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Clinical outcomes post percutaneous patent ductus arteriosus closure in adults
Journal Pre-proof Clinical outcomes post percutaneous patent ductus arteriosus closure in adults William M. Wilson, MBBS, Ashish Shah, Mark D. Osten, MD, Lee N. Benson, MD, Natalie Abraha, BSc, Daniel Breitner, Eric M. Horlick, MDCM PII:
S0828-282X(19)31450-3
DOI:
https://doi.org/10.1016/j.cjca.2019.11.025
Reference:
CJCA 3533
To appear in:
Canadian Journal of Cardiology
Received Date: 22 August 2019 Revised Date:
5 November 2019
Accepted Date: 21 November 2019
Please cite this article as: Wilson WM, Shah A, Osten MD, Benson LN, Abraha N, Breitner D, Horlick EM, Clinical outcomes post percutaneous patent ductus arteriosus closure in adults, Canadian Journal of Cardiology (2019), doi: https://doi.org/10.1016/j.cjca.2019.11.025. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier Inc. on behalf of the Canadian Cardiovascular Society.
Clinical outcomes post percutaneous patent ductus arteriosus closure in adults
William M Wilson MBBS1, Ashish Shah2, Mark D Osten MD2, Lee N Benson MD2, Natalie Abraha BSc2, Daniel Breitner2, Eric M Horlick MDCM2
1
Royal Melbourne Hospital, Melbourne, Australia
2
Toronto Congenital Cardiac Centre for Adults, Toronto General Hospital, Toronto,
Canada
Short title: PDA closure in adults Word count: 4315
Address for correspondence: Eric Horlick, Toronto Congenital Cardiac Centre for Adults, Peter Munk Cardiac Centre, University Health Network and University of Toronto, Toronto, Ontario, Canada. T: +14163403835 F: +14163403000 E: [email protected]
1
Brief Summary
Little published data exists for device PDA closure in adults. We describe outcomes of 141 adults undergoing device PDA closure at a single centre over a 16-year period. Device closure was feasible in 100% of cases using an AmplatzerTM device, most commonly an ADO1 occluder. No major complications occurred.
2
Abstract
Background: There is little published data regarding percutaneous patent ductus arteriosus closure in adults. We aim to describe the outcomes of adult patients undergoing PDA closure at a single tertiary referral centre.
Methods: All adults who underwent device PDA closure at our centre between 20012017 were identified and enrolled into the study. Available clinical data and imaging data was reviewed.
Results: 141 patients were identified with a mean age of 43±15 years. LV dilatation was present in 27% and pulmonary hypertension in 36% of patients. Most ducts (74%) were type A morphology. Mean ductal diameter at the pulmonary artery end was 4.1±1.9mm and mean length was 10.0±4.7mm. Wire passage from the pulmonary artery was achieved in 79%. Procedural success rate was 100% and an Amplatzer device was deployed in all successful cases (ADO1 Duct OccluderTM in 97%). There was a small residual shunt in 6% at the time of closure and only 2 patients had a residual leak on echocardiography at a median of 3 month follow-up. No major complications occurred.
Conclusions: Transcatheter PDA closure using the Amplatzer Duct OccluderTM is very effective in adults across all duct morphologies and associated with a very low complication rate.
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Introduction:
A patent ductus arteriosus (PDA) is a persistent fetal vascular connection between the aorta and main pulmonary artery (PA), accounting for 5-10% of all congenital heart defects 1. Clinical manifestations are defined by the degree of shunting across the connection. Patients with a small PDA are often diagnosed incidentally when a continuous cardiac murmur is heard. Larger shunts can manifest as exertional dyspnea or heart failure, or alternatively as Eisenmenger syndrome (cyanosis) if severe pulmonary vascular disease leading to pulmonary hypertension with shunt reversal occurs. Indications for PDA closure include: symptoms associated with a significant left to right shunt, left-sided volume overload (left atrial or left ventricular enlargement), or reversible pulmonary artery hypertension.2 Closure in these settings results in resolution of symptoms and a reduced likelihood of progressive pulmonary arterial hypertension. Many cardiologists advocate closure of an ‘audible’ PDA to prevent long-term complications of PDA, in particular endarteritis. Percutaneous closure was first performed in 1967 using the Porstmann method. 3 Currently, percutaneous closure, most commonly performed using the Amplatzer duct occluder (ADO1), is the treatment of choice in adults although surgical closure may be required in certain scenarios (for example, very large PDA, aneurysms, or infection).2 Efficacy and complications of percutaneous closure have been well described in the paediatric literature 4-11 but little data exists in adults 12-15.
