Patent Foramen Ovale and Stroke
This review summarizes the current state of knowledge about the relationship of patent foramen ovale (PFO) with ischemic stroke. Initial sections discuss the studies that identified this association. Subsequent sections discuss the detection techniques for PFO and other variables that may cause a PFO to be a conduit of paradoxical embolization. Finally, a section is devoted to summarizing the studies that assessed the strategies for preventing recurrent ischemic events in patients with PFO.
Cryptogenic Stroke and PFO
In ≈40% of patients with acute ischemic stroke, the cause remains undefined.1 PFO is a hemodynamically insignificant interatrial communication present in >25% of the adult population. During fetal life, because the lungs do not receive blood flow, blood returning to the right atrium is shunted through a PFO to the left atrium. Postnatally, PFO closes spontaneously in ≈75% of the population. However, in a portion of adults, by maintaining a direct communication between the right- and left-sided circulation, PFO can serve as a conduit for paradoxical embolization.
In 1877, Cohnheim2 described the association of PFO with stroke in a young woman with cerebral arterial embolism. However, it has been difficult to diagnose PFO in vivo until the development of echocardiography and its ability to image the interatrial shunting with an injection of saline contrast. With the use of contrast echocardiography, a strong association of cryptogenic stroke with PFO has become evident in patients <55 years of age (Table 1).3–8
Because stroke occurs more frequently in older population, with only 3% of cerebral infarctions occurring in patients <40 years of age, the number of stroke patients with PFO ≥40 years of age is much larger than in the younger patients.9 Several studies reported the association of PFO with cryptogenic stroke …