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Tex Heart Inst J. 2000; 27(1): 81–82.
PMCID: PMC101035

The Significance of a Patent Foramen Ovale

To the Editor:

I read with interest the case report by Maraj et al 1 of hypoxia due to patent foramen ovale (PFO) in the absence of pulmonary hypertension. I wish to make a few comments.

First, PFO is indeed a frequent anatomic finding in normal people, more than the figure of 20% as reported by the authors. It was present in 27.3% of normal subjects in a large autopsy series published in 1984. 2

Second, in addition to the 2 postulated mechanisms for right-to-left shunting via a PFO in the absence of pulmonary hypertension as discussed by the authors, I would like to mention a 3rd possibility—a persistent Eustachian valve. This was present in the case we reported in 1983. 3

Third, platypnea-orthodeoxia is a relatively uncommon but serious syndrome of arterial hypoxia and breathlessness in the upright position caused by interatrial or intrapulmonary shunting. The most common cause is an interatrial right-to-left shunt through either a PFO or an atrial septal defect. 4 Platypnea-orthodeoxia can be explained on the basis of positional modification of abnormal shunting. Standing upright can stretch the interatrial communication, be it a PFO or an atrial septal defect, thus allowing more streaming of venous blood from the inferior vena cava through the defect, whether or not a persistent Eustachian valve coexists.

Fourth, besides platypnea-orthodeoxia, PFO may also be responsible for paradoxical embolism in the presence of either established or induced pulmonary hypertension. 5 The diagnosis of paradoxical embolism can now be made antemortem. 5–7

Fifth, when treatment is indicated for PFO, nowadays it can be done nonsurgically by transcatheter closure. 8,9 This approach avoids the morbidity, mortality, and increased expenses associated with open heart surgery. 10,11 As we enter the new millennium, most patients with PFO can be treated in the cardiac catheterization laboratory instead of in the operating room. 12

References

1. Maraj R, Ahmed O, Fraifeld M, Jacobs LE, Yazdanfar S, Kotler MN. Hypoxia due to patent foramen ovale in the absence of pulmonary hypertension. Tex Heart Inst J 1999;26:306–8. [PMC free article] [PubMed]
2. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20. [PubMed]
3. Bashour T, Kabbani S, Saalouke M, Cheng TO. Persistent Eustachian valve causing severe cyanosis in atrial septal defect with normal right heart pressures. Angiology 1983;34:79–83. [PubMed]
4. Cheng TO. Platypnea-orthodeoxia syndrome: etiology, differential diagnosis, and management. Cathet Cardiovasc Intervent 1999;47:64–6. [PubMed]
5. Cheng TO. Paradoxical embolism. A diagnostic challenge and its detection during life. Circulation 1976;53:565–8. [PubMed]
6. Cheng TO. Echocardiography and paradoxical embolism. Ann Intern Med 1981;95:515. [PubMed]
7. Cheng TO. Echocardiography in ischaemic cerebrovascular disease. Br Med J (Clin Res Ed) 1987;295:856.
8. Cheng TO. Pulmonary embolism, patent foramen ovale and paradoxical embolism. J Cardiovasc Surg 1999;40:769. [PubMed]
9. Cheng TO. Potential source of cerebral embolism in migraine with aura: a transcranial Doppler study. Neurology 1999;53:2213–4. [PubMed]
10. Cheng TO. Paradoxic embolism. Am Heart J 1996;131:1238. [PubMed]
11. Cheng TO. Impending paradoxical embolism. Arch Intern Med 1998;158:1720. [PubMed]
12. Cheng TO. Coexistent atrial septal defect and mitral stenosis (Lutembacher syndrome): An ideal combination for percutaneous treatment. Cathet Cardiovasc Intervent 1999;48:205–6. [PubMed]

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