Methods:
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Study population This is a retrospective study of all adults patients (age > 18 years) who underwent device closure of a PDA at our institution, the Toronto Congenital Cardiac Centre for Adults (TCCCA) between 01 June 2001 and 29 June 2017. Indications for closure included: left atrial and/or ventricular enlargement, pulmonary hypertension with net left to right shunt >1.5:1, prior endarteritis, or the presence of an audible murmur attributable to the PDA in the absence of symptoms or other indications for closure.16, 17
Intervention was not performed for the small, silent duct. Research and Ethics
Board at Toronto General Hospital approval was obtained as well as a waiver for patient consent. Procedure All procedures were performed under local anaesthesia and sedation. Intravenous heparin (100IU/kg) was given after femoral cannulation and all patients received a single dose of antibiotics at the time of the procedure. Arterial and venous sheaths were inserted. After collection of haemodynamic data, aortography was performed in the descending aorta (lateral and 30 degree right anterior oblique projection). Initial attempts to cross the duct were made with a standard straight 0.035-inch wire (uncoated or coated) via a Gensini 8 French angiographic catheter, which was passed into the descending aorta and allowed exchange for an AmplatzerTM extra-stiff wire (St Jude Medical, MN, USA). If wire passage across the duct could not be achieved from the venous side, a straight wire was passed from the aortic side, usually via a Judkins left 4.0 diagnostic catheter, which was then snared in the pulmonary artery and externalized via the femoral vein. A 180-degree AmplatzerTM torque view sheath (St Jude Medical, MN, USA) was used to deliver the AmplatzerTM devices. Repeat
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aortography was performed after device release. All patients had an echocardiogram the day after the procedure.
Data collection Data was collected from hospital paper and electronic medical records, as well as from review of the procedural angiographic images. Demographic variables, including age, gender, body mass index (BMI), and associated medical conditions were extracted. Left ventricle (LV) dilatation was defined as indexed left ventricular end diastolic diameter (LVEDDi) more than 32mm/m2 in women and 31mm/m2 in men. Pulmonary hypertension was defined as a mean PA pressure > 25mmHg (at catheterization at time of procedure). Angiographic data recorded from review of preprocedural and procedural images included PDA diameter and PDA morphology, which was classified as A to E according to the Krichenko angiographic classification (Figure 1).18 Procedural data collected included percutaneous access and sheath size, direction of wire crossing of the duct (antegrade or retrograde), device type and size. Technical success was defined as device implantation in the appropriate position without complication and with little or no residual flow angiographically at the conclusion of the case or on inpatient echocardiography after the procedure. Procedural success was defined as technical success without an in-hospital complication (death, myocardial infarction (MI), stroke). An unfavourable outcome during follow-up was defined as embolization, persistent haemolysis, residual leak requiring a further procedure or flow impairment in adjacent structures.
Statistical analysis Mean and standard deviation or median and interquartile range, as appropriate, were
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calculated for continuous variables. Counts and percentages were calculated for categorical variables. Pre and post procedural angiographic measurements and hemodynamic data for continuous variables were compared using the paired t-test and for categorical variables using Fisher’s exact or chi squared tests. All tests were be performed at an alpha of 5%. Statistical analyses were performed using SPSS statistics Version 22 (IBM Corporation, Armonk, NY, USA)
Results We identified one hundred and forty one consecutive adults who had undergone device closure of a PDA at the TCCCA between 2001 and 2017. Patient demographics are presented in Table 1. Mean age (standard deviation) at the time of the procedure was 43±15 years and 24% were male. No patient had undergone previous surgical ligation. Three patients had undergone previous transcatheter PDA closure using coils or a Rashkind device but had significant residual shunting. Approximately half of patients (45%) were symptomatic (dyspnea on exertion, chest pain, palpitations or dizziness) at the time of diagnosis whilst 2.9% presented in heart failure and 0.6% presented with endocarditis. Based on echocardiography performed before the procedure, LV enlargement was evident in 27%. LV dysfunction was present in 10%. Morphology of the duct was A 74%, B 2%, C 5%, D 1%, E 18%. Mean ductal diameter at the PA end was 4.0±1.5mm (range 1-14mm), whilst the mean diameter at the aortic side was 7.8±3.3mm (range 1.5-19mm). The PA diameter was the narrowest dimension in 99% of patients. In 16% of cases, the narrowest PDA diameter was >5mm. Mean PDA length was 10.0± 4.7mm (median 9, range 2-17mm). Mean PA pressure at time of closure was 25±9mmHg (median 23mmHg, range 137
