Patent Foramen Ovale Closure

Abstract

HomeCirculationVol. 119, No. 23Patent Foramen Ovale Closure Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBPatent Foramen Ovale ClosureLet’s Keep the Heart in Mind Doff B. McElhinney, MD Doff B. McElhinneyDoff B. McElhinney From the Department of Cardiology, Children’s Hospital and Department of Pediatrics, Harvard Medical School, Boston, Mass. Search for more papers by this author Originally published1 Jun 2009https://doi.org/10.1161/CIRCULATIONAHA.109.871228Circulation. 2009;119:2967–2968Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 1, 2009: Previous Version 1 Setting aside the controversial questions of whether closing a patent foramen ovale (PFO) is indicated or effective for the prevention of recurrent stroke or the treatment of migraine headaches, what is the physiological impact of implanting a transcatheter device in the atrial septum? In this issue of Circulation, Wöhrle and his colleagues address 1 aspect of this question, reporting the results of a study in which they assessed atrioventricular and semilunar valve function in 102 patients before and after transcatheter PFO closure.1 The authors evaluated valvar competence before, the day following, and 12 months after PFO closure and found no significant change in aortic regurgitation (AR) or regurgitation of the other cardiac valves. On their own, these findings might be passed off as predictable and modestly novel. Viewed in the context of a recent article by Schoen et al in Heart, however, they are noteworthy.2 Accordingly, to appreciate the study by Wöhrle et al fully, it should be read as a counterpoint to the report by Schoen et al, which was a surprise to many in its description of new or increased AR in 10% of 170 patients who underwent transcatheter closure of a PFO and 9% of 70 in whom a device was placed to close an atrial septal defect.2Article see p 3002Before simply accepting the apparently contradictory findings of these 2 studies, however, it is worth acknowledging several basic methodological differences. The first difference is the means by which valvar regurgitation was assessed. In contrast to Schoen et al, who evaluated valvar function with transesophageal echocardiography 3, 6, and 12 months after catheterization, Wöhrle et al assessed the function of the aortic and other valves with cardiac magnetic resonance imaging. Schoen et al graded AR according to a standard ordinal scale, with no data on quantitative indices used to assign the grade of AR, whereas Wöhrle et al reported the AR fraction as a continuous variable. The second methodological difference is the manner in which data were presented and analyzed. Schoen et al assessed progression or development of regurgitation by reporting the proportion of patients with mild or greater regurgitation, without any statistical analysis. They also provided no explicit mention or denial of patients in whom AR may have improved from mild to less than mild, offsetting the reported trend of progression. In contrast, Wöhrle et al compared continuous data at 3 time points using paired analysis, and in a secondary description, reported the number of patients with an AR fraction >5%. In these respects, the 2 studies are not directly comparable.Beyond these methodological differences, there are unexpected and unexplained findings in both studies that give pause. The prevalence of mild AR at the time of preimplantation echocardiography in the series of Schoen et al was surprisingly high (16% to 17%). Almost all of the newly documented AR during follow-up was mild as well, suggesting either a biased population or systematically generous assessment of AR, an incongruity that begs for more detailed data. By the same token, the figures presented by Wöhrle et al depict a pronounced within-patient variability in regurgitant fraction measurements for all 4 valves across the 3 time points, which suggests either more substantial interstudy variability than their discussion acknowledged or true changes in regurgitant fraction in a number of patients that were neither explained nor discussed.In the final analysis, despite important differences in methodology and several less important discrepancies in findings, these 2 studies actually support the same conclusion: Development of or progression to an important degree of AR is a rare outcome 1 year after transcatheter closure of interatrial defects. However, that is not to say that the book should be closed on this issue. Whether intracardiac atrial septal closure devices contribute to valvar dysfunction 12 months after