Mechanisms linking T‐wave alternans to spontaneous initiation of ventricular arrhythmias in rabbit models of long QT syndrome

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12833-list-0001">T‐wave alternans (TWA) and T‐wave lability (TWL) are precursors of ventricular arrhythmias in long QT syndrome; however, the mechanistic link remains to be clarified.Computer simulations show that action potential duration (APD) prolongation and slowed heart rates promote APD alternans and chaos, manifesting as TWA and TWL, respectively.Regional APD alternans and chaos can exacerbate pre‐existing or induce de novo APD dispersion, which combines with enhanced I Ca,L to result in premature ventricular complexes (PVCs) originating from the APD gradient region.These PVCs can directly degenerate into re‐entrant arrhythmias without the need for an additional tissue substrate or further exacerbate the APD dispersion to cause spontaneous initiation of ventricular arrhythmias.Experiments conducted in transgenic long QT rabbits show that PVC alternans occurs at slow heart rates, preceding spontaneous intuition of ventricular arrhythmias.