General description of procedure, equipment, technique
Epidemiology, pathophysiology, and classification
Various developmental or acquired anomalies may lead to intracardiac shunting.
Patent foramen ovale (PFO) refers to the nonclosure of the potential space between septum primum and secundum (analogous to a flap valve) located at the superior and inferior margin of the foramen ovale.
During fetal development, foramen ovale allows for oxygenated blood (coming from the umbilical cord via the inferior vena cava [IVC] which is directed to the interatrial septum by the Eustachian valve) to enter systemic circulation. This channel fuses closed after birth as pulmonary pressures drop and the left atrial (LA) pressure stays above that of the right atrium (RA).
In approximately one fourth of the population, foramen ovale remains patent leading to shunting mainly from right to left.
FO has been associated with paradoxical embolization complicated by left-sided events including stroke, myocardial infarction, and peripheral embolism. It is also associated with orthodeoxia/platypnea, migraine headaches, high altitude pulmonary edema, and obstructive sleep apnea exacerbations.
Atrial septal defects (ASDs) result from abnormal embryologic development of the septum between the two atria. ASDs account for 10% of all congenital heart defects and occur in 1 in 1,500 live births. Associated congenital malformations occur in approximately 30% of the new ASD cases and a diagnosis of ASD requires full evaluation of the cardiovascular system. Long-term sequela of untreated ASDs includes premature death, atrial arrhythmias, right-sided heart failure, and paradoxical embolism among others. There are four types of ASDs:
Secundum ASDs account for the majority of cases (75%) and are located in the mid and anterior septum at the region of the fossa ovalis. However, these defects can affect the septum posteroinferiorly toward the IVC, inferiorly toward the atrioventricular (AV) junction, posteriorly to coronary sinus, or superiorly to the superior vena cava (SVC).
Primum ASDs (endocardial cushion defects) constitute 10% to 15% of all ASD cases and are located inferiorly toward the AV junction. This type of ASD is usually associated AV canal defects and cleft anterior mitral valve leaflet.
Sinus venosus ASDs account for 5% to 10% of cases and are located superiorly near the SVC or rarely inferiorly near the IVC. This defect results from failure of complete fusion of the sinus venosus chamber into the right atrium. In approximately 90% of the cases, there is associated anomalous venous drainage of the right pulmonary veins into the right atrium.
Coronary sinus defects are rare and account for less than 1% of all ASD cases. These are due to failure of separation of coronary sinus from the left atrium, leaving a shunt from the left atrium to the right atrium via the coronary sinus. Partial or complete anomalous pulmonary venous return and persistent left SVC are associated with these types of defects.
Ventricular septal defects (VSDs) are among the most common congenital heart anomalies accounting for 20% of all isolated defects. The majority of the small VSDs (75%) close in the first 2 years of life while larger defects are less likely to close spontaneously. The long-term sequela of untreated VSDs include pulmonary vascular disease/Eisenmenger’s syndrome, sudden cardiac death, atrial and ventricular arrhythmias, aortic insufficiency, right and subsequent left ventricular dysfunction due to volume overload, and infective endocarditis among others. There are several types of VSDs:
Type 1 (supracristal) defects are caudal to the pulmonary valve in the infundibular portion of the right ventricular outflow tract.
Type 2 (perimembranous) defects are those that involve the membranous septum.
Type 3 (inlet) defects are those that are in the inlet portion of the muscular septum inferior the AV valves.
Type 4 (muscular) defects are located most inferiorly in the muscular part of the septum.
Indications and patient selection
Indications for closure
PFOs had historically been closed surgically. However, advances in percutaneous techniques have enabled us to address these defects in a minimally invasive manner. Importantly, in the United States, the U.S. Food and Drug Administration (FDA) has not approved the use of any closure devices for PFO treatment pending results from ongoing randomized controlled trials. Despite this, the ASD closure devices (discussed below) are being used to close PFOs in an off-label fashion.
Incidentally discovered PFOs in asymptomatic patients do not require any treatment or follow-up.
If the presence of PFO is implicated in embolic events in a patient, the treatment is controversial. In the setting of unexplained recurrent embolic stroke despite optimal medical therapy, closure of PFO may be considered (American Heart Association [AHA]/American Stroke Association [ASA] Class IIb recommendation).