68mmHg); 36% had an elevated mean PA pressure (ie >25mmHg) and 8% had moderate pulmonary hypertension (ie mean PA pressure 35-45mmHg, all with PA systolic:Ao systolic ratio <0.5). One patient had severe pulmonary hypertension (mean PA pressure 68mmHg, PA systolic:Ao systolic ratio 0.9)
Procedural details Aside from two patients who had general anaesthesia, all cases were performed under local anaesthesia. Wire passage across the duct was achieved from the venous side (antegrade from PA) in 85% and from the arterial side (retrograde from aorta) in 15%. The need for a retrograde approach appeared to relate duct size (mean minimal duct diameter smaller in those requiring retrograde wire crossing (2.8±0.9mm versus 3.5±1.3mm, p=0.01). Sizing of the defect was largely performed via angiography. Balloon sizing was only required in 2 cases with large type B defects. Mean device waist diameter was 9.4±1.9mm (range 5-18mm). The device used was ADO1 occluder in 97% (n=136) of cases. ADO1 device sizes included: 5/4 n=2, 6/4 n=7, 8/6 n=50, 10/8 n=52, 12/10 n=25. Other devices used included an AmplatzerTM Muscular VSD device in 3 patients (6mm, 10mm, 18mm), an AmplatzerTM Septal Occluder (ASO) device in 1 (13mm) and an AmplatzerTM Vascular Plug 4 (6mm device) in 1. The Muscular VSD and ASO devices were used in patients with significant pulmonary hypertension and large ducts, where a double disc device was felt to be preferable. Mean fluoroscopy time was 14.3±8.8 minutes (range 4-50). The device was successfully deployed in 100% of patients. Trivial flow was present on aortography after device deployment in 35% of patients. Residual shunting was graded as small (ie. ‘smoke’ or jet <2mm diameter) in all with residual flow. Technical success (stable device and none-trivial residual shunt either 8
angiographically during the case or on echocardiography after the procedure) was achieved in 99% of patients. No major procedural complications were observed (no deaths, no device embolization, no perforation or tamponade, no thrombotic event, no encroachment on aorta or branch pulmonary artery). A minor vascular access complication occurred in one patient who developed a groin hematoma.
Follow-up Clinical follow-up was available in 90% of patients at a mean of 7 months after the procedure (median = 2 months, range 1-144 months) and an echocardiogram available in 61% (n=70) of patients at median of 3 months after the procedure. There was a residual leak in two patients (a small leak across an 11mm window-like PDA closed with a 13mm ASO and a small leak across an ADO1 10/8mm device). There were no cases of endocarditis nor embolization. In the 61% of patients who had a follow up echocardiogram in the first year, there was evidence of LV remodeling with mean LVEDDi 27.5±4.7mm/m2 (LVEDDi 30.3±4.3 pre-procedure, p<0.001) and mean LVESDi 18.3±3.2mm/m2 (LVESDi 19.9±3.6 pre-procedure, p=0.0008). In those with LV dysfunction (n=14), LV function improved to normal in all except one patient. In those patients with pulmonary hypertension present at catheterization pre-closure, the majority had normal pulmonary pressures at follow-up (RVSP was >50mmHg in two patients only).
Discussion
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In this study, we evaluated the procedural and short-term outcomes of a cohort of adults to have undergone percutaneous PDA closure. The main finding of this singlecentre study is that device PDA closure in adults is a highly effective and very safe procedure. The majority of evidence for PDA device occlusion relates to the paediatric population. In children, coil occlusion is usually very effective, in particular for small PDAs (<3mm diameter). Success rates are high in children (95% occlusion rate was documented at one year in 1258 patients in the European Paediatric Cardiology Registry) with a ‘suboptimal’ outcome (abandoned procedure, persistent hemolysis, residual leak requiring a further procedure, flow impairment in adjacent structures or duct recanalization) occurring in up to 10% of cases. 4 A suboptimal outcome was more likely to occur in larger ducts or tubular shaped ducts in this European registry. Our series is the largest reported series of adults with PDA closure with previous reports in adults ranging from 21 to 69 patients 12-15, 19. The range of duct morphologies and mean minimal duct diameter was similar in our study to the previous series with similar high procedural success rates documented using the AmplatzerTM Duct Occluder (ADO) device. Almost 100% PDA occlusion rate at mid and long-term follow-up has been documented in other series.12, 13, 19
Technique PDA closure in adults is technically feasible and successful in most cases. Imaging of the duct is usually achieved by aortogram at the time of closure, which can be suboptimal in larger ducts or short ducts (eg type B); in these cases, balloon sizing (eg AmplatzerTM sizing balloon) may be useful and also provide information regarding distensibility. A high cineangiographic frame rate may be required to capture the
