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. Author manuscript; available in PMC: 2014 Nov 1.
Published in final edited form as: Heart Rhythm. 2013 Aug 1;10(11):10.1016/j.hrthm.2013.07.047. doi: 10.1016/j.hrthm.2013.07.047

Figure 2.

Figure 2

Effect of cilostazol to reverse the repolarization defects underlying the electrocardiographic and arrhythmic manifestations of Brugada syndrome in a coronary-perfused right ventricular wedge model. Recordings were obtained at a basic cycle length of 1000 ms. Each shows transmembrane action potentials (APs) recorded from 2 epicardial (Epi) sites and 1 (Endo) endocardial site together with an ECG, all simultaneously recorded. The Ito agonist NS5806 increases notch and J wave parameters but does not induce arrhythmic activity. The addition of verapamil leads to marked accentuation of the Epi AP notch, giving rise to a large J wave, appearing as an ST segment elevation. Loss of the dome at Epi 2 results in development of phase 2 reentry. Cilostazol (5 μM) reverses these repolarization defects, restoring AP duration homogeneity, normalizing the ECG and abolishing all arrhythmic activity. Cilostazol (10 μM) further reduced notch and J wave parameters. The Brugada phenotype promptly reappears after washout of cilostazol. Time calibrations for the recordings are indicated on the right of the figure. The top trace is a stimulus marker.