Basis for the Induction of Tissue-Level Phase-2 Reentry as a Repolarization Disorder in the Brugada Syndrome

Figure 4

Induction of reentrant activity by phase-2 reentry (P2R) in epicardial tissue layers. The upper part of the  cm tissue represents normal epicardium, whereas the bottom part represents Brugada-affected epicardial tissue (left: lost-dome Brugada; right: delayed-dome Brugada). (a) Under stimulation from the lost-dome region, an antidromic P2R originates from the delayed-dome region, re-exciting the lost-dome epicardium and forming a stable reentry when the normal epicardial region recovers. (b) Under stimulation from the delayed-dome region, the orthodromic P2R is unable to find excitable normal epicardial tissue, and sustained reentry is not induced for this tissue size. (c) Under homogeneous epicardial activation, P2R develops analogously to the antidromic reentry case. Tissue coupling was decreased by 20% in order to accommodate the reentrant wave in the 6 × 6 cm domain. Color bar denotes transmembrane potential.

(a) Stimulation from lost-dome

(b) Stimulation from delayed-dome

(c) Stimulation from Purkinje network