Can Posterior Fossa Lesions Be A Place For Preventive Patent Foramen Ovale Transcatheter Closure?

Case 1. A 40-year-old woman presented for elective posterior fossa craniectomy. She had a past history of headache, dizziness, diplopia, and transient ischaemic attacks. A diagnosis of Chiari type I malformation was made with magnetic resonance imaging study which revealed caudal displacement of the cerebellar tonsils, crowding of the foramen magnum, and a 3 x 2.5 cm lesion consistent with a meningioma in the right temporal lobe. The patient’s weight and height were 53 Kg and 162 cm, respectively; she had no history of cardiopulmonary, renal or liver diseases and she wasn’t receiving any type of drugs before operation. Her blood pressure was 110/70 mmHg supine with no postural hypotension. Her resting heart rate was 60 beats/min with normal heart rate variability in response to respiration and the Valsalva maneuver. Cervical spine mobility was normal and airway and neurological examinations were unremarkable. Standard preoperative evaluation included: 1) laboratory studies, i.e. complete blood and coagulation profile, blood grouping, renal and liver function tests, tumor marker, whose values were all within normal limits; 2) imaging studies, i.e. plain X-rayed skull, cerebral angiography, transthoracic (TTE) and subsequently contrast transesophageal (cTEE) echocardiography, and if that was the case contrast transcranial Doppler (cTCD) ultrasonography of the middle cerebral artery. The plain X-rayed skull showed no signs of chronic intracranial hypertension or calcification, and cerebral angiography was useful to assess no vascular supply of the meningioma. TTE demonstrated normal size and contraction of heart chambers and an atrial septal aneurysm; subsequently, a bidirectional shunting through a PFO was disclosed by cTEE. Agitated saline cTCD, performed by using a 2-MHz pulsed probe, revealed 18 high-intensity transient signals at rest and a grade 2-curtain pattern (uncountable microbubbles) with Valsalva strain. Due to the well-known increased risk of air embolism and hemodynamic instability in patients with right-to-left shunt undergoing neurosurgical procedures in the sitting position, the patient was scheduled for neurosurgery in the prone position. Intra-operatively, two episodes of cardiovascular instability were detected, monitoring ECG, pulse oximetry (sPO2), end-tidal carbon dioxide partial pressure (PETCO2) and non-invasive blood pressure. The first one was hemodynamically insignificant and occurred after anaesthesia induction meanwhile the patient was turned from supine to prone position, when the anesthesiologist noted a transient decrease in arterial pressure, sPO2 and PETCO2, which was resolved without any specific management. A second severe episode occurred during midline incision from the inion to the upper cervical vertebra, and was associated with a decrease of PETCO2, blood pressure, oxygen saturation, cardiac index, and an increase in pulmonary artery pressure. The differential diagnosis at this time included pulmonary embolism with air or thrombus, pneumothorax, displacement of the endotracheal tube with a failure of ventilation and a mechanical malfunction of the anesthesia machine or circle breathing system. A physical check of the anesthesia machine, breathing tubes and the patient were performed to confirm that the lungs were being appropriately ventilated. A presumptive diagnosis of VAE was made, the incision was closed and the procedure was aborted without significant complications, with an immediate recovery of arterial blood pressure, sPO2 and PETCO2. Post-operatively, the results of the patient’s neurological examination were unchanged from those of the preoperative status. Invasive management of PFO was suggested and the patient was referred to our hospital for consideration of elective transcatheter PFO closure as a “late” primary prevention of paradoxical VAE. Cardiac catheterization was performed through the right femoral vein and a flow-directed catheter was easily passed through the interatrial communication. Oxygen saturation, measured while the patient was breathing 100% oxygen and haemodynamic data are displayed in Table 1; the aortic oxygen saturation was obtained by percutaneous measurement of oxygen saturation by pulse oximetry. The right-sided pressures were entirely normal and the mean right atrial pressure was 1 mmHg less than the left atrial one; furthermore, there was no evidence of an intra-cardiac shunt. Percutaneous closure of the interatrial communication was performed under local anaesthesia and intracardiac echocardiography (ICE) guide and monitoring, using a 9F–9MHz Ultra ICE™ catheter-based ultrasound transducer (EP Technologies, Boston Scientific Corp., San Jose, Calif., USA), after puncture of the left femoral vein, as previously described.7 Two standardized orthogonal sections were used to obtain ICE-derived fossa ovalis measurements and to assess optimal device deployment: the transverse section on the aortic valve plane in the short axis of the body (Figure 1A), and the longitudinal section on the 4-chamber plane in the long-axis of the heart (Figure 1B). The latter view was also used to monitor