Atrial Fibrillation and Fibrosis: Beyond the Cardiomyocyte Centric View

Figure 2

Increased susceptibility to atrial flutter/fibrillation (AF) in hearts. (a) Rapid-pacing-induced AF in hearts under isoproterenol and acetylcholine treatment. The pseudo-ECG showed that rapid pacing at 30 Hz induced AF which lasted for 28 seconds. The regular fibrillatory (F) waves indicating atrial flutter is zoomed in on the right. Both macro- and microreentry were drivers for the AF in hearts. The reentrant circuits are shown in the activation maps on the left; maps in the middle show the dominant frequency (or the reciprocal of the averaged cycle length) at various locations. During macroreentry, dominant frequency was uniform. In contrast, during microreentry, dominant frequency was locally higher in the microreentry circuit area. On the right are the sample optical action potentials (OAPs), whose locations were marked by numbers in the frequency maps. Abbreviations are the same as those in Figure 1. (b) Spontaneous AF occurred under Isoproterenol (Iso) and acetylcholine (ACh) treatment. As shown in OAPs and activation maps, the heart was under slow stable IVC rhythm, and then one of the IVC beats triggered a rapid burst of atrial activity. Representative OAP trace from the IVC region is shown. (c) Percentage of animals with AF inducibility in the control and groups (sAF: spontaneous AF; pAF: pacing-induced AF) (reprinted with permission from [4]).

(a) Pacing-induced AF in heart

(b) Spontaneous AF in heart

(c) AF%