Is closure of patent foramen ovale to prevent ischaemic stroke ever justified?

摘要

The foramen ovale is a tunnel in the interatrial septum of the fetal heart that allows oxygenated placental blood to bypass the lungs and flow into the systemic circulation. At birth, inflation of the lungs causes physiological closure of the foramen, and in most people the interatrial communication seals completely over time. In around a quarter of the population, however, incomplete closure of the foramen results in a persistent (or patent) foramen ovale that provides a potential route for bloodbome material from the venous circulation to enter the systemic circulation. Case reports of thrombus straddling a patent foramen ovale confirm that material from the venous circulation can pass through the interatrial communication and cause systemic embolism to the brain and other organs,1 but the frequency and clinical relevance of this phenomenon are controversial. Case-control studies to assess whether patent foramen ovale is more common in people with stroke are confounded by selection and case ascertainment biases and have produced conflicting results. Nevertheless, meta-analyses of these studies support an association between a patent foramen ovale and stroke without an identifiable cause ("cryptogenic stroke"), especially in young patients (age <55 years). Differences in the prevalence of conventional risk factors for stroke, and in patterns of ischaemic brain injury, also suggest discrepant mechanisms of stroke in those with and without a patent foramen ovale.