all of the stages of the device deployment and to interrogate the device and surrounding structures before and after its release (Figure 2). The ICE examination of the atrial septum from the right atrial chamber showed an intact and a redundant fossa ovalis with the guidewire eccentrically located in the inferior (Figure 1A) and anterior (Figure 1B) aspect of the septum primum. The two orthogonal ICE axes of the fossa ovalis were 12.8 mm and 14.4 mm on the transverse and longitudinal planes, respectively. A 25 mm Amplatzer PFO Occluder device was chosen in order to close the PFO and to primarily incorporate the atrial septal aneurysm in the closure. The prosthesis was successfully implanted, the patient had an uncomplicated post-operative course, and she was discharged the day after with the prescription of aspirin and infective endocarditis prophylaxis for 6 months. The follow-up investigations (cTEE and cTCD) at 3 months enhanced complete catching of the atrial septal aneurysm without residual right-to-left shunting. This preventive strategy allowed to subsequently complete the neurosurgical procedure in the prone position with no adverse events. Case 2. An 18-year-old female patient with a past history of sudden headache and vomiting had an initial diagnosis of intracranial arteriovenous malformation, consisting with small (2.3 cm) cavernous hemangioma in the territory of the right posterior cerebral artery, made at the time of her first hemorrhage. Due to the location of the arteriovenous malformation, the lesion must be approached with posterior craniotomy in the operative sitting position. Contrast echocardiography assessment was performed as a screening technique in order to detect intracardiac shunting, revealing the presence of a PFO. The patient was transferred to our hospital department and the authors prepared this high-risk patient with prophylactic percutaneous PFO closure (“early” primary prevention), in order to anticipate the potential for hemodynamic instability and pardoxical air embolism during neurosurgical procedure in the sitting position. Catheter-based PFO closure with a 25 mm Amplatzer PFO Occluder prosthesis deployment was performed with optimal intra-cardiac echocardiographic result. How Would You Manage This Case? Steven L. Goldberg, MD University of Washington, Seattle, Washington The FDA has provided restricted approval for two different devices for percutaneous closure of a patent foramen ovale, for patients suffering from multiple strokes, and have failed medical therapy. Currently, the interventional cardiology and neurology communities are struggling together to understand which patients with patent foramen ovales benefit from closure. However, we are also becoming more cognizant of individuals with patent foramen ovales who may benefit from closure even though they suffer from other conditions besides spontaneous strokes. Some of these conditions are stroke-like, such as neurologic events associated with scuba diving, but some are quite different conditions. These include right to left shunting causing hypoxemia, such as in patients with pulmonary hypertension, certain congenital heart diseases, platypnea-orthodeoxia, and perhaps even acute mountain sickness. In these cases, the “offending” agent is not thrombus, but deoxygenated blood. Routine perioperative circumstances may promote the right to left passage of blood across a patent foramen ovale, by elevating the pressure in the right atrium relative to the left atrium. These circumstances include mechanical ventilation, the introduction of air during central venous catheter placement, or other common scenarios. Another example of PFO related pathology is outlined by the authors of the above vignettes. In this case, the “offending” agent is air, which commonly enters the venous blood stream during neurosurgical procedures in the sitting position. Significant venous air embolism has been described in approximately three out of four patients undergoing posterior fossa surgery in the sitting position. Some experts propose that all patients being considered for posterior fossa surgery be screened for patent foramen ovale, and the sitting approach avoided when one is found. Alternatively, there is some theoretic sense in closing these defects, potentially making it possible to perform this surgery by the otherwise preferred approach. It seems to make sense, and the authors are correct in stating that percutaneous closure of a patent foramen ovale carries little morbidity risk. Is there a benefit to closing patent foramen ovales in these uncommon scenarios? Because the conditions are rare, we do not have data supporting an invasive approach, nor can we expect to have such data in the foreseeable future. In one of the cases presented closure was undertaken after the patient manifested some instability during neurosurgery, but in the other vignette it was done prophylactically. However, I suspect we will be called upon with increasing frequency by our neurosurgical colleagues to consider percutaneous closure of these defects, and if initial outcomes are favorable, these may be routinely done prophylactically. I think it is a very good idea to have avoided a transesophageal