Figure 4.

Radiofrequency ablation of the epicardial surface abolishes the BrS ECG and suppresses arrhythmogenesis in coronary-perfused canine right ventricular wedge model of BrS. Transmembrane action potentials (AP) were simultaneously recorded from one endocardial (Endo) and two epicardial (Epi) sites together with epicardial bipolar electrograms (EG) and a transmural pseudo-ECG. The epicardial bipolar EGs were recorded at 10-1000 Hz bandwidth (black trace), and were simultaneously band-pass filtered at 30-200Hz, 50-200Hz and 100-200Hz (green traces). Column 1: Control. Column 2: Recorded 45 min after the addition of the I_to-agonist NS5806 (4μM) to the coronary perfusate. Column 3: Recorded 45 min after the concentration of NS5806 was raised to 8μM. High and low frequency late potentials (LP) are apparent in the EG recordings resulting from progressive delay in the appearance of the second upstroke of the Epi AP secondary to accentuation of the AP notch. Column 4: Recorded 15 min after the addition of the I_Ca-blocker verapamil (1μM) to the coronary perfusate. Column 5: Recorded after 40 min of exposure to verapamil (1μM). Loss of the AP dome at Epi1 but not Epi2 gives rise to a phase 2 reentrant beat, which precipitates polymorphic VT. Column 6: Recorded 2h after radiofrequency ablation of the epicardial surface, and 1h after reintroduction of the provocative agents to the perfusate (in the same concentration as before ablation). APs are now recorded from the deep subepicardium- midmyocardium (Mid1, Mid2) instead of the epicardial surface. Ablation markedly suppressed the BrS phenotype and abolished all arrhythmic activity. Modified from ¹⁶⁸, with permission.