Key result
Three-dimensional electroanatomic mapping and histology showed the cardiac fulcrum is rich in neurofilaments adjacent to the AV node, with left ventricular activation completing at 116.6±2.15 ms.
Why the study?
This investigation analyzed the anatomical, histological, and functional relationship between the cardiac fulcrum and the atrioventricular node across human, bovine, porcine, and anuran hearts.
Observational (n=101)
No
Histological and 3D electroanatomical mapping analyses demonstrate that the cardiac fulcrum and AV node form an interconnected neurofilament-rich electromechanical unit supporting the helical continuous myocardium model of ventricular activation and torsion.
Observed fulcrum-AV node contiguity may indicate electromechanical coupling; leaves open clinical relevance for pacing and demands further study.
Objective: In the present investigation, the anatomical and histological relationship of the Cardiac Fulcrum with the atrioventricular node in hearts of the human, bovine, porcine and anuran species was analyzed, as well as the possible functionality between both structures and the actions derived from said electromechanical unit. Material and methods:The methods used in this research to explain consisted of:1) The use of 96 hearts from a morgue, slaughterhouse and breeding grounds: a) 17 human hearts (three at 8, 16, and 23 weeks of gestation, respectively; four infants at 30 days, 36 days, 10 weeks, and 27 weeks; one 4-year-old child; one 10-year-old child; and eight adults with an average weight of 300 g); b) 59 two-year-old bovine hearts weighing between 1300 and 1900 g (average 1650 g); c) 10 porcine hearts (400 g); 10 de anuros (Rhinella arenarum) 2) Histological and histochemical analysis of the anatomical samples. 3) Immunostaining technique for neurofilaments.4) The endo-and epicardial electrical activation of the left ventricle was studied in 5 humans using three-dimensional electroanatomical mapping. Results:We observed that in all the species studied (human, bovine, and porcine), the fulcrum has a central area and two poles.It is in close contact with the atrioventricular node.The fulcrum and the atrioventricular node regulate and modulate the body's afferent information before converting it into the depolarization wave.Conclusion: During this investigation, in both human and other species' hearts, histological analysis revealed that the fulcrum (the beginning and end of the continuous myocardium) is adjacent to the AV node, defining a space rich in plexuses with interconnected neurofilaments between both structures.The structural relationship between myocardial stimulation and its mechanical product was analyzed, based on the assumption that this electromechanical unit is undergoing a continuous process of self-organization in which time plays a fundamental role as a fourth dimension added to the three spatial dimensions.The mechanical consequence of the initiation of stimulation in the anatomical and functional unit between the AV node and the cardiac fulcrum, and the continuity of myocardial activation up to the anisotropic zone at the contiguity between the descending and ascending segments, is what generates myocardial torsion through the sequential opposition of movements.Each heartbeat is then a result of a reading of fluctuations in an external and internal environment, which enters through the autonomic system to the AV node in sync with the Fulcrum that generates rhythmic feedback with coupling and decoupling similar to a self-organizing process.
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Jorge Carlos Trainini (2026) conducted an observational in Cardiac anatomy and electrophysiology (arrhythmias in the 5 living human subjects) (n=101). Histological/immunohistochemical analysis and 3D endo-epicardial electroanatomic mapping (MET) was evaluated on Total left ventricular endo-epicardial electrical activation propagation time and anatomical relation of the cardiac fulcrum and AV node. Three-dimensional electroanatomic mapping and histology showed the cardiac fulcrum is rich in neurofilaments adjacent to the AV node, with left ventricular activation completing at 116.6±2.15 ms.
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