echocardiogram. The use of transcranial Doppler, transthoracic and/or intracardiac echocardiography (for diagnosis) makes it unnecessary to subject the at-risk individual to the potential pressure fluctuations from placing the transesophageal echo probe. Intracardiac echo is used by many routinely anyway in the placement of these devices, obviating the need for transesophageal echo, so this would have been standard operating procedure. One significant concern I have, however, is how to manage the antithrombotic regimen. Antiplatet therapy is routinely given after implantation of a PFO closure device, but that is likely problematic in an individual undergoing a neurosurgical procedure. Although clot forming on a PFO occlusion device is rare, it has been well-described. Recent reports have suggested it might be more common with the CardioSEAL device than the Amplatzer, but this has not been tested in a formal manner. It is of interest that in both of the described cases an Amplatzer device was used. Nonetheless, it would be preferable to place such patients on aspirin as soon as it was felt to be safe by the neurosurgeons. John J. Young, MD and Joseph K. Choo, MD The Lindner Center for Research & Education The Ohio Heart Health Center, Cincinnati, Ohio Percutaneous transvenous closure of atrial septal defects (ASD) and patent foramen ovale has been successfully performed since the mid-1970’s, but only in recent years has the technique become widespread. Early devices were difficult to deploy, required large delivery sheaths, and were more prone to complications.¹ Patent foramen ovale has been identified as a source of paradoxical embolism presenting as cryptogenic stroke, peripheral embolism, brain abscess, and decompression sickness in underwater divers. Patients with PFO and paradoxical embolism are at increased risk of recurrent systemic thromboembolic events, ranging from 3.2% to 3.8% per year.² The optimal management of these patients remains controversial, with long-term anticoagulation, surgical closure, and percutaneous transcatheter closure being proposed as therapeutic options. Transcatheter techniques to close PFOs have been used with increasing frequency during the last few years as these devices evolve. Of the modern devices, the Amplatzer septal occluder and PFO devices are, in our opinion, the most versatile and practical to use. In our experience of nearly 100 patients presenting with symptomatic ASD or PFO, the Amplatzer devices have been universally successful in carefully selected patients with minimal complications. Intracardiac echocardiography (ICE), as an adjunct to biplane fluoroscopy, is now utilized exclusively for guidance of these procedures allowing us to avoid the potential complications associated with general anesthesia and indwelling transesophageal echocardiographic (TEE) probes.³ This strategy provides a safe and effective approach to transcatheter closure of PFO with a high success rate, low incidence of hospital complications, and low frequency of recurrent systemic embolic events. To date, most of the clinical experience with these devices has been in symptomatic patients as a secondary preventative strategy under a human device exemption (HDE), compassionate use or emergency clinical indication. The initial and intermediate results of a phase 1 U.S. mulitcenter trial of patients undergoing transcatheter PFO closure utilizing the Amplatzer device were recently reported.⁴ Fifty patients (28 male)underwent catheter closure of their PFO's at a mean age of 41±11 years. Device implantation was sucessful in all patients with no complications related to the device. At a mean follow-up of 16.5 ± 7.2 months, there were no deaths or recurrent neurological or peripheral embolic events. The conclusion was that the Amplatzer PFO device was a safe and effective method for preventing recurrent embolic events. Larger randomized clinical trials comparing device closure versus medical therapy are underway. The current two case studies describe another subset of patients with PFO at increased risk of embolic complications during neurosurgical procedures. The unique clinical risks associated with these procedures, physical and hemodynamic considerations depending on surgical positioning, and the potential for rapid entry of air into the venous system, predispose these patients to the risk of paradoxical emboli as well outlined by the authors. There are very little data regarding the prophylactic closure of PFOs (primary prevention) in any patient population. Known associated conditions (migraine headache for example) that may improve following percutaneous closure of PFO, have not been studied in prospective randomized trials. While these data are currently lacking, it would seem reasonable based on the safety and low morbidity related to transcatheter closure, that high-risk neurosurgical patients as described be considered for PFO closure. However, timing of surgical intervention following transcatheter closure of PFO should be carefully considered. Following closure, a residual shunt is not uncommonly seen immediately after deployment of the PFO device that may persist for months depending on the type of device.