To further elucidate the potential role of IFN-γ in AF susceptibility, we performed optical mapping of the heart using rats. Although IFN-γ perfusion did not significantly alter AERP or APD, it precipitated a reduction in conduction velocity (P < 0.05; Figure 7B–D). Moreover, IFN-γ was found to induce notable alternans in action potentials and calcium transients (Figure 7E and F; P < 0.05), a precursor to arrhythmogenic activity. Most notably, these electrophysiological perturbations translated into an increased AF induction probability and a substantial prolongation of AF episodes (Figure 7G–I; P < 0.01)

A. Schematic diagram of the optical mapping system used for analyzing the rat heart. The hearts were perfused with recombinant rat IFN-γ or a vehicle control in each panel. B. AERP 3 measurements in S1-S2 mode, with premature S2 stimuli ranging from 60 to 20 ms (n = 11 each). C. APD30 and APD80 maps and quantification, with S1S1 stimulation at 6 Hz (n = 11 each). D. Comparison of the conduction velocity, with S1S1 stimulation at 6 Hz (n = 11 each). E-F. The amplitude maps along with profiles tracing normal or the alternans of both action potentials and calcium transients at indicated sites, at a cycle length of 80 ms (n = 11 each). G. Recordings of action potential and pseudo-ECG after 50Hz pacing and phase maps showing normal or rotor signal. H-I. Comparison of the AF incidence and duration after 50Hz pacing (n = 11 each). Student’s t test in B and D. Two-way ANOVA in C. Fisher’s exact test in F. Wilcoxon rank-sum test in H and I. *, p < 0.05; **, p < 0.01. Scale bar (ms): 40 in E

Cardiovasc Res. 2025 Apr 15;121(1):97-112.

doi: 10.1093/cvr/cvae222. PMID: 39382426.