Disclosures: NonePulmonary vein isolation (PVI) has become established as an effective therapy for paroxysmal atrial fibrillation (AF). The mechanistic basis of PVI, as a strategy to isolate ectopic foci that trigger AF paroxysms, is sound. The therapeutic tools to achieve PVI are robust, and the outcomes, albeit imperfect, are satisfactory. Although PVI failures do exist, the majority are due to technical failures, ie, the inability to achieve durable PVI, and only a relative minority can be attributed to nonpulmonary vein triggers. In essence, the mechanistic paradigm of trigger ablation remains unchallenged for paroxysmal AF. Although purely a temporal-pattern characteristic, paroxysmal AF in its prototypical form occurs in structurally normal hearts, and trigger elimination without extensive substrate modification is generally sufficient.On the other hand, the treatment of nonparoxysmal forms of AF remains challenging. Persistent AF most commonly arises in the context of aged atria, and often coexists with hypertensive heart disease, diabetes, sleep apnea, and other comorbidities. Even in the presence of structurally normal hearts with normal left ventricular ejection fraction, high left atrial pressures, left atrial scar, and varying degrees of diastolic dysfunction are common in persistent AF. By definition, persistent AF patients are in continuous AF for at least a week, but some for months or even years. The coexistence of structural atrial disease and the prolonged temporal persistence are inconsistent with an exclusive relevance of triggers initiating AF, and suggest that a substrate maintaining AF is perhaps a more valid therapeutic target. Identifying accurately such substrate-regions mechanistically involved in the maintenance of AF-has proven extremely difficult. It is likely that no single region is solely responsible for the maintenance of AF, and that interindividual and intraindividual variations in AF maintenance mechanisms exist. Strategies to improve ablation outcomes by extending lesion sets beyond PVI have failed in randomized clinical trials. Reasons may be technical; if ablation lesion sets are incomplete, no benefit is to be expected, but also could be because mechanistically the additional lesions fail to impact AF.Although it is likely that no single or fixed anatomical location can be expected to be a universally valid ablation target, the ligament and vein of Marshall (LOM and VOM) appear plausible contributors to AF generation and maintenance. Located in the epicardial aspect of the left atrial ridge, the VOM colocalizes with abundant sympathetic and parasympathetic innervation that can modulate atrial myocyte physiology to create a profibrillatory state. It has associated complex myocardial architecture with discrete LOM-atrial connections. It can be a source of ectopic AF triggers (for review, see Rodríguez-Mañero et al 1 ). In addition, the VOM is a true atrial vein with direct communication with the underlying myocardium, 2,3 which encompasses the left atrial ridge, and most imp...