⁵ The majority of patients treated with the Amplatzer device have less residual shunting at 6 months follow-up compared to other devices, but the exact extent and timing of this issue is unknown. Presumably, the device is occlusive enough to prevent thromboembolic events even with small residual shunts, but the ability to prevent air emboli immediately post-deployment requires study before this can be recommended as “prophylactic” in these neurosurgical patients. In addition, there is no uniform approach to antiplatelet or anticoagulation therapy following transcatheter closure of PFOs (with or without the known associated antiphospholipid antibodies)⁶ which may impact the timing and risk of subsequent surgical intervention. Percutaneous transcatheter closure of PFOs has evolved into a safe and effective strategy for the prevention of recurrent thromboembolic events in patients with a prior episode. The efficacy for primary prevention of thromboembolic events, other associated clinical conditions, or as in the presented cases — air emboli, requires further study. References: 1. Harper RW, Mottram PM, McGaw DJ. Closure of secundum atrial septal defects with the amplatzer septal occluder device: Techniques and problems. Cathet Cardiovasc Interv 2002;57:508–524. 2. Martin F, Sanchez PL, Doherty E, et al. Percutaneous transcatheter closure of patent foramen ovale in patients with paradoxical embolism. Circulation 2002;106:1121–1126. 3. Zanchetta M, Rigatelli G, Onorato E. Intracardiac echocardiography and transcranial doppler ultrasound to guide closure of patent foramen ovale. J Invas Cardiol 2003;15:93–96. 4. Hong TE, Thaler D, Brorson J, et al. Transcatheter closure of patent foramen ovale associated with paradoxical embolism using the amplatzer PFO occluder: Initial and intermediate-term results of the U.S. multicenter clinical trial. Cathet Cardiovasc Interv 2003;60:524–528. 5. Schwerzmann M, Windecker S, Wahl A, et al. Percutaneous closure of patent foramen ovale: Impact of device design on safety and efficacy. Heart 2004;90:186–190. 6. Dodge SM, Hassell K, Anderson CA, et al. Antiphospholipid antibodies are common in patients referred for percutaneous patent foramen ovale closure. Cathet Cardiovasc Interv 2004;61:123–127. Expanding Indications for Transcatheter Closure Patent Foramen Ovale Ashraf Nagm, MD Interventional Pediatric Cardiology Fellow P. Syamasundar Rao, MD Professor & Director, Division of Pediatric Cardiology University of Texas-Houston Medical School Memorial Hermann Hosptial, Houston, Texas Since the initial reports by Mills,¹ Bridges,² Rao^3,4 and their colleagues of transcatheter occlusion of patent foramen ovale (PFO) with King and Mills’, clamshell and buttoned devices respectively, to prevent recurrence of cerebrovascular accidents presumably related to paradoxical embolism via the PFO, a number of other investigators, referenced elsewhere5 and by the authors of the preceding report, have adopted the concept and technique. Transcatheter closure of PFOs or atrial septal defects, hereafter referred to as atrial defects (ADs) was extended to closure of ADs with right-to-left atrial shunts associated with previously treated complex congenital cardiac anomalies, including Fontan fenestrations⁶ and platypnea-orthodeoxia syndrome.⁷ More recently, closure of ADs has been attempted in the management of atrial right-to-left shunts associated with right ventricular infarction, decompression illness⁸ and migrane.⁹ Now, it seems, there is yet another indication to close ADs, as alluded to in the preceding presentation. In this interesting article the authors shed light on potential risks during neurosurgical operations and how to prevent such complications. From the interventional point of view this article suggests a new indication for transcatheter occlusion of ADs to prevent potential paradoxical embolism in the setting of venous air embolism (VAE) during neurosurgery. As alluded to in the article, the incidence of VAE is 10–17% in the prone position and 7–76% in the sitting position. As summarized nicely by the authors, the cardiovascular instability due to VAE during neurosurgery has two major mechanisms, pulmonary air embolism and systemic air embolism, the latter is presumably due to paradoxical embolism via ADs. It is unlikely that pulmonary embolism will be altered by occlusion of ADs. The transcatheter occlusion of ADs in patients with history of stroke (or transient ischemic attacks) unexplained by other etiology has become the standard of care because the postulated role of PFO in paradoxical embolism cannot be ruled out. One might argue that this might not be the case in neurosurgery patients with ADs with no history of neurological incidents. However, the hemodynamic changes accompanying induction of anesthesia and the changes in intravascular fluid distribution and cardiac filling pressures would predispose any patient with an AD to the risk of paradoxical embolism. Because the venous blood return from inferior vena cava is preferentially directed towards the foramen ovale while that from the superior vena cava towards the right ventricle, the VAE during neurosurgery, particularly in sitting position, is more likely to produce pulmonary