Catheter-Based Closure of the Patent Foramen Ovale
2009; Lippincott Williams & Wilkins; Volume: 120; Issue: 18 Linguagem: Inglês
10.1161/circulationaha.109.903427
ISSN1524-4539
Autores Tópico(s)Takotsubo Cardiomyopathy and Associated Phenomena
ResumoHomeCirculationVol. 120, No. 18Catheter-Based Closure of the Patent Foramen Ovale Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBCatheter-Based Closure of the Patent Foramen Ovale Bernhard Meier, MD Bernhard MeierBernhard Meier From Cardiology, Cardiovascular Department, University Hospital, Bern, Switzerland. Originally published3 Nov 2009https://doi.org/10.1161/CIRCULATIONAHA.109.903427Circulation. 2009;120:1837–1841Case presentation: A 34-year-old woman was admitted for chest pain lasting 5 hours. She had been in excellent health except for migraine attacks with rare aura that kept her away from work about twice a month. She took no medication except for birth control pills. The ECG was unrevealing, but cardiac biomarkers were elevated. Emergency cardiac catheterization showed an occluded small left circumflex coronary artery (Figure 1) and a corresponding small akinetic area in the left ventriculogram. No attempt at coronary recanalization was made because the symptoms had abated, the injured myocardium was akinetic, and there were no collaterals. However, a catheter was introduced into the right atrium, and contrast medium injection proved the suspected patent foramen ovale (PFO; Figure 2 and Movies I and II in the online-only Data Supplement). An Amplatzer PFO occluder was implanted in <10 minutes. The patient was discharged 36 hours later after her cardiac biomarkers had normalized. Download figureDownload PowerPointFigure 1. Right anterior oblique view of the left coronary artery showing an abrupt occlusion (presumably embolic) of a small left circumflex coronary artery (arrow).Download figureDownload PowerPointFigure 2. Left, Angiographic proof of a PFO (dashed arrow) by contrast medium injection at the PFO entrance in the right atrium (RA). Right, Situation after implantation of an Amplatzer 25-mm PFO occluder (left atrium [LA] disk, 25 mm; RA disk, 18 mm). See also Movies I and II in the online-only Data Supplement. SS indicates septum secundum; SP, septum primum.Several lessons are to be gleaned from this case: (1) paradoxical embolism does not necessarily require clinically apparent deep vein thrombosis; (2) paradoxical embolism is not confined to the brain; (3) if coronary artery disease had been present, the connection to paradoxical embolism would probably have been missed; (4) attention was correctly directed primarily at the PFO with a potential to obviate subsequent infarctions of brain, heart, or other sensitive organs; (5) echocardiography is not mandatory to prove a PFO or to close it; (6) migraine symptoms may be linked to the PFO and influenced by PFO closure; and (7) someday, workup for migraine may include screening for a PFO, and treatment for migraine may include closure of a PFO, which, in this case, would have prevented the myocardial infarction.Qualification of PFO as a DiseaseFigure 3 and Movie III in the online-only Data Supplement show a large clot caught in the act of slipping through the PFO, proving the potential of a PFO to cause harm. However, the formation of such a large thrombus that will find its way to and through the PFO is an exquisite rarity. Such a problem can also be demonstrated with magnetic resonance (which is not true for the PFO itself) or computed tomography.1Download figureDownload PowerPointFigure 3. Large thrombus stuck in the PFO and about to break into halves. LA indicates left atrium; RA, right atrium; SP, septum primum; and SS, septum secundum.The PFO accounts for ≈95% of right-to-left shunts.2 The remainder are mainly pulmonary arteriovenous fistulas (≈4%) or atrial septal defects (≈1%). The prevalence of a PFO ranges from 15% to 25% in autopsy studies,3,4 7% to 24% with transthoracic echocardiography,5,6 and 20% to 40% with transesophageal echocardiography in patients with a history of cerebral events.7,8 Tiny emboli (a few millimeters in size) that can form anywhere in the venous system are the culprits. Such emboli are absent in children and young adults with few exceptions but tend to occur with increasing frequency with age, particularly after 50 years of age.9 Most thrombi will emerge from the inferior vena cava. Both an atrial septal aneurysm (ASA), which is a flagellate central part of the septum primum forming the lower rim of the foramen ovale, and a Eustachian valve, which is a ledge extending the vena cava onto the foramen ovale, increase the chance for such clots to hit the foramen ovale and pass through it should it be open. Incessant motion in the case of the ASA and the continuous blood pounding the foramen in the case of the Eustachian valve render the fusion of the septum primum and septum secundum after birth all but impossible. The ASA and Eustachian valve increase the duration of time the flap-like PFO is actually gaping. In the case of the ASA, this may occur with every heartbeat.It is assumed that one or both of these features are present in 2% to 4% of the population. These individuals may account for most of the mishaps attributable to the PFO, a feature present in 20% to 30% of the general population. Screening for such ominous PFO combinations (with ASA and/or Eustachian valve) may therefore make sense.10 Yet, current guidelines of regulatory bodies concentrate on conservative therapeutic options (Table 1).11–14Table 1. Management of Patients With PFO After Cerebral Events According to Current Guidelines for PFO Closure by the American College of Chest