For a long time, lack of knowledge regarding the physiopathology of atrial fibrillation (AF) limited the development of interventional techniques for treating it. Demonstrations that paroxysmal AF was triggered by extrasystoles and tachycardias mainly originating from inside the pulmonary veins ushered in a new era for treatment of AF. Since then, electrical isolation of the pulmonary veins has been the standard treatment for AF. Among specialists, achieving lasting electrical isolation of the pulmonary veins has been the main technical challenge, which has gradually been overcome in recent years with the implementation of new technology for more effective ablation, given that reconnections or previously isolated veins are the main cause of recurrences observed in these patients.

The challenge has been greater in patients with persistent AF, owing to its more complex physiopathology, which involves additional mechanisms that are little known, in addition to the pulmonary venous foci. It is known that metabolic alterations induced by excessive atrial work during repeated episodes of AF initially induce atrial electrical remodeling, characterized by functional and transient changes in ion channels of cell membranes that modulate atrial electrical activity, thus facilitating the appearance of trigger foci in other regions of the atria and conditions that favor increased persistence of AF.

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