rather than systemic air embolism. This might be the case in the first case described by the authors; this patient exhibited decreased blood pressure, oxygen saturation and cardiac index, and increased pulmonary artery pressure. However, the potential for paradoxical embolism via a PFO cannot be eliminated completely in any patient. That would make prophylactic transcatheter PFO occlusion justified. It is crucial to scrutinize the results of prophylactic transcatheter PFO occlusion on the outcome of neurosurgery in large groups of patients, prior to adopting this procedure as standard of care. Screening of neurosurgical patients at risk by contrast echocardiography with Valsalva may demonstrate intracardiac right-to left shunt through ADs. Once it is concluded that ADs should be closed percutaneously, the next step is selection of the type of device to be used for closure. Most of the devices that are used for closure of atrial septal defects¹⁰ can be used to close the PFOs. Three devices, namely, PFO-Star,¹¹ Amplatzer PFO Occluder¹² and inverted⁶ or hybrid¹³ buttoned devices are specifically designed to occlude PFOs. Although Amplatzer Septal Occluder¹⁴ is approved for closure of ostium secundum ASD and the CardioSeal can be used under humanitarian device exemption (HDE) to close Fontan fenestrations, none of the other devices are approved by the FDA for closure of PFOs. The devices are at various phases of FDA approved clinical trials. Hence the devices are available for use only at institutions participating in clinical trials. Consequently, comparative data on safety and effectiveness¹⁵ are hard to come by and therefore, it would be difficult to opine which device is best suited to close a given AD. The method of implantation is of course different with different devices and should be mastered by the cardiologist performing the procedure. We agree with the authors that intracardiac echocardiography under local anesthesia should be used instead of transesophageal echocardiography under general anesthesia for monitoring device implantation to close the ADs in this group of patients. In summary, we find this article very intuitive, paving way to a new horizon in prophylactic transcatheter occlusion of atrial defects. References: 1. Mills NL, King TD. Nonoperative closure of left-to-right shunts. J Thorac Cardiovasc Surg 1976; 72:371–378. 2. Bridges ND, Hellenbrand W, Latson L, et al. Transcatheter closure of patent foramen ovale after presumed paradoxical embolism. Circulation 1992;16:83–84. 3. Rao PS, Wilson AD, Levy JM, Chopra PS. Role of “buttoned” double-disk device in the management of atrial septal defects. Am Heart J 1992;123:191–200. 4. Ende DJ, Chopra PS, Rao PS. Transcatheter closure of atrial septal defect or patent foramen ovale with the buttoned device for prevention of recurrence of paradoxic embolism. Am J Cardiol 1996;78:233–236. 5. Windecker S, Meier B. Percutaneous closure of patent foramen ovale in patients with presumed paradoxical embolism. In Rao PS, Kern MJ (eds). Catheter-Based Devices for the Treatment of Noncoronary Cardiovascular Disease in Adults and Children. Lippincott, Williams & Wilkins, Philadelphia, PA, 2003, pp.111–118. 6. Rao PS, Chandar JS, Sideris EB. Role of inverted buttoned device in transcatheter occlusion of atrial septal defect or patent foramen ovale with right-to-left shunting associated with previously operated complex congenital cardiac anomalies. Am J Cardiol 1997;80:914–921. 7. Rao PS, Palacios IF, Bach RG, et al. Platypnea-orthodeoxia syndrome: Management by transcatheter buttoned device implantation. Cathet Cardiovasc Intervent 2001;54:77–82. 8. Wilmshurst P, Walsh K, Morrison WL. Transcatheter occlusion of foramen ovale with a buttoned device after neurological decompression illness in professional divers. Lancet 1996;348:752–753. 9. Wilmshurst P, Nightingale S, Walsh KP et al. Effect on migraine of closure cardiac right-to-left shunts to prevent recurrence of decompression illness, stroke or for haemodynamic reasons. Lancet 2000;356:1648–1651. 10. Rao PS. History of atrial septal occlusion devices. In Rao PS, Kern MJ (eds). Catheter-Based Devices for the Treatment of Noncoronary Cardiovascular Disease in Adults and Children. Lippincott, Williams & Wilkins, Philadelphia, PA, 2003, pp. 3–9. 11. Braun MU, Fassbender D, Schoen SP, et al. Transcatheter closure of patent foramen ovale in patients with cerebral ischemia. J Am Coll Cardiol 2002;39:2019–2025. 12. Han Y, Gu X, Titus JL, et al. New self-expanding patent foramen ovale occlusion device. Cathet Cardiovasc Intervent 1999;47:370–376. 13. Rao PS. Transcatheter closure of atrial septal defects with right-to-left shunts. In Rao PS, Kern MJ (eds). Catheter Based Devices for the Treatment of Noncoronary Cardiovascular Disease in Adults and Children. Lippincott, Williams & Wilkins, Philadelphia, PA, 2003, pp.119–128. 14. Masura J, Gavora P, Formanek A, et al. Transcatheter occlusion of secundum atrial septal defects using a new self-expanding Amplatzer septal occluder: Initial human experience. J Am Coll Cardiol 1997; 42: 388–393. 15. Rao PS. Summary and comparison of atrial septal defect closure devices. Current Intervent Cardiol Reports 2000;2:367–376.