A case of infra-nodal Wenckebach conduction block with alternating bundle branch block

Background Atrioventricular (AV) node normally has decremental conduction property and a longer refractory period than His-Purkinje system (HPS). This results in AV conduction delay or block at the level of AV node in response to short-coupled atrial premature beats. Prolonged refractoriness in HPS can produce unusual physiological patterns of AV conduction such as conduction delay or infra-nodal block in the distal elements of HPS. Case presentation We present a case in which atrial premature stimulation produces infra-nodal Wenckebach conduction block which initiates long-short cycle sequence within the bundle branches resulted in alternating bundle branch block and atypical pattern of Ashman phenomenon. Conclusions This case highlights the importance of recognizing the unusual physiological AV conduction patterns of HPS. The long-short cycle sequence in the bundle branches of distal HPS and linking phenomenon can result in alternating bundle branch block without the presence of HPS disease.

Ventricular transmural decremental conduction explains short t-peak-t-end interval in “in silico” ECG reconstruction model

Introduction In chronic hepatic cirrhosis (CHC), T-wave peak to T-wave end interval (TPTE) has shown prognostic value for survival and liver transplantation. Altered cellular ionic regulatory systems may produce decremental conduction in ventricular endocardial to epicardial activation wavefront propagation and ECG waveforms, particularly the T-wave. It was investigated whether ventricular transmural activation wavefront conduction may affect T-wave shape and impact TPTE duration, using “in silico” ECG reconstruction. Methods Mammalian-derived ventricular endocardial to epicardial AP waveforms (APW) were simulated and deployed in 10 discrete layers in homogeneous impedance ventricular wedge-like model. A uniform conduction model was employed to mimic normal heart, in which the speed of propagation of the activation wavefront was nonzero and constant in all layers. In CHC heart, a decremental conduction model was employed, in which the speed of propagation of the activation wavefront was maximal at the endocardial layer and exponentially decayed to greater than zero speed at the epicardial layer. ECG was computed as the sum of dipoles weighted by the inverse of the squared distance to an observation electrode arbitrarily located outside the wedge. One dipole was one layer thick, and its charge was assumed as the time-integral of the current generated by the difference of potential between adjacent APW, from endocardial to epicardial layers. ECG was reconstructed in one axis. Results Two-dimensional transmural APW distribution and respective reconstructed ECGs are presented in Figures 1 and 2. In uniform endocardial to epicardial transmural conduction model, QRS complex was taller and shorter as well as TPTE was larger (Fig. 1) than respective counterparts in decremental conduction model (Fig. 2). Additionally, peak-amplitude of the T-wave as well as the maximal slope of the TPTE were lower in decremental as compared to uniform conduction model. Conclusion Using “in silico” ECG reconstruction, decrementally conducted model of epicardial to endocardial ventricular transmural activation wavefront propagation yields wider and lower amplitude QRS complex as well as shorter TPTE, as compared to respective counterparts in uniformly conducted activation wavefront model. Ventricular transmural decremental conduction model offers an insight into electrophysiological background of ECG findings in CHC. (NCT01433848) Transmural APW distribution vs ECG Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Universidade do Estado do Rio de Janeiro; Rio de Janeiro, RJ - Brazil

Purkinje Fibers in Canine False Tendons: New Anatomical and Electrophysiological Findings

Introduction. Purkinje system and false tendons (FTs) are related to ventricular arrhythmia, but the association between Purkinje fibers and FTs is not clear. This study investigated the associations of anatomical and electrophysiological characteristics between Purkinje fibers and FTs. Methods and Results. We optimized the protocol of Lugol’s iodine solution staining of Purkinje fibers to study the anatomical structure and originated a novel electrophysiological mapping method, named the direct visual mapping (DVM) method, to study the electrophysiological characteristics. By using the above-mentioned innovations in 12 dogs, we found the following. (1) There was no Purkinje fiber found 0.5 cm–1.0 cm below the valve annulus or on the leaflets or chordae tendineae of the mitral valve or adjacent to the top 1/3 of the papillary muscle. (2) Purkinje fibers existed in all FTs, including smaller and tiny FTs. (3) The Purkinje fibers contained in the FTs extended from the proximal to the distal end, and their electrophysiological characteristics were similar to the fibers on the endocardium, including anterograde, retrograde, and decremental conduction and automaticity. Conclusions. Purkinje fibers are commonly found in FTs. The electrophysiological characteristics of the Purkinje fibers contained in FTs are similar to the fibers on the endocardium. FTs might have an anatomical and electrophysiological basis for ventricular arrhythmia.

Anatomy and physiology of the atrioventricular node

The atrioventricular node (AVN) and the surrounding area is a crucial part of the cardiac conduction system. It consists of specialized tissue located at the base of the atrial septum within the triangle of Koch. The inherent physiological function of the AVN is to delay cardiac impulse propagation between the atria and the ventricles, and to function as a backup pacemaker in the setting of sinoatrial node dysfunction or advanced atrioventricular (AV) block. AV nodal conduction and pacemaker activity are under strict control by the autonomic nervous system. Due to the unique property of decremental conduction, the AVN protects the heart from an excessive ventricular rate during rapid atrial arrhythmias. On the other hand, the AVN is also an important source of brady- and tachyarrhythmias, and a target for various pharmacological and non-pharmacological arrhythmia therapies.

Pre-excitation related to Mahaim physiology

Rare accessory pathways, such as Mahaim fibres, have been postulated to result in cardiac pre-excitation. However, most lack the histopathological correlation that has been demonstrated for the Wolff–Parkinson–White pattern. This chapter will discuss the Mahaim fibre tachycardias with left bundle branch block pattern. Mahaim fibres are characterized by the presence of different accessory pathways with decremental conduction (Mahaim physiology, i.e. conduction slows at faster heart rates), which only conducts in an antegrade fashion. The Mahaim fibres have a different anatomical location and distribution that characteristically terminate in the ventricles into or near the conducting system and are responsible for the constellation of electrophysiological features that define Mahaim tachycardias. Similar to other types of pre-excitation syndromes, there are two treatment options available for the treatment of Mahaim fibre tachycardias: pharmacological therapy and/or curative ablation. Catheter ablation offers the greatest chance at definitive therapy for symptomatic patients experiencing frequent Mahaim tachycardias.