Abstract
The arrhythmogenic role of increased dispersion of repolarization (Dispersion) in monophasic action potentials (MAPs) was studied in 12 open-chest dogs. Following exposure of the heart by pericardial cradle, four MAPS were recorded simultaneously from the right and left ventricular surfaces using the suction electrode technique. Maximum dispersion (maxDIS) was defined as the greatest Dispersion between any two of the four MAPS in atrial pacing and ventricular premature stimulation (VPS). Dispersion was increased by warming the heart with a heat lamp and regional cooling with a cold saline (2-4°C) drip. In control experiments maxDIS in atrial pacing (PCL: 500 ms) was 21±10 ms. MaxDIS was increased when the VPS was applied at the right ventricular apex (RVa) (maxDIS: 73±17 ms), at the left ventricular base (LVb) (maxDIS: 78±34 ms), and at the left ventricular apex (LVa) (maxDIS: 89±20 ms). Ventricular fibrillation, however was not induced by any VPSs. Warming the heart and regional cooling increased Dispersion from the control value to 180±58 ms (p<0.001), mainly because of the increased MAP duration difference (ΔMAPD) in atrial pacing, but no ventricular fibrillation occurred spontaneously. VPS applied at the LVa induced ventricular fibrillation following marked increase of maxDIS, which was due to added contributions of AMAPD and the maximal difference between activation times (ΔAT). With RVb cooling ventricular fibrillation was induced in 16/20 cases (80%) (maxDIS: 286±124 ms), with RVa cooling in 6/9 cases (67%) (maxDIS: 263±109 ms), and with LVb cooling in 11/23 cases (48%) (maxDIS: 172±67 ms). There was significant linear correlation between maxDIS and ΔAT (r=0.88, p<0.01), and also AMAPD (r=0.80, p<0.01).
We conclude that the increased Dispersion plays an important role in the induction of ventricular fibrillation. This temperature gradient model is a favorable tool to study the role of Dispersion as one of the important factors which induce ventricular fibrillation.