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balloon waist if stability of the inflated balloon is an issue. CT aortography before the procedure can be of value in defining the size and characteristics of the duct, and excluding other causes of continuous murmurs including coronary fistula, aortopulmonary collaterals, and anomalous connections between the internal mammary arteries and the lung circulation due to TB or other pulmonary disease. The main challenge of the procedure in adults is crossing the duct with a wire. This can be achieved from the venous aspect in most cases (85% in our series) using a Gensini diagnostic catheter and a straight wire. Otherwise, retrograde crossing from the aorta is usually straight-forward using a JL4 diagnostic catheter; snaring of an exchange length angled GlidewireTM (Terumo Medical, Japan) with an EN SnareTM (Merit Medical, UT, USA) or an AmplatzTM Gooseneck snare (Medtronic, MN, USA) in the branch pulmonary artery allows externalization of the wire and subsequent delivery of a multipurpose catheter from the venous side across the duct to the aorta. Once a multipurpose catheter is positioned across the duct, an AmplatzTM extra-stiff exchange length wire is delivered to the aorta over which the appropriate sized Amplatzer delivery sheath can be delivered (usually 6 or 7 French). Hypotension at this stage of the procedure may relate to severe tricuspid insufficiency due to valve splinting by a stiff wire and sheath (usually resolves once the delivery equipment is withdrawn). The selected device is then deployed in the duct; the anterior border of the trachea in the lateral projection represents a good anatomic landmark to mark the aortic aspect of the duct and guide device deployment. The most commonly used device in adults is the AmplatzerTM ADO1 occluder. It is a versatile device that can be used in all duct morphologies 12, 13, as evidenced in this study where the device was used for 97% of cases. The commonest device sizes employed are 8/6mm and 10/8mm; it can be used to treat ducts up to 12mm in
11
diameter (using the 16/14mm device). It is suggested that the device waist diameter (at aorta) should be > 2mm larger than the minimum duct diameter; we would recommend assuming that the true ductal diameter is usually larger than the angiographic measurement (ductal spasm may contribute for example), thus one should select the next size up from that which would be selected based on minimum duct diameter plus 2mm (Figure 2). The Occlutech OccluderTM (Occlutech, Germany) was recently introduced with some potential advantages including: wider core at pulmonary aspect and longer lengths for better stability; prominent screw attachment at pulmonary end to facilitate easy snaring if need be and absence of distal clamp at aortic end. It is available up to 24/18mm (diameter) and 16mm length. The CeraTM occluder device (Lifetech Scientific, Shenzen, China) is also useful for larger ducts (available up to 26/24mm)19. The use of AmplatzerTM Muscular VSD devices is also described for larger ducts (Figure 3), in particular in the setting of pulmonary hypertension, where the double disc design can prevent embolization20, 21. These devices are symmetrical and can also be delivered from the aortic side, which has been associated with shorter procedure times and lower radiation exposure22. Other devices available include the ADO2 device (can treat ducts <5.5mm diameter) and vascular plugs (such as AmplatzerTM vascular plugs 2 and 4, which some have advocated as being suitable for long, tubular ducts, in particular ductal types C, D, or E) 23; the role of these devices in adults is likely in smaller ducts that may be difficult to cross antegrade from the pulmonary artery as they can easily be delivered in a retrograde fashion from the aorta.
Complications
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Complications of device closure in adults were rare in this study and others 12, 13, 15, 19, 24
. Obstruction of the aorta or branch pulmonary arteries is rarely an issue in adults. A
residual leak is uncommon but can be seen in irregular and calcified ducts where there may not be adequate conformation of device. Haemolysis can occur due to residual leak in very large ducts, but usually settles with time5. Transient left ventricular systolic dysfunction has been reported after PDA closure, in particular with large shunts and pre-existing LV dysfunction or pulmonary hypertension; this may relate to preload reduction with a sudden afterload increase25, 26, but rarely translates into pulmonary oedema post closure and pre-procedure diuretic use is rarely required. Device embolization is very uncommon in adults, likely relating to the ability to generously oversize devices without fear of obstruction of the LPA or aorta. A chest x-ray and transthoracic echocardiogram are performed after the procedure to ensure stable device position and document any residual shunting. Patients with no residual shunt, normal LV size and function with normal pulmonary pressures do not warrant follow-up beyond 6 months. Otherwise, review 1 to 3 yearly is reasonable. Persistent LV systolic dysfunction was reported in approximately 10% of patients in a study of 45 adults to undergo PDA closure in a South Korean study by Jeong et al. 27 In that study, pre-closure LVEF was the best index to predict late LVEF after closure.
