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(Circulation. 2000;101:838.)
© 2000 American Heart Association, Inc.

Editorials

Patent Foramen Ovale Is Indicted, but the Case Hasn’t Gone to Trial

James E. Lock, MD

From the Department of Cardiology, Children’s Hospital, Boston, Mass.

Correspondence to James E. Lock, MD, Department of Cardiology, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115.

In humans, birth itself is primarily a cardiorespiratory event. The fetus has outgrown its inefficient circulatory dependence on the mother and needs an effective oxygen-delivery system: the umbilical cord clamps off, the lungs aerate, the ductus arteriosus involutes, and the foramen ovale seals shut. A patent foramen ovale (PFO) is, by far, the most commonly persistent abnormality of fetal origin, occurring in 10% to 15% of the normal adult population. Because the thin, left-sided septum primum is pushed against the thicker septum secundum by higher left atrial pressures, a PFO only permits intracardiac shunting during those transient periods (eg, sudden changes in intrathoracic pressures or right heart compliance) when right atrial pressure exceeds left atrial pressure.

Although common, a PFO is invariably, or almost invariably, benign. The key word here is almost. The first real suspicion of pathological potential came from case reports.¹ One such report² included a picture of the heart from a patient who died of a stroke; incredibly, a large thrombus straddled the patient’s persistently patent foramen ovale. A formal indictment of the PFO as a source of embolic stroke was lodged by Lechat et al in 1988,³ when they reported that patients with an embolic stroke of unknown cause had a much higher incidence of PFOs than control subjects. Although this finding was challenged by some studies that used differing diagnostic techniques, the large majority of studies now support the notion that the presence of a PFO is strongly associated with the occurrence of an embolic . . . [Full Text of this Article]

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