How to Recognize Epicardial Origin of Ventricular Tachycardias?

Abstract

Percutaneous pericardial access for epicardial mapping and ablation of ventricular arrhythmias has expanded considerably in recent years. After its description in patients with Chagas disease, the technique has provided relevant in-formation on the arrhythmia substrate in other cardiomyopathies and has improved the results of ablation procedures in various clinical settings. Electrocardiographic criteria proposed for the recognition of the epicardial origin of ventricular tachycardias are mainly based on analysis of the first QRS components. Ventricular activation at the epicardium has a slow initial component reflecting the transmural activation and influenced by the absence of Purkinje system in the epicardium. Various parameters (pseudodelta wave, intrinsicoid deflection and shortest RS interval) of these initial intervals predict an epicardial origin in patients with scar-related ventricular tachycardias with right bundle branch block morphology. Using the same concept, the maximum deflection index was defined for the location of idiopathic epicardial tachycardias remote from the aortic root. Electrocardiogram criteria based on the morphology of the first component of the QRS (q wave in lead I) have been proposed in patients with nonischemic cardiomyopathy. All these criteria seem to be substrate-specific and have several limitations. Other information, including type of underlying heart disease, previous failed endocardial ablation, and evidence of epicardial scar on magnetic resonance imaging, can help to plan the ablation procedure and decide on an epicardial approach.

Premature ventricular contraction-induced cardiomyopathy: Related clinical and electrophysiologic parameters

“…It is admitted that a longer QRS duration, especially in the presence of a LBBB, may participate in the alteration of LV function, because of the electrical and therefore likely associated mechanical dyssynchrony (30,31). Epicardial PVCs have been shown to have longer QRS duration than other PVCs (26) probably because of the paucity of Purkinje fibers in the epicardium and thus engaged in local conduction from the focus (32). Our data confirm this statement, although PVC duration was not linked to the presence of CMP.…”

Localization of Origins of Premature Ventricular Contraction by Means of Convolutional Neural Network From 12-Lead ECG

“…[27], [28] On ECG, epicardial VT is reflected as a slow onset of the QRS because the initial part of the wave front progresses slowly until it reaches the Purkinje system at the subendocardium. [29] The intracardiac delay of electrical conduction produces a slurred initial part of the QRS complex (pseudo Δ wave) [30] So the initial part (first half) of the QRS is critical for the detection of an epicardial or endocardial focus. In this study, we use the first half of QRS complexes generated by the ventricle computer model as input to the CNN to classify between an epicardial ectopic beat and an endocardial ectopic beat.…”

Insight of Electrocardiographic and Electrophysiological Parameters on The Left Ventricular Function in Patients with Ventricular Arrhythmia from Left Ventricular Summit

“…The initial part of the wavefront progresses slowly through the myocardial wall until reaching the Purkinje system at the subendocardium. This slow transmural activation is reflected as the slow onset of the QRS on the surface electrocardiogram 29 and prolonged transmural activation by measuring the AEAD [epi-endo]. To the best of our knowledge, this is the first study to demonstrate the relationship between PVC-induced cardiomyopathy and AEAD [epi-endo], a novel parameter associated with LV dysfunction in patients with LVS VA, which reflects the depth of intramural foci.…”