Dynamics of Intramural and Transmural Reentry During Ventricular Fibrillation in Isolated Swine Ventricles

Abstract

Abstract-The intramural dynamics of ventricular fibrillation (VF) remain poorly understood. Recent investigations have suggested that stable intramural reentry may underlie the mechanisms of VF. We performed optical mapping studies of VF in isolated swine right ventricles (RVs) and left ventricles (LVs). Nine RV walls were cut obliquely in their distal edge exposing the transmural surface. Six LV wedge preparations were also studied. Results showed that intramural reentry was present. In RV, 28 of 44 VF episodes showed reentry; 15% of the activation pathways were reentrant. Except for 4 episodes, reentry was transmural, involving subendocardial structures as the papillary muscle (PM) or trabeculae. In LV, reentry was observed in 27 of 27 VF episodes; 23% of the activations were part of reentrant pathways (PϽ0.05 compared with RV). All LV reentrant pathways were truly intramural (confined to the wall) and were frequently located at the PM insertion. In both ventricles, reentry was spatially and temporally unstable. Histological studies showed abrupt changes in fiber orientation at sites of reentry and wave splitting. Connexin 40 immunostaining demonstrated intramyocardial Purkinje fibers at sites of reentry in the PM root and around endocardial trabeculae. Our results confirm that reentry is frequent-but unstable-in the myocardial wall during VF. In RV, reentry is mostly transmural and requires participation of subendocardial structures. The LV has a greater incidence of reentry and is intramural. Anisotropic anatomic structures played key roles in the generation of wave splitting and in the maintenance of reentry. Key Words: intramural reentry Ⅲ fibrillation Ⅲ anisotropy Ⅲ Purkinje Ⅲ papillary muscle O ur current knowledge of the activation dynamics that take place during ventricular fibrillation (VF) derives from multiple endocardial and/or epicardial mapping studies. [1][2][3][4][5] On the basis of these data, VF has been characterized by spatiotemporal heterogeneity because of the coexistence of both organized reentry and fragmented wavelets. 3,4,6,7 However, the intramural dynamics of VF remain largely unexplored because of the lack of an experimental model that allows for intramural mapping of VF. Recent studies 8,9 have suggested that rapid and stable intramural reentry might serve as the source of VF. Intramural reentry has been previously demonstrated during ventricular tachycardia or fibrillation, 1,10 -13 but whether stable intramural reentry occurs during VF and to what extent is it required to maintain VF are unanswered questions. We have developed an experimental model to study intramural patterns of activation during VF. Our results confirm that reentry is indeed frequently seen in the myocardial wall. Substantial differences are noted between right ventricle (RV) and left ventricle (LV). We also demonstrate that anatomic structures played key roles in the generation of wave splitting and in the maintenance of reentry. Materials and Methods RV PreparationThe experimental model has been previously...

Mother Rotors and the Mechanisms of D600-Induced Type 2 Ventricular Fibrillation

“…3 Furthermore, an abrupt change of fiber orientation or a specific spatial distribution of the Purkinje-muscle junction at the PM base can be associated with conduction delay and reentry formation. 4,19 An important finding of the present study is that the mother rotors during type 2 VF were not randomly distributed throughout the ventricles. Rather, they clus- tered around the PM region.…”

“…Optically recorded voltage signals were spatiotemporally filtered to reduce noise. 4,5 Phase mapping 7 was performed to evaluate the location and evolution of phase singularities (PSs) in VF. For cumulative PS display (ie, a PS map) over long acquisition intervals (typically 600 frames), PSs were identified by an automated PS tracking algorithm.…”

“…2 However, the nature of this focal source during type 2 VF remains unclear. We [3][4][5] previously demonstrated that the papillary muscle (PM) can serve as a site for anchoring reentry. An anchored stationary scroll wave can have a longer life span and can function as a mother rotor.…”

A Tale of Two Fibrillations

“…The anatomic heterogeneities, which are naturally present, also facilitate conduction blocks and wavebreaks through the source-sink mismatches. 13 For example, epicardial coronary arteries, 14 papillary muscles, 15 transmural sites with abrupt fiber orientation changes, 16 and increased fibrosis resulting from cardiomyopathy 17 can all serve as sites of wavebreaks. With the more recent appreciation that dynamic factors related to electrical restitution also play a key role in facilitating wavebreak, an updated version of the Multiple Wavelet Hypothesis emphasizes that the synergy between dynamic factors and preexisting tissue heterogeneities are the fundamental cause of wavebreaks perpetuating VF.…”

Spatial Distribution of Phase Singularities in Ventricular Fibrillation

“…9,10 For right ventricular (RV) studies, the RV wall was excised, perfused with Tyrode's solution, and placed in a tissue bath. Optical mapping during VF was performed on the endocardial surface (nϭ12) as well as the epicardial surface (nϭ9).…”