In young patients after the first paradoxical thromboembolic event, PFO closure can be considered if the patient has a large PFO, thrombophilia, and no other cause of stroke.
In orthodeoxia/platypnea syndromes, the closure of PFO is the definitive treatment.
Observational data suggest that PFO closure frequently exerts a beneficial effect in patients with intractable migraines. The single randomized controlled trial performed to-date has not shown that PFO closure leads to a lower frequency of migraine attacks, however.
ASD closure can be considered for several indications. While secundum ASDs can be closed percutaneously, anatomy permitting, the primum, sinus venosus, and coronary sinus ASDs require surgical treatment. In order for percutaneous closure to be entertained, the ASD maximum diameter should be less than 40 mm as measured by echocardiography. Current indications include:
Right atrial (RA) and right ventricular enlargement by echocardiography with or without symptoms (American College of Cardiology [ACC]/AHA Class I recommendation).
Documented or verified paradoxical embolization events or orthodeoxia/platypnea (ACC/AHA Class IIa recommendation).
Net left-to-right shunt (pulmonary blood flow [Qp]/systemic blood flow [Qs] >1.5) with pulmonary artery (PA) pressure less than two thirds of systemic pressure, pulmonary vascular resistance (PVR) less than two thirds of systemic vascular resistance (SVR), or when responsive to pulmonary vasodilators or test occlusion of the defect (ACC/AHA Class IIb recommendation).
VSD closure is usually performed via a surgical approach for the following indications:
Presence of significant VSD with a net left-to-right shunt with Qp/Qs greater than 2.0 and/or worsening ventricular function due to pressure or volume overload (ACC/AHA Class I recommendation).
Recurrent endocarditis (ACC/AHA Class I recommendation).
Closure of defects with Qp/Qs greater than 1.5 can also be considered with PA pressure less than two thirds of systemic pressure, PVR less than two thirds of SVR, or in the setting of left ventricular (LV) systolic or diastolic dysfunction (ACC/AHA Class IIa recommendation).
Type 4 (muscular) VSDs can be closed with a device percutaneously when the above indications are present.
In postmyocardial infarction with ventricular septal rupture cases, the role of surgical closure is established despite poor outcomes with or without closure. Percutaneous closure in this setting is investigational and can be performed in selected cases.
Contraindications to PFO/ASD/VSD closure
Any of these invasive procedures are contraindicated in patients with serious comorbidities and unfavorable long-term outcomes. As with any invasive procedure, the risks and benefits of the procedure should be weighed carefully. Contraindications to specific defects are outlined below:
PFO closure is contraindicated:
If PFO is discovered incidentally without associated symptoms. It should be noted that approximately one fourth of the population has PFO and the overwhelming majority of these patients have no symptoms/adverse sequela associated with the PFO.
Percutaneous ASD closure is contraindicated:
For ASDs less than 5 mm for hemodynamic reasons unless paradoxical embolism is documented
In patients with severe irreversible/fixed pulmonary hypertension (PVR >10 to 12 Woods units) and no evidence of left-to-right shunt
In patients with an unsuitable anatomy, with deficient rims including superior, inferior, or posterior rims. A deficient anterior rim is not a contraindication for percutaneous closure; however, it should be performed with caution if present
In patients with severe mitral regurgitation where the mitral valve should be simultaneously treated to prevent an increase in LA pressure
In primum, sinus venosus, and coronary sinus defects, as well as those with associated congenital anomalies that also need treatment. These cases are best treated surgically.
VSD closure is contraindicated:
In patients with severe irreversible/fixed pulmonary hypertension (PVR >7 Woods units). In these situations, the VSD acts as a pop-off valve that unloads the right ventricle allowing for maintenance of cardiac output
In restrictive VSD cases, where the defect is not associated with any hemodynamic consequences
Patients with severe pulmonary hypertension require particular attention and caution, as some patients might still benefit from closure of the defects if pulmonary pressure improves on specific pulmonary hypertension regimens. Therefore, pulmonary vasodilatory challenge and a therapeutic medication trial in collaboration with a pulmonary hypertension specialist might be of critical importance before a final decision is rendered.
