Figure 1. Fundamental arrhythmogenic mechanisms and antiarrhythmic therapies.

Ectopic activity, often resulting from delayed or early afterdepolarizations (DADs or EADs, respectively), and reentry, promoted by short and heterogeneous effective refractory periods, Ca²⁺-driven repolarization alternans and slow heterogeneous conduction, are the predominant arrhythmogenic mechanisms involved in the initiation and maintenance of cardiac arrhythmias. Both mechanisms are influenced by interactions between the genetic predisposition, environmental factors, and (non-) cardiovascular diseases. Almost all AADs exhibit both pro- and antiarrhythmic effects. For example, Class I AADs (blocking cardiac Na⁺ channels) decrease excitability, reducing the likelihood of ectopic activity and prolong effective refractory period, reducing reentry, but can promote reentry by slowing conduction velocity. Similarly, Class III AADs prolong effective refractory period, reducing reentry, but can promote EAD-mediated ectopic activity.