Physicians,11American Association of Neurology,12American Heart Association/American Stroke Association,13and European Stroke Organisation14TherapyRecommended byACCP indicates American College of Chest Physicians; AAN, American Association of Neurology; AHA/ASA, American Heart Association/American Stroke Association; and ESO, European Stroke Organisation.PFO closure in patients with recurrent cryptogenic stroke despite medical therapyAANAntiplatelet therapyAAN, AHA/ASA, ESO, ACCPWarfarin in the presence of deep vein thrombosisAHA/ASA, ESO, ACCPWarfarin in the presence of coagulation abnormalitiesAHA/ASAWarfarin rather than antiplatelet agents in the presence of ASAAANThe ASA has been a regularly cited cause for cerebral ischemic stroke. Really at fault, however, is the PFO that typically went undetected in the early transthoracic echocardiograms showing only the ASA in patients with cryptogenic stroke.Most analyses corroborate the PFO as a stroke risk, at least for cryptogenic stroke. A number of studies appeared to prove the ominous role of a PFO without acknowledging it. In a 20-year population-based cohort study in Denmark15 of almost 200 000 people, an increase in risk of myocardial infarction or stroke was recorded immediately after a clinically apparent venous thromboembolic event. The risk decreased over the subsequent year but never quite normalized.The true peril of the PFO emerges from a study already a decade old.16 In patients with clinically apparent pulmonary embolism, the mere presence of a PFO increased mortality from 14% to 33% and systemic embolism from 2% to 28% (P 200 000 PFOs have been closed percutaneously since, with more than a dozen device designs. Success rates, defined as no significant residual shunt at the latest follow-up echocardiography, vary between 50% and 100%.20 Randomized controlled trials comparing devices are scarce.Complications include cardiac perforation or air embolization during implantation, induced atrial fibrillation, nonspecific malaise attributed to nickel allergy, and puncture site problems. Puncture site problems were the only significant complications in the past 1000 cases at our center and occurred in <1%.Thrombosis on the device during follow-up varies significantly between device families. A German registry found no thrombus with transesophageal echocardiography at 4 weeks on 292 Amplatzer occluders (AGA Medical, Plymouth, Minn), 1 (1%) on 161 Helex occluders (WL Gore and Associates, Newark, Del), 3 (7%) on 127 PFO Star occluders (Cardia Inc., Burnsville, Minn), and 7 (7%) on 100 CardioSEAL/STARFlex occluders (NMT Medical, Boston, Mass).21PFO Closure TechniquesPercutaneous ClosureThe simplest technique described so far includes the Amplatzer PFO occluder. It takes 600 patients.ConclusionsSeeking a PFO should be part of the workup for stroke, and the term cryptogenic should be pushed beyond the exclusion of a PFO. This would result in the new stroke classification drafted in Table 6. Table 6. Revisited Ischemic Stroke ClassificationArterial Occlusion Brachiocephalic Common carotid Internal carotid Vertebral Intracerebral LacunarArterial Embolus for Plaque, Ulcer, or Dissection Ascending aortic Brachiocephalic Common carotid Internal carotid Vertebral IntracerebralCardiac Embolus From Left atrium Left atrial appendage Left atrial foramen pouch Left ventricle Myxoma or other tumor Vegetation (endocarditis)Paradoxical Embolus PFO Atrial septal defect Pulmonary fistulaPulmonary Venous Bed EmbolusCryptogenicFollow-Up of Case VignetteThe patient was placed on aspirin for 6 months, at which time a transesophageal echocardiography showed complete closure of the PFO. Therefore, aspirin was discontinued. She switched from birth control pills to an intrauterine device. In the 7 years since, she had noted a marked reduction in headache days and complete abolition of aura.The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/120/18/1837/DC1.DisclosuresDr Meier has received research support and honoraria from, served on the speakers' bureau for, and been a consultant to or on the advisory board for AGA Medical.FootnotesCorrespondence to Bernhard Meier, MD, Professor and Chairman of Cardiology, Cardiovascular Department, University Hospital, 3010 Bern, Switzerland. E-mail [email protected] References 1 Fukumoto A, Yaku H, Doi K, Ito H, Numata S, Hayashida K, Inoue T, Akabame S, Oda Y, Matsubara H, Nishimura T. Images in cardiovascular medicine: continuous thrombus in the right and left atria penetrating the patent foramen ovalles. Circulation. 2005; 112: e143–e144.LinkGoogle Scholar2 Weber F, Goriup A. Prevalence of right-to-left shunts in active fighter pilots. 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Int J Cardiol. 2005; 101: 77–82.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Andreis A, Agnoletti G and Scacciatella P (2020) Incidental diagnosis of four pulmonary arteriovenous fistulas during patent foramen ovale closure: a case report, Cardiology in the Young, 10.1017/S1047951120002152, 30:9, (1363-1365), Online publication date: 1-Sep-2020. Erbel R and Diener H (2019) Herz und Hirn – zwei Begriffe, ein zentrales ProblemHeart and brain—two terms, one central problem, Herz, 10.1007/s00059-019-4810-y, 44:4, (287-288), Online publication date: 1-Jun-2019. Blanche C, Noble S, Roffi M, Testuz A, Müller H, Meyer P, Bonvini J and Bonvini R (2013) Platypnea–orthodeoxia syndrome in the elderly treated by percutaneous patent foramen ovale closure: A case series and literature review, European Journal of Internal Medicine, 10.1016/j.ejim.2013.08.698, 24:8, (813-817), Online publication date: 1-Dec-2013. 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