Patients with LV dysfunction (systolic or diastolic) might have increased left-to-right shunting due to elevated LV/LA pressures if they are not medically optimized. Patients with LV dysfunction should be optimized before closing the defect as patients might go in acute LV failure and pulmonary edema with closure.
Details of how the procedure is performed
Assessment, procedural specifics, and aftercare
Several tools are at the disposal of the diagnostician for accurate assessment of the presence and severity of the defect.
Physical examination is not very helpful in the diagnosis of PFO. In patients with hypoxia related to orthodeoxia/platypnea, bedside maneuvers or ambulation with measurement of oxygen saturation might be of value in detecting symptoms. A high index of suspicion is necessary in patients with cryptogenic stroke, shortness of breath, and unexplained embolic events.
In patients with ASDs, right ventricular (RV) heave/lift might be present with evidence for right-sided ejection murmur consistent with increased blood flow across the pulmonic valve. Tricuspid middiastolic murmur at the left lower sternal border might also be present due to increased flow. A wide and fixed split S2 sound is a hallmark of ASD and a loud P2 suggests pulmonary hypertension. Although infrequent, in advanced cases with pulmonary hypertension, reversal of shunt leads to right-to-left flow with cyanosis and hypoxia.
VSD can be usually detected by auscultation. The typical physical examination finding is a systolic murmur at the left lower sternal border with amplitude corresponding to the velocity of the defect. In small/restrictive VSD, the murmur is loud and often pansystolic. Larger defects lead to softer murmurs that stop short of S2 (due to pressure equalization before S2). As in the case of ASDs, high flow across the right ventricle might lead to RV lift/heave with wide split S2 and a loud P2 component. If there is reversal of the shunt, cyanosis and hypoxia might be present.
ECG is usually normal in patients with PFO.
ECG in patients with ASD might show right (secundum) or left axis deviation (primum). The p-wave axis might be abnormal and the PR might be prolonged. Incomplete right bundle branch block is frequently present. Crochetage (a notch seen in QRS in leads II and III) can be seen in secundum ASD cases.
ECG is normal in patients with restrictive VSDs. In significant defects, there might be evidence for LA enlargement and LV dilation due to volume overload. If pulmonary hypertension is present, right ventricular hypertrophy and right axis deviation might also be present.
Advances in echocardiography have enabled us to more accurately assess the atrial and ventricular septum.
In patients with PFO or ASDs, two-dimensional transthoracic evaluation (TTE) with color flow mapping and Doppler assessment can establish the presence, location, and size of these defects. Use of agitated saline has enabled improved detection of right-to-left shunts in PFO (bubbles seen on the left side within five heartbeats suggest intracardiac, whereas more than five beats suggests intrapulmonary shunting). Valsalva maneuver, cough, or sharp nasal sniff can transiently increase the RA pressure and might provoke shunting right-to-left for improved detection of these defects.
The anatomy of the VSD can also be seen with TTE with color flow and Doppler assessment. The higher the velocity, the smaller the defect and less hemodynamically significant the lesion will be.
While a transthoracic echocardiography is very useful in diagnosing the septal defects, it’s not uncommon that the diagnosis might be missed due to image quality, body habitus, and underlying lung disease. Transesophageal echocardiography (TEE) is very helpful when diagnosis is in question and provides with invaluable information for accurate assessment of the location of the lesion as well as its hemodynamic impact.
TEE is also very valuable when planning a percutaneous or surgical closure. In an ASD, rims of the defect can be evaluated carefully to make sure that these have sufficient (>5mm) room for device placement (except the anterior rim).
Patients with ASDs might also have other congenital anomalies—importantly anomalous pulmonary venous connections. TEE is useful in assessing the locations of the pulmonary veins before a percutaneous approach is undertaken.
During the procedure, intracardiac echocardiography (ICE) can be used very effectively as it is helpful in defining the anatomy in crossing the septum and establishing the rims as it guides the placement of the device. The use of TEE versus ICE depends on the operator and the institution.
Transcranial Doppler assessment:
If the bubble study is inconclusive in the echocardiogram or if the degree of shunting is not clearly determined, a transcranial Doppler assessment might be of value where the bubbles arriving at the brain are counted over a set period of time. The higher number of bubbles counted the more significant the right-to-left shunt (curtain sign).
