Electropathological Substrate of Long-Standing Persistent Atrial Fibrillation in Patients With Structural Heart Disease

Abstract

Background-The electropathological substrate of persistent atrial fibrillation (AF) in humans is largely unknown. The aim of this study was to compare the spatiotemporal characteristics of the fibrillatory process in patients with normal sinus rhythm and long-standing persistent AF. Methods and Results-During cardiac surgery, epicardial mapping (244 electrodes) of the right atrium (RA), the left lateral wall (LA), and the posterior left atrium (PV) was performed in 24 patients with long-standing persistent AF. Twenty-five patients with normal sinus rhythm, in whom AF was induced by rapid pacing, served as a reference group. A mapping algorithm was developed that separated the complex fibrillation process into its individual elements (wave mapping). Parameters used to characterize the substrate of AF were (1) the total length of interwave conduction block, (2) the number of fibrillation waves, and (3) the ratio of block to collision of fibrillation waves (dissociation index). In 4403 maps of persistent AF, no evidence for the presence of stable foci or rotors was found. Instead, many narrow wavelets propagated simultaneously through the atrial wall. The lateral boundaries of these waves were formed by lines of interwave conduction block, predominantly oriented parallel to the atrial musculature. Lines of block were not fixed but continuously changed on a beat-to-beat basis. In patients with persistent AF, the total length of block in the RA was more than 6-fold higher than during acute AF (median, 21.1 versus 3.4 mm/cm 2 ; PϽ0.0001). The highest degree of interwave conduction block was found in the PV area (33.0 mm/cm 2 ). The number of fibrillation waves during persistent AF was 4.5/cm 2 compared with 2.3 during acute AF, and the dissociation index was 7.3 versus 1.5 (PϽ0.0001). The interindividual variation of these parameters among patients was high. Conclusions-Electric dissociation of neighboring atrial muscle bundles is a key element in the development of the substrate of human AF. The degree of the pathological changes can be measured on an individual basis by electrophysiological parameters in the spatial domain. (Circ Arrhythm Electrophysiol. 2010;3:606-615.)

Three‐dimensional Integrated Functional, Structural, and Computational Mapping to Define the Structural “Fingerprints” of Heart‐Specific Atrial Fibrillation Drivers in Human Heart Ex Vivo

“…However, most studies accept the importance of atrial structure, and all mechanisms would benefit from a method that can quantify the contribution of atrial structural substrates to AF maintenance 32, 33, 34, 35, 36, 37, 38, 39. Spach and colleagues were the first to report local conduction delay and morphological changes in electrical signals caused by abrupt changes in myofiber orientations and geometric tissue variations in the dog atria ex vivo 40.…”

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

“…U pacjentów z AF i towarzyszącymi stanami sprzyjającymi AF stwierdza się również nacieczenie przedsionków tkanką tłuszczową, nacieki zapalne, przerost miocytów, martwicę oraz amyloidozę [81][82][83][84]. Przebudowa strukturalna wywołuje rozkojarzenie elektryczne między pęczkami włókien mięśniowych i miejscową niejednorodność przewodzenia [85], co sprzyja pobudzeniom nawrotnym (re-entry) i podtrzymaniu arytmii [86]. U wielu pacjentów ten proces przebudowy strukturalnej następuje przed wystąpieniem AF [78].…”

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

“…On one side are those who promote variants of the original idea of Gordon Moe that fibrillation, whether atrial or ventricular, results from the continued random propagation of multiple independent electric waves that move independently throughout the atria. 234,235 On the other side are those who adhere to the theory that fibrillation is a consequence of the continued activity of a few vortices (rotors) that spin at high frequencies, generating 'fibrillatory conduction'. 236,237 In either case, arrhythmia maintenance is favoured by abbreviated APD/refractory period.…”