placement is one thing; whether they contribute to dysfunction 12 years after placement is another. This question is important not only for valvar dysfunction but for other adverse outcomes that might result from placement of an intracardiac device.In the field of structural interventional cardiology, a nearly ubiquitous topic of discussion these days is erosion. There is a growing literature documenting erosion of closure devices through the right or left atrium and into the aorta or pericardial space, often with fatal consequences.3–6 No one truly understands why this occurs, although, as is common with such conundrums, many theories have been advanced. Some suggest that device undersizing allows rotation and consequent erosion; others propose that oversizing of devices leads to abutment against adjacent structures and residual deformation stress; still others argue that the degree of septal motion or excursion can play a role, and so on. None of these hypotheses is proven, and it is likely that no single theory correctly explains all cases. Certainly, the clinical context is unpredictable: Some erosions are recognized at the time of implantation, and some are diagnosed years later.3,4 Despite the complexity of this problem, which ought to defy categorical solutions, it is common to hear or read of strategies for avoiding erosion that are no more substantiated than the underlying cause of the problem. The points of this digression are (1) that intracardiac complications related to atrial septal closure devices are real and relevant even if uncommon, and (2) that the problems of erosion and aortic root function (ie, aortic valve function) may be closely related, and “solutions” to the problem of erosion should take into account the possibility that distortion of the aortic root and commissural framework may have implications for aortic valve function.As with erosion, the possible mechanisms by which atrial septal device placement cause AR are speculative. Schoen et al rationalized the delayed and progressive appearance of AR in their cohort by proposing that it was not the device per se that altered aortic valve function and caused AR but tissue overgrowth of the device exerting traction on the noncoronary sinus and leaflet.2 Given that evaluation of explanted septal occlusion devices confirms a progressive biological response to the foreign body, with an initial deposition of fibrin and blood cells followed by fibroblastic ingrowth and organization, as well as a mild chronic inflammatory response,7 the hypothetical cause of AR proposed by Schoen et al is plausible. However, it seems just as likely that any distortion of the aortic root or valve is more closely related to the device. The progressive increase in the frequency of AR from 3 to 12 months, if valid, may simply be a stochastic time-dependent phenomenon that is influenced by various device- and patient-related factors, including conformational changes of the device and its relationship with adjacent structures, which are known to occur.8,9 Among the many studies evaluating atrial and ventricular function after atrial septal device placement, several have hinted at the potential mechanical or electromechanical importance of a stiff device in the atrial septum,10,11 but no obviously attributable impairment of cardiac function has been described. In any event, the short- and long-term effects of these conformational changes and of a rigid device covering much of the atrial septum are unknown and should not be taken for granted. Atrial strain rate imaging, which allows discrimination of septal and device deformation patterns, may help provide further insight into this question.12How do the studies by Wöhrle et al1 and Schoen et al,2 along with the growing literature on device erosions,3–6 inform us about the relative risks and benefits of atrial septal device placement? Given the current state of knowledge, it is difficult to argue that the beneficial effects on atrial and ventricular volume and function that result from atrial septal defect closure are outweighed by any adverse mechanical effect of placing a device in the septum. Whether this is true for PFO closure remains to be seen. As the debate about PFO closure continues, clearly the most important issue remains whether and for what particular indications the procedure is effective. Indeed, the future of transcatheter PFO closure may hang on the answers to these questions. Regardless of whether transcatheter PFO closure proliferates further, comes to serve a more circumscribed set of indications, or largely disappears, septal