Patent (open) foramen ovale (PFO) is a common anomaly, affecting approximately a quarter of the adult population. In most people PFO never causes a health problem, but paradoxical embolism of venous thrombi with deleterious consequences has been well described in the setting of deep venous thrombosis and right heart pressure overload—that is, after severe pulmonary embolism.¹ After the initial seminal reports^2,3 many studies have confirmed a statistical association between unexplained, presumably embolic ischaemic neurologic events in young patients and the presence of a PFO, indicating that these events might be caused by paradoxical embolism from—mostly clinically inapparent—venous thrombosis.

The difficulty, hence, is to define under which circumstances (other than severe pulmonary embolism) PFO constitutes a risk high enough to warrant treatment, and to define optimal treatment. Unfortunately, this is an exercise in weighing several relatively small risks: the risk of recurrence of an ischaemic event, the risk of anticoagulation treatment, the risk of a procedural complication of closure (for example, device embolisation), and the risk of a post-procedural complication (for example, thromboembolism from a device). Assessment is further complicated by an index event, paradoxical embolism, which is almost never directly observed and usually only inferred. Therefore, neither whether the event is embolic nor whether other embolic sources are “ruled out” constitute iron-clad facts in clinical practice.

OTHER PATHOMECHANISMS

Other conceivable pathomechanisms have been suggested. In this mini-symposium, Amarenco reports that his group did not find an increased frequency of thrombophilia in patients …