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Indications for the closure of patent foramen ovale
  1. Michael J Landzberg,
  2. Paul Khairy
  1. Boston Adult Congenital Heart (BACH) Service, Children’s Hospital and Brigham and Women’s Hospital, Boston, USA
  1. Correspondence to:
    Michael J Landzberg
    MD, Boston Adult Congenital Heart (BACH) Service, Department of Cardiology, Children’s Hospital and Brigham and Women’s Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA; michael.landzbergcardio.chboston.org

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The foramen ovale, while vital to our formative development, assumes mischievous potential if it persists post-utero. Similar to other vestigial structures, presence of a patent foramen ovale (PFO) appears to carry no physiologic or survival benefit for normal individuals. In states of abnormal right sided cardiac or pulmonary vascular capacitance or resistance, PFO has been implicated in worsening hypoxaemia caused by right to left intracardiac passage of deoxygenated blood (see box). More recently, a causative role of PFO in much more commonly occurring syndromes, including embolic ischaemic stroke, migraine with aura, and cerebral and cutaneous decompression disease, has been suggested. Highlighting cryptogenic embolic stroke associated with PFO, we will systematically review the evidence for these relations, discuss therapeutic potentials, and propose guidelines for therapeutic decisions as we await the completion of randomised controlled interventional trials.

CRYPTOGENIC STROKE AND PFO

Incidence

Stroke databases suggest that despite intensive evaluation, approximately 40% of all patients suffering ischaemic strokes (80% of all stroke victims) remain without clearly identifiable precipitant or cause (2002 heart and stroke statistical update, American Heart Association). In 1989, Webster and Lechat separately reported small case–control series with increased prevalence of PFO in patients with cryptogenic stroke (CS).12 To date, these descriptive series have been followed only by additional case–control studies, without prospective collection of primary occurrence of CS + PFO in a well defined population. While these case–control series have significant limitations, meta-analysis by Overell and colleagues suggested a strong correlation between PFO and primary occurrence of CS.3 In this analysis, prevalence of CS + PFO in persons of all ages was three times greater (95% confidence interval (CI) 2.0 to 4.3) than in non-stroke controls; this relation was even more compelling in persons with CS aged < 55 years of age, where PFO prevalence was five times greater (95% CI 3.2 …

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