Indications for closure Indications for PDA closure are largely similar in adults and children. Closure is indicated in all patients with evidence of LV volume overload (LV dilation ± dysfunction) and in those with pulmonary hypertension (without evidence for Eisenmenger physiology). Expert opinion is largely in favor of device closure of small PDAs that are audible (continuous murmur) without evidence of a
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haemodynamically significant shunt (ie normal LV size and normal pulmonary pressures) to avoid PDA-related complications, such as endarteritis (10% lifetime risk) and pulmonary hypertension. In adults, duct closure is reasonable in the presence of a systolic murmur only if there exists any LV enlargement or elevation of pulmonary pressures. A ‘clinically silent’ small duct is likely best managed conservatively, however, a small risk of endarteritis remains. One issue that requires consideration on occasion is what severity of pulmonary hypertension represents a contra-indication to closure. In general, closure is safe as long as there is a residual left-to-right shunt and no features of Eisenmenger physiology. Zabal et al. studied 168 selected patients (mean age 10±14 years) with a PDA and elevated systolic pressure (>50mmHg, mean PASP 64±16mmHg, mean PVR 3.7±2.1 Wood units); device closure using AmplatzerTM devices (ADO1 86%, muscular VSD device 11%, ASO device 2%) was safe with an immediate drop in pulmonary artery pressures, which continued to decline over time (PASP 30±8mmHg at median of 30 months post closure).28 Zhang et al. reported findings after test occlusion of the PDA in 137 patients with severe pulmonary hypertension. They described an approach of observing haemodynamics post device deployment but before release (rather than test occlusion using a balloon); an invasively derived ratio of PA systolic pressure to aortic systolic pressure of greater than 0.5 after trial occlusion (using the device) reliably predicted the presence of late pulmonary hypertension.29
Limitations
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This was a retrospective study where information was mostly extracted from paper and electronic medical records. The follow-up duration was relatively short and echocardiographic assessment at follow-up incomplete.
Conclusion Transcatheter PDA closure using the AmplatzerTM Duct Occluder is very effective in adults across all duct morphologies and associated with a very low complication rate.
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Disclosures
Eric Horlick is a consultant for Abbott Structural Heart Disease and is supported by the Peter Munk Chair in Structural Heart Disease Intervention. Mark D. Osten is a consultant for Abbott Structural Heart. The Peter Munk Cardiac Centre receives unrestricted research and educational grants from Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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References
1. Hammerman C. Patent ductus arteriosus. Clinical relevance of prostaglandins and prostaglandin inhibitors in PDA pathophysiology and treatment. Clin Perinatol. 1995;22:457-79. 2. Stout KK, Daniels CJ, Aboulhosn JA, Bozkurt B, Broberg CS, Colman JM, Crumb SR, Dearani JA, Fuller S, Gurvitz M, Khairy P, Landzberg MJ, Saidi A, Valente AM and Van Hare GF. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology. 2019;73:1494-1563. 3. Porstmann W, Wierny L and Warnke H. [The closure of the patent ductus arteriosus without thoractomy. (preliminary report)]. Thoraxchir Vask Chir. 1967;15:199-203. 4. Magee AG, Huggon IC, Seed PT, Qureshi SA, Tynan M and Association for European C. Transcatheter coil occlusion of the arterial duct; results of the European Registry. European heart journal. 2001;22:1817-21. 5. Pass RH, Hijazi Z, Hsu DT, Lewis V and Hellenbrand WE. Multicenter USA Amplatzer patent ductus arteriosus occlusion device trial: initial and one-year results. Journal of the American College of Cardiology. 2004;44:513-9. 6. Faella HJ and Hijazi ZM. Closure of the patent ductus arteriosus with the amplatzer PDA device: immediate results of the international clinical trial. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2000;51:50-4. 7. Tometzki AJ, Arnold R, Peart I, Sreeram N, Abdulhamed JM, Godman MJ, Patel RG, Kitchiner DJ, Bu'Lock FA and Walsh KP. Transcatheter occlusion of the patent ductus arteriosus with Cook detachable coils. Heart. 1996;76:531-5. 8. Jang GY, Son CS, Lee JW, Lee JY and Kim SJ. Complications after transcatheter closure of patent ductus arteriosus. Journal of Korean medical science. 2007;22:484-90. 9. Wang JK, Wu MH, Lin MT, Chiu SN, Chen CA and Chiu HH. Transcatheter closure of moderate-to-large patent ductus arteriosus in infants using Amplatzer duct occluder. Circulation journal : official journal of the Japanese Circulation Society. 2010;74:361-4. 10. Ghasemi A, Pandya S, Reddy SV, Turner DR, Du W, Navabi MA, Mirzaaghayan MR, Kiani A, Sloan K and Forbes TJ. Trans-catheter closure of patent ductus arteriosus-What is the best device? Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2010;76:687-95. 11. Brunetti MA, Ringel R, Owada C, Coulson J, Jennings JM, Hoyer MH and Everett AD. Percutaneous closure of patent ductus arteriosus: a multiinstitutional registry comparing multiple devices. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2010;76:696-702.
