiating VF.
Section snippets
Study population
We retrospectively analyzed data of 4560 patients who underwent catheter ablation for ventricular arrhythmias at the Hospital of the University of Pennsylvania. Between May 2007 and January 2022, 42 patients (0.9%) presented with VPDs initiating VF (group 1). Metabolic and toxicologic etiologies were excluded, and no structural or electrical causes were identified after extensive clinical investigation. Patients with apparently normal hearts were defined by normal 2-dimensional echocardiography
Study population clinical characteristics
Between May 2007 and January 2022, 42 patients with apparent structurally normal heart underwent catheter ablation of VPDs initiating VF (group 1). Of these 42 patients, 31 (74%) presented with sudden cardiac arrest and only 5 (11%) had a family history of SCD. Of the remaining 11 patients (26%), 10 presented with syncope and 1 with documentation of episodes of nonsustained PMVT with no symptoms. Fourteen patients underwent genetic testing. Of these patients, 5 (35%) demonstrated a variant of
Acute and long-term outcome of catheter ablation for VF triggers
In 29 of 40 patients (72.5%) in group 1, VPDs occurred in sufficient number to be targeted based on activation and pacemapping, with a goal of eliminating at least> 80% of VPDs. At the end of the first procedure, VPDs were completely abolished (16 patients) or at least >80% reduced from baseline (12 patients) in 28 of these 29 patients (96.6%) in group 1. In 11 patients (27.5%) in group 1, VPDs were not elicited or were rare during EP study, and an ablation strategy based on only pacemapping
Discussion
This is the first study describing the prevalence of sinus rhythm ECG abnormalities in patients with apparent structurally normal heart and VPDs initiating episodes of VF. Unique to our study, VF frequently occurred in the setting of ECG depolarization abnormalities that include a reduced QRS amplitude, QRSf, and/or the presence of an ER pattern. These ECG abnormalities are much more common than noted in a reference population of patients with later coupled VPDs that do not initiate VF.
The
Conclusion
A reduced QRS amplitude (<0.55 mV) in aVF, QRSf in ≥2 contiguous leads, and/or an ER pattern are frequently (81%) observed in patients with VPDs initiating VF and suggest an underlying subclinical structural cardiac abnormality in the presence of apparent normal imaging and EAM studies. VPDs initiating VF typically originate from the distal Purkinje system/PAPs and can be successfully eliminated with catheter ablation.
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Cited by (0)
Funding Sources: This work was supported by the Richard T. and Angela Clark Innovation Fund in Cardiovascular Medicine; the Mark S. Marchlinski EP Research and Education Fund; and the Winkelman Family Fund in Cardiovascular Innovation.
Disclosures: Dr Marchlinski has served as consultant for Abbott Medical, Biosense Webster, Biotronik, and Medtronic Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.