Magnetic resonance imaging:
Magnetic resonance imaging (MRI) is useful in cases where defects are not readily visualized by echocardiography. Direct visualization with hemodynamic and volumetric measurements are attainable with estimation of the severity of the shunt. MRI can also be helpful in assessing associated congenital anomalies including anomalous pulmonary vein return.
Computed tomography is not routinely used in detecting septal defects; however, it can be helpful in delineating the anatomy to assess for associated congenital anomalies including anomalous pulmonary vein return. This imaging technique should be used judiciously in younger patients due to radiation exposure.
Routine cardiac catheterization is not necessary in uncomplicated cases; however in patients where diagnosis is in question, shunt quantification or ventriculograms might be of use. In patients with pulmonary hypertension, direct pulmonary pressure measurements with assessment of vasoreactivity might also be of value.
Several devices are available for closure of septal defects.
There currently are two FDA-approved devices in the United States for ASD closure. These devices are used off-label for PFO closure as well.
AMPLATZER Septal Occluder (St. Jude Medical, St. Paul, MN)
GORE HELEX Septal Occluder (WL Gore & Associates, Flagstaff, AZ).
There is only one FDA-approved device for congenital muscular VSD closure:
AMPLATZER Muscular VSD Occluder (St. Jude, St. Paul, MN) for up to 18 mm defects. For defects larger than 18 mm, a research protocol should be in place for proceeding with intervention.
No devices are approved for postmyocardial infarction ventricular septal rupture closure except for humanitarian/compassionate use.
Several other devices are used outside of the United States: AMPLATZER Membranous VSD Occluder (St. Jude, St. Paul, MN) and the PFM VSD Coil (PFM Medical, Koln, Germany) in Europe.
Access and procedural details:
For ASD closure, conscious sedation is sufficient in most cases as the use of intracardiac echocardiography (ICE) supplanted the use of continuous TEE monitoring. For VSD closure, both conscious sedation and general anesthesia are reasonable depending on the stability of the patient.
For ASD closure, usually two venous sheaths are necessary (one for device placement and other for ICE). If TEE is being used for imaging, only one sheath for device delivery should suffice.
We use a J-tipped guidewire with Goodale-Lubin (GL) catheter to cross the PFO/ASD using fluoroscopic and echocardiographic guidance. We then move the GL catheter to the left upper pulmonary vein (LUPV) for anchoring over the guidewire. The J-wire is then exchanged for an 0.035″ extra-stiff guidewire. We use stop-flow technique for sizing the defect. This is accomplished by advancing a sizing balloon to the defect over the extra-stiff wire and inflating the balloon while flow through the defect is monitored by ICE or TEE. Inflation is stopped when shunt flow stops. The stop-flow technique allows for optimal sizing of the ASD.
For VSD closure, several approaches are possible:
Initial planning might include venous access with the guidewire traversing the atrial septum via a transseptal puncture, through the mitral valve and the VSD; finally with externalization of the wire through the internal jugular vein or the IVC using a snare device.
Alternatively, a retrograde aortic approach can be used with the wire across the aortic valve, then the defect with wire externalization to the internal jugular vein using a snare device.
Finally, a wire can be passed from the venous system directly to the right ventricle and then into the left ventricle without externalization (particularly for apical defects).
A diagnostic coronary catheter is usually used as the wire is advanced to cross these defects and this catheter can also be used to help guide the wire into the pulmonary artery (when defect is crossed left-to-right) where the wire is snared (snaring in the right ventricle can be problematic as the snare might catch on the tricuspid valve apparatus). Once the defect is crossed with the wire and distal end of the wire is snared, the closure device can be advanced. Intravenous heparin administration is necessary to a goal activated clotting time of greater than 250 seconds.
The Amplatzer device is made of nitinol wire mesh and is a self-expanding, double disk device with a connecting middle waist of varying dimensions. Polyester fabric is sewn in each disk and impede blood flow when placed across the defect (Figure 1 and Figure 2).
This device is approved by the FDA for ASD closure, however it is also used off-label for PFO closure. Different versions of the device with structural variations are used for VSD closures as well.
The device is sized according to the diameter of its middle waist and comes in several sizes ranging from 4 to 38mm. The right and the left atrial disks are larger than the middle waist by approximately 8 to 16mm depending on the device waist. The right atrial disk is usually smaller than the left-sided disk.