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12. Hong TE, Hellenbrand WE, Hijazi ZM and Amplatzer I. Transcatheter closure of patent ductus arteriosus in adults using the Amplatzer duct occluder: initial results and follow-up. Indian Heart J. 2002;54:384-9. 13. Behjati-Ardakani M, Rafiei M, Behjati-Ardakani MA, Vafaeenasab M and Sarebanhassanabadi M. Long-term Results of Transcatheter Closure of Patent Ductus Arteriosus in Adolescents and Adults with Amplatzer Duct Occluder. N Am J Med Sci. 2015;7:208-11. 14. Bonhoeffer P, Borghi A, Onorato E and Carminati M. Transfemoral closure of patent ductus arteriosus in adult patients. Int J Cardiol. 1993;39:181-6. 15. Bentham JR, Thomson JD and Gibbs JL. Transcatheter closure of persistent ductus arteriosus in adults. J Interv Cardiol. 2012;25:501-4. 16. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, del Nido P, Fasules JW, Graham TP, Jr., Hijazi ZM, Hunt SA, King ME, Landzberg MJ, Miner PD, Radford MJ, Walsh EP, Webb GD, Smith SC, Jr., Jacobs AK, Adams CD, Anderson JL, Antman EM, Buller CE, Creager MA, Ettinger SM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Page RL, Riegel B, Tarkington LG, Yancy CW, American College of C, American Heart Association Task Force on Practice G, American Society of E, Heart Rhythm S, International Society for Adult Congenital Heart D, Society for Cardiovascular A, Interventions and Society of Thoracic S. 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. Journal of the American College of Cardiology. 2008;52:e143-263. 17. Silversides CK, Salehian O, Oechslin E, Schwerzmann M, Vonder Muhll I, Khairy P, Horlick E, Landzberg M, Meijboom F, Warnes C and Therrien J. Canadian Cardiovascular Society 2009 Consensus Conference on the management of adults with congenital heart disease: complex congenital cardiac lesions. Can J Cardiol. 2010;26:e98-117. 18. Krichenko A, Benson LN, Burrows P, Moes CA, McLaughlin P and Freedom RM. Angiographic classification of the isolated, persistently patent ductus arteriosus and implications for percutaneous catheter occlusion. Am J Cardiol. 1989;63:877-80. 19. P S, Jose J and George OK. Contemporary outcomes of percutaneous closure of patent ductus arteriosus in adolescents and adults. Indian Heart J. 2018;70:308-315. 20. Fernando R, Koranne K, Loyalka P, Kar B and Gregoric I. Patent ductus arteriosus closure using an Amplatzer() ventricular septal defect closure device. Experimental and clinical cardiology. 2013;18:e50-4. 21. Eicken A, Balling G, Gildein HP, Genz T, Kaemmerer H and Hess J. Transcatheter closure of a non-restrictive patent ductus arteriosus with an Amplatzer muscular ventricular septal defect occluder. Int J Cardiol. 2007;117:e40-2. 22. Liddy S, Oslizlok P and Walsh KP. Comparison of the results of transcatheter closure of patent ductus arteriosus with newer Amplatzer devices. 18
Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2013;82:253-9. 23. Gillespie MJ, Golden A, Sivarajan VB and Rome JJ. Transcatheter closure of patent ductus venosus with the Amplatzer vascular plug in twin brothers. Pediatric cardiology. 2006;27:142-5. 24. Al-Hamash SM, Wahab HA, Khalid ZH and Nasser IV. Transcatheter closure of patent ductus arteriosus using ado device: retrospective study of 149 patients. Heart Views. 2012;13:1-6. 25. Galal MO, Arfi MA, Nicole S, Payot M, Hussain A and Qureshi S. Left ventricular systolic dysfunction after transcatheter closure of a large patent ductus arteriosus. J Coll Physicians Surg Pak. 2005;15:723-5. 26. Tilahun B and Tefera E. Transient left ventricular systolic dysfunction following surgical closure of large patent ductus arteriosus among children and adolescents operated at the cardiac centre, Ethiopia. J Cardiothorac Surg. 2013;8:139. 27. Jeong YH, Yun TJ, Song JM, Park JJ, Seo DM, Koh JK, Lee SW, Kim MJ, Kang DH and Song JK. Left ventricular remodeling and change of systolic function after closure of patent ductus arteriosus in adults: device and surgical closure. Am Heart J. 2007;154:436-40. 28. Zabal C, Garcia-Montes JA, Buendia-Hernandez A, Calderon-Colmenero J, Patino-Bahena E, Juanico-Enriquez A and Attie F. Percutaneous closure of hypertensive ductus arteriosus. Heart. 2010;96:625-9. 29. Zhang DZ, Zhu XY, Lv B, Cui CS, Han XM, Sheng XT, Wang QG and Zhang P. Trial occlusion to assess the risk of persistent pulmonary arterial hypertension after closure of a large patent ductus arteriosus in adolescents and adults with elevated pulmonary artery pressure. Circ Cardiovasc Interv. 2014;7:473-81.
