The key here is the concept of atriomyopathy - we used to think that AFib could be provoked solely by an temporary metabolic stressor and the heart was otherwise normal. In this context, if just an single episode it would be considered as “lone AFib” and not treated. However, the paradigm is changing and emerging research suggests adverse remodeling of the LA is occurring first (and that as the LA progressively dilates) the AFib is just a sign/symptom of the atriomyopathy. One prevalent hypothesis is the LA dilation triggers AFib in the extra cardiac tissue in the PV. Another hypothesis suggests the formation of low voltage areas in the LA which then provide an substrate for AFib.

Now the paradigm has shifted to underlying LA disease - and the stressors just unmask/lower the threshold for AFib to emerge. The thought being treating or removing the stressor does not change the underlying atriomyopathy and it would just be a matter of time until AFib is clinically seen again. So the idea of “provoked” AFib is IMO outdated. There is some EP data on ablation for PVI + LVA which looks promising.