Figure 1.

Site-specific prolongation of repolarization prevents postinfarction tachycardia. A, left: Transversal section of the pig heart at the level of the apex showing infarcted myocardium based on autofluorescence. Middle: Schematic drawing of the left anterior wall indicates the location of the multielectrode and the stimulus electrode. Right: Tracing shows pronounced fractionated potentials initiated by the third premature stimulus (s4), which were only present at the location of the red dots in the grid. B: Map showing the activation and repolarization sequence before (top) and after (bottom) sotalol injection at basic cycle length (s1). Note local prolongation of repolarization (±25 ms) at the location where fractionated potentials were present. C: Local electrograms before and after local injection of sotalol. D:Upper trace shows a monomorphic tachycardia induced by premature stimulation (s1-s2-s3-s4). After local sotalol injection, only a single extra beat was induced (lower trace). Bar graph shows the decrease in arrhythmia inducibility. Superimposed red line indicates the simultaneous increase in local repolarization time of S1 in the area with fractionated potentials. E, left:In silico reconstruction of the left ventricular septal and free wall showing noninfarcted myocardium in red, gray zone in green, and scar in yellow.Middle: Potential distribution shows the activation front exiting the infarcted myocardium resulting in sustained reentry, of which the first cycle is shown at the right. F, left: Region in purple shows prolonged repolarization (±50 ms) near the exit site. Middle: Activation front exiting the infarcted myocardium at a different location than before site-specific prolongation of repolarization, resulting in only a single reentrant beat (right). LV = left ventricle; RV = right ventricle.