There is a variation of the Amplatzer device—i.e., a cribriform device that is similar in its nitinol and polyester patch content with the exception of a thinner or minimal waist with atrial disks of equal sizes. This device can be used for multifenestrated secundum ASDs or off-label for PFO closure.
Placement of the Amplatzer device requires careful flushing and preparation of the device. The delivery sheath is advanced over the extra-stiff guidewire into the left atrium. The Amplatzer device is then loaded onto the delivery cable and advanced to the left atrium. The LA disk is advanced out of the catheter to expand to its original shape in the left atrium after which the catheter and the LA disk are pulled back as a unit to abut against the interatrial septum as confirmed by fluoroscopy and with ICE imaging. The RA disk is then deployed by withdrawing the sheath further and this disk advanced to the septum. After satisfactory position is confirmed via imaging, the device is then released from the cable entirely.
Approved by the FDA for closure of secundum ASDs, the device consists of a single nitinol wire covered by polytetrafluoroethylene (PTFE) with a LA eyelet, a center eyelet, and a RA eyelet (Figure 3 and Figure 4). This device is used off-label for closure of PFO defects as well.
The Helex device comes in various sizes (15, 20, 25, 30, and 35 mm) and has a complicated structure; however it is effective and very well tolerated by patients.
After adequate preparation and careful flushing of the Helex device, the delivery catheter is advanced to the left atrium over the extra-stiff guidewire. The guidewire is then removed and LA disk is deployed, after which the device is retracted to the atrial septum so that the center eyelet centers itself on the ASD/PFO as this is verified fluoroscopically and on ICE images. The RA eyelet is then released, after which the mandrel is retracted with deployment of the locking loop.
The device is then released. If the placement is not satisfactory at this point however, there is a retrieval cord that can be used to retract the entire device altogether.
Following septal closure, patients are allowed to recover in a telemetry floor overnight, where they are monitored for atrial and/or ventricular arrhythmias and other possible acute complications. An ECG and a chest X-ray, as well as an echocardiogram with color Doppler assessment, is recommended for determination of the location of the device and the residual shunt.
These procedures (including a TEE) are ideally repeated in 6 months to assess for any residual shunt. Follow up thereafter can be annual for the first 2 years and subsequently every 3 to 5 years. Any new development of shortness of breath, exercise intolerance, and new arrhythmias should prompt repetition of the above work up to assess for device integrity.
Patients are routinely kept on aspirin and clopidogrel for approximately 6 months—when the device is fully endothelialized. Clopidogrel can then be discontinued.
Aspirin is typically used long term. Procedural prophylaxis for infective endocarditis is also recommended for a duration of 6 months as the foreign material might be a nidus for infection until device is endothelialized.
If there is significant residual shunt after 6 months, however, this may prevent full endothelialization of the device and so endocarditis prophylaxis should be continued indefinitely.
Procedural success with closure (percutaneous or open surgical)
Success rates for septal defect closures with percutaneous approaches are greater than 95%. The open surgical approach grants a direct visualization of the defect and primary closure using suture and/or patch techniques.
Surgical treatment remains the gold standard for primum, sinus venosus, coronary sinus ASDs, and all types of VSDs. The standard of care for secundum ASD and PFOs, however, is to close these percutaneously using the above devices.
In selected patients with VSDs, percutaneous devices can be used as well. In the event of complications with devices and inappropriate results with percutaneous intervention, surgery remains a viable option.
It should be noted that in patients with ASD, the earlier the closure of a significant defect, the better the outcome in terms of prevention of arrhythmias, greater longevity, and right-sided heart failure.
While a successful surgical closure eliminates the shunting immediately, there may be residual shunting initially with percutaneous devices. This residual shunt usually improves as the devices self-center and get endothelialized leading to excellent long term outcomes.
Alternative and/or additional procedures to consider
In the absence of any indications for closure of the septal defects, monitoring for symptoms and/or medical treatment is appropriate. Percutaneous procedures, while minimally invasive, are associated with risks as well; as such a thorough informed consent is mandatory as is the case for open surgical approach.
Most PFOs are found incidentally in asymptomatic patients and do not warrant any monitoring or medications.