occlusion devices have been implanted in thousands of patients where they will remain for decades, not months. As long as these devices remain in situ, the burden of proof relative to their safety will and should be borne by practitioners, device manufacturers, and regulatory agencies. As we have learned from the still-unfolding story of device erosions,3,4 and as cases of complete atrioventricular block several years after transcatheter ventricular septal defect closure should remind us,13 these are not simply short-term concerns, and we do not fully understand how intracardiac devices will impact cardiac function over time. So, as we rightly continue to consider how PFO closure impacts the brain, let’s be sure to keep the heart in mind.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.DisclosuresNone.FootnotesCorrespondence to Doff B. McElhinney, MD, Department of Cardiology, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail [email protected] References 1 Wöhrle J, Kochs M, Spiess J, Nusser T, Hombach V, Merkle N. Impact of percutaneous device implantation for closure of patent foramen ovale on valve insufficiencies. Circulation. 2009; 119: 3002–3008.LinkGoogle Scholar2 Schoen SP, Boscheri A, Lange SA, Braun MU, Fuhrmann J, Kappert U, Strasser RH. Incidence of aortic valve regurgitation and outcome after percutaneous closure of atrial septal defects and patent foramen ovale. Heart. 2008; 94: 844–847.CrossrefMedlineGoogle Scholar3 Divekar A, Gaamangwe T, Shaikh N, Raabe M, Ducas J. Cardiac perforation after device closure of atrial septal defects with the Amplatzer septal occluder. J Am Coll Cardiol. 2005; 45: 1213–1218.CrossrefMedlineGoogle Scholar4 Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv. 2004; 63: 496–502.CrossrefMedlineGoogle Scholar5 Delaney JW, Li JS, Rhodes JF. Major complications associated with transcatheter atrial septal occluder implantation: a review of the medical literature and the manufacturer and user facility device experience (MAUDE) database. Congenit Heart Dis. 2007; 2: 256–264.CrossrefMedlineGoogle Scholar6 Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand W, Kleinman CS. PFO closure complications from the AGA registry. Catheter Cardiovasc Interv. 2008; 72: 74–79.MedlineGoogle Scholar7 Sigler M, Jux C. Biocompatibility of septal defect closure devices. Heart. 2007; 93: 444–449.CrossrefMedlineGoogle Scholar8 Kitano M, Yazaki S, Sugiyama H, Yamada O. The influence of morphological changes in amplatzer device on the atrial and aortic walls following transcatheter closure of atrial septal defects. J Interv Cardiol. 2009; 22: 83–91.CrossrefMedlineGoogle Scholar9 Cao QL, Du ZD, Joseph A, Koenig P, Heitschmidt M, Rhodes J, Hijazi ZM. Immediate and six-month results of the profile of the Amplatzer septal occluder as assessed by transesophageal echocardiography. Am J Cardiol. 2001; 88: 754–759.CrossrefMedlineGoogle Scholar10 Eyskens B, Ganame J, Claus P, Boshoff D, Gewillig M, Mertens L. Ultrasonic strain rate and strain imaging of the right ventricle in children before and after percutaneous closure of an atrial septal defect. J Am Soc Echocardiogr. 2006; 19: 994–1000.CrossrefMedlineGoogle Scholar11 Santoro G, Pascotto M, Caputo S, Gaio G, Iacono C, Caso I, Sarubbi B, Carrozza M, Russo MG, Calabrò R. Short-term electrogeometric atrial remodelling after percutaneous atrial septal defect closure. J Cardiovasc Med (Hagerstown). 2008; 9: 789–793.CrossrefMedlineGoogle Scholar12 Di Salvo G, Pacileo G, Caso P, Verrengia M, Rea A, Santoro G, Giovanna Russo M, Calabrò R. Strain rate imaging is a superior method for the assessment of regional myocardial function compared with Doppler tissue imaging: a study on patients with transcatheter device closure of atrial septal defect. J Am Soc Echocardiogr. 2005; 18: 398–400.CrossrefMedlineGoogle Scholar13 Predescu D, Chaturvedi RR, Friedberg MK, Benson LN, Ozawa A, Lee KJ. Complete heart block associated with device closure of perimembranous ventricular septal defects. J Thorac Cardiovasc Surg. 2008; 136: 1223–1228.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Ward C, Harrison J and Bashore T (2012) Adult Congenital Heart Disease Cardiovascular Clinical Trials, 10.1002/9781118399378.ch10, (274-295), Online publication date: 2-Nov-2012. June 16, 2009Vol 119, Issue 23 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.109.871228PMID: 19487590 Originally publishedJune 1, 2009 Keywordsatriumheart defects, congenitalEditorialspatent foramen ovaleatrial septal defectsPDF download Advertisement SubjectsCerebrovascular Disease/StrokeTreatment