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Tables Table 1. Patient characteristics Table 2. Imaging parameters
Figures Figure 1. Krichenko classification
Figure 2. Case – 24 year old with shortness of breath and a continuous murmur. LV dilatation is evident on echocardiography with a PDA. a. Aortogram demonstrates a type A PDA with a minimum diameter of ~6mm (Black arrow). White arrow indicates anterior border of trachea, which serves as a marker for the aortic aspect of the PDA (in the lateral projection) b. Successful Device closure was performed using a 12/10 ADO1 device deployed from the pulmonary artery (minimum diameter + 2mm is 8mm, therefore one size larger is selected). Compression of device waist evident.
Figure 3. 42 year old female with dyspnea and a large PDA with associated LV dilatation, moderate pulmonary hypertension a. CT aortogram demonstrating type B ‘window-like’ duct (8 x 10mm) b. Successful device closure using a 10mm muscular VSD device deployed from the pulmonary artery. Minor residual leak post deployment with haemolysis thereafter, which settled over the following weeks.
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Table 1. Patient baseline characteristics Characteristic Age (years), mean ±SD Male, n (%) BMI (kg/m2), mean ±SD Down syndrome, mean (%) Co-morbidities, n (%) Atrial fibrillation Hypertension Pacemaker Coronary fistula Diabetes Stroke Other congenital heart conditions ASD VSD AS (moderate) Previous cardiac surgery (VSD)
n = 141 42.8 ± 15.4 34 (24) 25.2 ± 5.2 3 (2) 6 (4) 6 (4) 2 (1) 2 (1) 3 (2) 2 (1) 2 (1) 3 (2) 1 (1) 2 (1)
Prior endocarditis 1 AS = aortic stenosis; ASD = atrial septal defect; BMI = body mass index; VSD = ventricular septal defect
Characteristic Age (years), median (range) Male, n (%) BMI (kg/m2), median (range) Down syndrome, mean (%) Co-morbidities, n (%) Atrial fibrillation Hypertension Pacemaker Coronary fistula Diabetes Stroke Other congenital heart conditions ASD VSD AS (moderate)
n = 141 41 (18-82) 34 (24) 24 (15-49) 3 (2) 6 (4) 6 (4) 2 (1) 2 (1) 3 (2) 2 (1) 2 (1) 3 (2) 1 (1)
Previous cardiac surgery (VSD)
2 (1)
Prior endocarditis
1
Table 2. Imaging parameters
n = 141, Median (range) Echocardiogram pre closure LVEDDi LVESDi LVEF RVSP Aortogram pre/at time of closure PDA diameter at PA (mm) PDA diameter at aorta (mm) PDA length (mm)
30 (19-44) 20 (14-34) 62 (33-74) 31(14-74) 4.0 ± 1.5mm (1-14) 7 (1.5-19) 9 (2-17)
Pulmonary hypertension Systolic PA pressure (mmHg) Mean PA pressure (mmHg)
36% 32 (18-105) 23 (13-68)
PA systolic:Aorta systolic PCWP (mmHg) Coronary disease
0.3 (0.2-0.9) 13 (6-29) Nil
LVEDDi = Left ventricular end-diastolic diameter (indexed); LVEF = left ventricular ejection fraction; LVESDi = left ventricular end-systolic diameter (indexed); LVSP = Left ventricular systolic pressure; PA = pulmonary artery; PCWP = pulmonary capillary wedge pressure; RVSP = right ventricular systolic pressure.
S0828-282X(19)31450-3
DOI:
https://doi.org/10.1016/j.cjca.2019.11.025
Reference:
CJCA 3533
To appear in:
Canadian Journal of Cardiology
Received Date: 22 August 2019 Revised Date:
5 November 2019
Accepted Date: 21 November 2019
Please cite this article as: Wilson WM, Shah A, Osten MD, Benson LN, Abraha N, Breitner D, Horlick EM, Clinical outcomes post percutaneous patent ductus arteriosus closure in adults, Canadian Journal of Cardiology (2019), doi: https://doi.org/10.1016/j.cjca.2019.11.025. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier Inc. on behalf of the Canadian Cardiovascular Society.
Clinical outcomes post percutaneous patent ductus arteriosus closure in adults
William M Wilson MBBS1, Ashish Shah2, Mark D Osten MD2, Lee N Benson MD2, Natalie Abraha BSc2, Daniel Breitner2, Eric M Horlick MDCM2
1
Royal Melbourne Hospital, Melbourne, Australia
2
Toronto Congenital Cardiac Centre for Adults, Toronto General Hospital, Toronto,
Canada
Short title: PDA closure in adults Word count: 4315
Address for correspondence: Eric Horlick, Toronto Congenital Cardiac Centre for Adults, Peter Munk Cardiac Centre, University Health Network and University of Toronto, Toronto, Ontario, Canada. T: +14163403835 F: +14163403000 E: [email protected]
1
Brief Summary
Little published data exists for device PDA closure in adults. We describe outcomes of 141 adults undergoing device PDA closure at a single centre over a 16-year period. Device closure was feasible in 100% of cases using an AmplatzerTM device, most commonly an ADO1 occluder. No major complications occurred.
