Heart · 2011 · 101 citations · 20 references
MedicineNeurologySurgeryCerebrovascular SurgeryClinical NeuroscienceNeurocritical CareCerebrovascular DiseaseDiving SafetyNeurologic PrognosticationPatent Foramen OvalePatent Foramen Ovale ClosureStrokeClosure IndicationsNeurological Adverse EventsNeurological DisabilityPatent Foramen Ovale AssessmentPatent Foramen Ovale PrevalencePercutaneous Closure DevicesPercutaneous Patent Foramen Ovale ClosureSurgical Patent Foramen Ovale Closure
OBJECTIVE: To test the effect of patent foramen ovale (PFO) closure on neurological events in divers. DESIGN: Prospective, non-randomised, longitudinal three-arm study. SETTING: Tertiary referral centre. POPULATION: 104 scuba divers with a history of major decompression illness (DCI). INTERVENTION: Transcutaneous PFO closure. MAIN OUTCOME MEASURES: Baseline and three follow-up examinations with a questionnaire about health status and diving habits/accidents, transoesophageal echocardiography at baseline for PFO grading, cerebral MRI at all examinations. RESULTS: 39 divers had no PFO, 26 had a PFO and chose to undergo percutaneous closure and 39 had a PFO, but decided not to undergo closure. The total number of dives, including those performed before baseline and those during long-term follow-up, was 81,654; 18,394 dives during the follow-up period of 5.3 ± 0.3 years, during which there were a total of five major neurological DCI events-namely 0 in the no PFO group, 0.5 ± 2.5/10⁴ dives in the PFO closure group and 35.8 ± 102.5/10⁴ dives in the PFO no closure group (four events; p = 0.045 between the PFO groups). In the groups, no PFO, PFO closure and PFO no closure, there were 1.1 ± 2.6, 0.8 ± 1.4, 3.3 ± 6.9 ischaemic brain lesions, respectively, at follow-up (p = 0.039 between the PFO groups)-that is, 16 ± 42/10⁴ dives in the no PFO group, 6 ± 13/10⁴ dives in the PFO closure group and 104 ± 246/10⁴ dives in the PFO no closure group (overall p = 0.042; p = 0.024 between the PFO groups). CONCLUSION: PFO closure in continuing divers appears to prevent symptomatic (major DCI) and asymptomatic (ischaemic brain lesions) neurological events during long-term follow-up.
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