Abstract

To the Editor: Paradoxical embolism via a patent foramen ovale (PFO) has been suggested as a mechanism of otherwise unexplained, cryptogenic stroke.1 Paradoxical embolism, however, can be diagnosed only if there is evidence of a venous thrombosis coexisting with arterial embolism and right-to-left shunting via a PFO. When looking for venous thrombosis in suspected paradoxical embolism, the diagnostic yield depends on the interval between the event and the investigation and the used diagnostic methods.2 Diagnosing venous thrombosis in patients with suspected paradoxical embolism is sometimes difficult since the thrombosis (1) may be confined to the calf veins and thus only detectable by venography; (2) may be localized in places other than in the leg veins and thus not detectable by leg venography; (3) may be not the cause but the consequence of arterial embolism; or (4) may spontaneously dissolve, re-embolize, or recanalize.3 Due to these problems, a timely search for venous thrombosis is only rarely performed in patients with suspected paradoxical embolism, especially if they have no clinical symptoms of thrombosis. Several strategies are possible to overcome these obstacles. The first strategy is by improving noninvasive methods to visualize venous thrombosis in different locations, like magnetic resonance venography.4 Another strategy is by search for a clotting diathesis in patients with suspected paradoxical embolism. This indirect strategy is based on the assumption that hypercoagulability leads to a higher incidence of venous thrombosis and thus, in the presence of a PFO, might increase the possibility of paradoxical embolism. Hypercoagulability can be assessed by genetic testing for factor VG1691A mutation, prothrombinG20210A variant, and TT677 genotype of methylenetrahydrofolate reductase. The risk for venous thrombosis is increased 3- to 8-fold in heterozygous carriers of the factor VG1691A mutation, 3-fold in heterozygous carriers of the prothrombinG20210A variant, and …

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