In the setting of stroke, where PFO is felt to be a factor in the pathogenesis, patients should first be treated with antiplatelet agents or anticoagulation depending on the culprit etiology. If and when this medical approach fails, PFO closure can be entertained.
If the associated symptom is orthodeoxia/platypnea, percutaneous closure is recommended; however if not favored by the patient or clinical scenario, surgical closure can be considered.
If the ASD is not hemodynamically significant (as suggested by the above criteria), it can be monitored safely. However, there is really no proven role for medical management if the ASD is hemodynamically significant.
In the rare instances where patient does not wish to proceed or risk outweighs the benefit, diuretics or afterload reducing agents can be used to decrease left-sided pressures to diminish the left-to-right shunt to provide relief to the volume overloaded right ventricle.
In the presence of paradoxical embolus, use of antiplatelet agents or anticoagulants are necessary as above.
In pediatric patients, when a VSD is diagnosed and is small; watchful waiting is of value as the defect might close. In fact, when the defect is seen in adults and it is restrictive with no hemodynamic embarrassment of the right ventricle (Qp/Qs <1.5), pulmonary hypertension, or associated aortic insufficiency, patient can be monitored safely. Patients with moderate or large size defects have worse mortality in long term however and there is no real role for medical management in this patient population.
Complications and their management
Percutaneous and open surgical closure of septal defects are generally safe and well-tolerated. Given the invasive nature of these procedures however, significant risks are present and the risk/benefit assessment should be carefully performed before proceeding with an intervention.
Complications associated with percutaneous PFO or ASD closures
Serious complications associated with PFO and ASD closures are rare but present. Overall, the combined incidence of serious complications is in the 1 to 2% range in the published meta-analyses and include death, hemorrhage requiring blood transfusion, cardiac tamponade, and pulmonary embolization. Heart block and atrial arrhythmias can also be seen during procedure or follow up.
It is rare for a PFO closure device to get dislodged and embolize into the right- or the left-sided circulation; however, case reports have been published. Cases where the closure device, particularly the Amplatzer septal occluder, eroded through atrial tissue has been reported (incidence 0.1%). There are no documented cases of erosion in Helex device due to its softer components.
Thrombus might form on the device on either side and lead to embolic phenomenon. It is for this reason that the patients should stay on aspirin and clopidogrel therapy for approximately 6 months as the device gets endothelialized.
Risk of infective endocarditis is present in the initial few months after device implantation; however, it is reduced as the device gets endothelialized. Procedural prophylactic antibiotics are indicated until this is the case. If there is significant residual shunt, this might prevent full endothelialization of the device and longer term prophylaxis is the rule.
Residual shunts might be present after ASD and PFO device closures, however, this is not common. Usually, as the device gets centered on the defect and gets endothelialized, scar tissue formation together with the device leads to elimination of these residual shunts. In the rare instances where the shunt remains significant and large, a second device implantation or a surgical explantation and primary closure might be necessary.
Overall, studies have shown that percutaneous closure of secundum ASDs and PFOs are as effective as surgery. This makes the percutaneous approach procedure of choice if patients are deemed candidates.
Complications associated with percutaneous VSD closures
Complications associated with VSD closures depend on where the defect is located and the type of the device used.
Serious complications including device embolization, wire thrombus, and pericardial effusion with tamponade are rare complications and are best avoided with meticulous technique and thorough use of imaging modalities.
The most commonly reported complication during procedure or follow up is the development of complete heart block with perimembranous VSDs and it is felt to occur due to tissue edema. While usually transient, cases where pacemaker implantation was required have been reported.
Depending on the location and the size of the device, valve impingement by the device can lead to valvular regurgitation or stenosis. Use of TEE should be helpful in the prevention of these complications.
What’s the evidence?
The first two articles provide a framework where we can learn about the natural history of septal defects. The last article shows the prevalence of PFOs in the general population.
Campbell, M. “Natural history of atrial septal defect”. Br Heart J. vol. 32. 1970. pp. 820-826.
Campbell, M. “Natural history of ventricular septal defect”. Br Heart J. vol. 33. 1971. pp. 246-257.
Hagen, PT, Scholz, DG, Edwards, WD. “Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts”. Mayo Clin Proc. vol. 59. 1984. pp. 17-20.
