Percutaneous Catheter Ablation of Epicardial Accessory Pathways.

Radiofrequency (RF) catheter ablation is the treatment of choice in patients with accessory pathways (APs) and Wolff-Parkinson-White syndrome. Endocardial catheter ablation has limitations, including the inability to map and ablate intramural or subepicardial APs. Some of these difficulties can be overcome using an epicardial approach performed through the epicardial venous system or by percutaneous catheterisation of the pericardial space. When a suspected left inferior or infero-paraseptal AP is refractory to ablation or no early activation is found at the endocardium, a transvenous approach via the coronary sinus is warranted because such epicardial pathways can be in close proximity to the coronary venous system. Associated congenital abnormalities, such as right atrial appendage, right ventricle diverticulum, coronary sinus diverticulum and absence of coronary sinus ostium, may also hamper a successful outcome. Percutaneous epicardial subxiphoid approach should be considered when endocardial or transvenous mapping and ablation fails. Epicardial mapping may be successful. It can guide and enhance the effectiveness of endocardial ablation. The finding of no epicardial early activation leads to a more persistent new endocardial attempt. When both endocardial and epicardial ablation are unsuccessful, open-chest surgery is the only option to eliminate the AP.info:eu-repo/semantics/publishedVersio

Unusual source of tachycardia in an adolescent

Mahaim fiber tachycardia is an uncommon cause of palpitations among the pediatric population. This case report describes an adolescent female who presented with recurrent episodes of tachycardia with chest pain and dizziness. Her ECG showed tachycardia with wide QRS complexes and left bundle branch block pattern. Repeat ECG after adenosine treatment revealed sinus rhythm with persistence of the left bundle branch block pattern. Metoprolol was started however she continued to have episodes of sustained tachycardia

Bigeminy and the bifid papillary muscle

Various structural anomalies of the left ventricular papillary muscles have been observed in recent years. Many of these have been linked to electrocardiographic aberrations

Revisiting the Atrioventricular Conduction Axis for the 21st Century

\ua9 The Author(s) 2024. In this review, we summarise the ongoing debate surrounding the anatomy of the atrioventricular conduction axis and its relevance to pacing. We highlight previous disagreements and emphasise the importance of understanding the anatomical location of the axis. We give credit and support to the initial descriptions by His and Tawara, in particular their attention to the relationship of the atrioventricular conduction axis with the membranous septum. We express our disagreements with recent diagrams that incorrectly, in our opinion, depict the left bundle and right bundle branches. We offer our own latest understanding of the location and relationships of the atrioventricular conduction axis, including details of its development, and differences between human and animal hearts. We also emphasise the importance of understanding the relationship between the inferior pyramidal space and the inferoseptal recess so as appropriately to place the axis within the heart. We conclude by emphasising the need to consider the heart in the context of the body, describing its component parts by using attitudinally appropriate nomenclature

The Anatomy of the Atrioventricular Node

\ua9 2025 by the authors.The anatomical arrangement of the atrioventricular node has been likened to a riddle wrapped up in an enigma. There are several reasons for this alleged mystery, not least the marked variability in structure between different species. Lack of detailed knowledge of the location of the node relative to the atrial and ventricular septal structures has also contributed to previous misunderstandings. Recent studies comparing the findings of gross dissection with virtual dissection of living datasets, combined with access to a large number of serially sectioned human and animal hearts, have served to provide the evidence to solve the riddle. We summarise these findings in this review. We explain how the node is located within the atrial walls of the inferior pyramidal space. It becomes the non-branching component of the atrioventricular conduction axis as the axis extends through the plane of atrioventricular insulation to enter the infero-septal recess of the left ventricular outflow tract. The node itself is formed by contributions from the tricuspid and mitral vestibules, with extensive additional inputs from the base of the atrial septum. We show how knowledge of development enhances the appreciation of the arrangements and offers an explanation as to why, on occasion, there can be persisting nodoventricular connections. We discuss the findings relative to the circuits producing atrioventricular re-entry tachycardia. We conclude by emphasising the significance of the variation of the anatomical arrangements within different mammalian species

Mammalian γ2 AMPK regulates intrinsic heart rate.

AMPK is a conserved serine/threonine kinase whose activity maintains cellular energy homeostasis. Eukaryotic AMPK exists as αβγ complexes, whose regulatory γ subunit confers energy sensor function by binding adenine nucleotides. Humans bearing activating mutations in the γ2 subunit exhibit a phenotype including unexplained slowing of heart rate (bradycardia). Here, we show that γ2 AMPK activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate, including sarcolemmal hyperpolarization-activated current (I f) and ryanodine receptor-derived diastolic local subsarcolemmal Ca(2+) release. In contrast, loss of γ2 AMPK induces a reciprocal phenotype of increased heart rate, and prevents the adaptive intrinsic bradycardia of endurance training. Our results reveal that in mammals, for which heart rate is a key determinant of cardiac energy demand, AMPK functions in an organ-specific manner to maintain cardiac energy homeostasis and determines cardiac physiological adaptation to exercise by modulating intrinsic sinoatrial cell behavior