Abstract

Cardiac alternans are a precursor to arrhythmias. Spatially discordant alternans (SDA) in ventricles are especially arrhythmogenic as they can lead to ventricular tachycardia and fibrillation. Bidirectional ventricular tachycardia (BVT) is one of the rare arrhythmias. However, the underlying mechanism is still not clear. The normal electrical activity generated by the sinoatrial node propagates as an action potential wave in the heart. BVT occurs when the route of conduction changes in every other beat. In this study, we investigated the mechanism of BVT using mathematical models of cardiac tissue. The two-dimensional tissue was paced from two sites at a constant pacing cycle length. The stimulation site alternated every pacing cycle. We measured electrical alternans, which are defined as an alternating sequence of the action potential durations. We varied parameters in the model such as the distance between two sites and the pacing cycle length. We found that alternans amplitude was significantly amplified when the tissue was paced alternatively from two sites. SDA was formed even at slow heart rates. The alternans amplitude increased with the distance between the pacing sites. The nodal line was formed in the middle of the two pacing sites. This is arrhythmogenic since it can easily lead to a wave break that may initiate a spiral wave. Fast pacing with steep APD restitution is another mechanism of SDA. However, the nodal line is parallel to the wavefront. When tissue is paced rapidly and alternatively from two sites, APD distribution becomes more complex. Our study demonstrates that alternans can be formed by alternating pacing from two sites that mimics BVT.

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