Lechat, P, Mas, JL, Lascault, G. “Prevalence of patent foramen ovale in patients with stroke”. N Engl J Med. vol. 318. 1988. pp. 1148-1152.
Azarbal, B, Tobis, J, Suh, W. “Association of interatrial shunts and migraine headaches: impact of transcatheter closure”. J Am Coll Cardiol. vol. 45. 2005. pp. 489-492.
Sorrentino, M, Resnekov, L. “Patent foramen ovale associated with platypnea and orthodeoxia”. Chest. vol. 100. 1991. pp. 1157-1158.
Allemann, Y, Hutter, D, Lipp, E. “Patent foramen ovale and high-altitude pulmonary edema”. JAMA. vol. 296. 2006. pp. 2954-2958.
King, TD, Thomson, SL, Steiner, C. “Secundum atrial septal defect: nonoperative closure during cardiac catheterization”. JAMA. vol. 235. 1976. pp. 2506-2509.
Roos-Hesselink, JW, Meijboom, FJ, Spitaels, SE. “Excellent survival and low incidence of arrhythmias, stroke and heart failure long-term after surgical ASD closure at young age. A prospective follow-up study of 21-33 years”. Eur Heart J. vol. 24. 2003. pp. 190-7.
Attie, F, Rosas, M, Granados, N. “Surgical treatment for secundum atrial septal defects in patients >40 years old. A randomized clinical trial”. J Am Coll Cardiol. vol. 38. 2001. pp. 2035-2042.
Gatzoulis, MA, Freeman, MA, Siu, SC. “Atrial arrhythmia after surgical closure of atrial septal defects in adults”. N Engl J Med. vol. 340. 1999. pp. 839-846.
Du, ZD, Hijazi, ZM, Kleinman, CS. “Comparison between transcatheter and surgical closure of secundum atrial septal defect in children and adults: results of a multicenter nonrandomized trial”. J Am Coll Cardiol. vol. 39. 2002. pp. 1836-1844.
Hughes, ML, Maskell, G, Goh, TH. “Prospective comparison of costs and short term health outcomes of surgical versus device closure of atrial septal defect in children”. Heart. vol. 88. 2002. pp. 67-70.
Dowson, A, Mullen, MJ, Peatfield, R. “Migraine Intervention With STARFlex Technology (MIST) trial: a prospective, multicenter, double-blind, sham-controlled trial to evaluate the effectiveness of patent foramen ovale closure with STARFlex septal repair implant to resolve refractory migraine headache”. Circulation. vol. 117. 2008. pp. 1397-1404.
Amin, Z, Hijazi, ZM, Bass, JL. “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. vol. 63. 2004. pp. 496-502.
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. vol. 2. 2007. pp. 256-264.
Divekar, A, Gaamangwe, T, Shaikh, N. “Cardiac perforation after device closure of atrial septal defects with the Amplatzer septal occluder”. J Am Coll Cardiol. vol. 45. 2005. pp. 1213-1218.
Schoen, SP, Boscheri, A, Lange, SA. “Incidence of aortic valve regurgitation and outcome after percutaneous closure of atrial septal defects and patent foramen ovale”. Heart. vol. 94. 2008. pp. 844-847.
Warnes, CA, Williams, RG, Bashore, TM. “ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons”. J Am Coll Cardiol. vol. 52. 2008. pp. e143-263.
Wilson, W, Taubert, KA, Gewitz, M. “Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group”. Circulation. vol. 116. 2007. pp. 1736-1754.
Alkashkari, W, Cao, Q, Hijazi, ZM, Carroll, JD, Webb, JG. “Closure of atrial septal defects”. Structural Heart Disease Interventions. 2012. pp. 175-195.
Horlick, EM, Benson, LN, Osten, MD, Carroll, JD, Webb, JG. “Closure of ventricular septal defects in adults”. Structural Heart Disease Interventions. 2012. pp. 195-210.
Poommipanit, P, Tobis, J, Carroll, JD, Webb, JG. “Closure of patent foramen ovale”. Structural Heart Disease Interventions. 2012. pp. 159-173.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
- General description of procedure, equipment, technique
- Indications and patient selection
- Details of how the procedure is performed
- Alternative and/or additional procedures to consider
- Complications and their management
- What’s the evidence?