2
Abstract
Background: There is little published data regarding percutaneous patent ductus arteriosus closure in adults. We aim to describe the outcomes of adult patients undergoing PDA closure at a single tertiary referral centre.
Methods: All adults who underwent device PDA closure at our centre between 20012017 were identified and enrolled into the study. Available clinical data and imaging data was reviewed.
Results: 141 patients were identified with a mean age of 43±15 years. LV dilatation was present in 27% and pulmonary hypertension in 36% of patients. Most ducts (74%) were type A morphology. Mean ductal diameter at the pulmonary artery end was 4.1±1.9mm and mean length was 10.0±4.7mm. Wire passage from the pulmonary artery was achieved in 79%. Procedural success rate was 100% and an Amplatzer device was deployed in all successful cases (ADO1 Duct OccluderTM in 97%). There was a small residual shunt in 6% at the time of closure and only 2 patients had a residual leak on echocardiography at a median of 3 month follow-up. No major complications occurred.
Conclusions: Transcatheter PDA closure using the Amplatzer Duct OccluderTM is very effective in adults across all duct morphologies and associated with a very low complication rate.
3
Introduction:
A patent ductus arteriosus (PDA) is a persistent fetal vascular connection between the aorta and main pulmonary artery (PA), accounting for 5-10% of all congenital heart defects 1. Clinical manifestations are defined by the degree of shunting across the connection. Patients with a small PDA are often diagnosed incidentally when a continuous cardiac murmur is heard. Larger shunts can manifest as exertional dyspnea or heart failure, or alternatively as Eisenmenger syndrome (cyanosis) if severe pulmonary vascular disease leading to pulmonary hypertension with shunt reversal occurs. Indications for PDA closure include: symptoms associated with a significant left to right shunt, left-sided volume overload (left atrial or left ventricular enlargement), or reversible pulmonary artery hypertension.2 Closure in these settings results in resolution of symptoms and a reduced likelihood of progressive pulmonary arterial hypertension. Many cardiologists advocate closure of an ‘audible’ PDA to prevent long-term complications of PDA, in particular endarteritis. Percutaneous closure was first performed in 1967 using the Porstmann method. 3 Currently, percutaneous closure, most commonly performed using the Amplatzer duct occluder (ADO1), is the treatment of choice in adults although surgical closure may be required in certain scenarios (for example, very large PDA, aneurysms, or infection).2 Efficacy and complications of percutaneous closure have been well described in the paediatric literature 4-11 but little data exists in adults 12-15.
Methods:
4
Study population This is a retrospective study of all adults patients (age > 18 years) who underwent device closure of a PDA at our institution, the Toronto Congenital Cardiac Centre for Adults (TCCCA) between 01 June 2001 and 29 June 2017. Indications for closure included: left atrial and/or ventricular enlargement, pulmonary hypertension with net left to right shunt >1.5:1, prior endarteritis, or the presence of an audible murmur attributable to the PDA in the absence of symptoms or other indications for closure.16, 17
Intervention was not performed for the small, silent duct. Research and Ethics
Board at Toronto General Hospital approval was obtained as well as a waiver for patient consent. Procedure All procedures were performed under local anaesthesia and sedation. Intravenous heparin (100IU/kg) was given after femoral cannulation and all patients received a single dose of antibiotics at the time of the procedure. Arterial and venous sheaths were inserted. After collection of haemodynamic data, aortography was performed in the descending aorta (lateral and 30 degree right anterior oblique projection). Initial attempts to cross the duct were made with a standard straight 0.035-inch wire (uncoated or coated) via a Gensini 8 French angiographic catheter, which was passed into the descending aorta and allowed exchange for an AmplatzerTM extra-stiff wire (St Jude Medical, MN, USA). If wire passage across the duct could not be achieved from the venous side, a straight wire was passed from the aortic side, usually via a Judkins left 4.0 diagnostic catheter, which was then snared in the pulmonary artery and externalized via the femoral vein. A 180-degree AmplatzerTM torque view sheath (St Jude Medical, MN, USA) was used to deliver the AmplatzerTM devices. Repeat
5
aortography was performed after device release. All patients had an echocardiogram the day after the procedure.
Data collection Data was collected from hospital paper and electronic medical records, as well as from review of the procedural angiographic images. Demographic variables, including age, gender, body mass index (BMI), and associated medical conditions were extracted. Left ventricle (LV) dilatation was defined as indexed left ventricular end diastolic diameter (LVEDDi) more than 32mm/m2 in women and 31mm/m2 in men. Pulmonary hypertension was defined as a mean PA pressure > 25mmHg (at catheterization at time of procedure). Angiographic data recorded from review of preprocedural and procedural images included PDA diameter and PDA morphology, which was classified as A to E according to the Krichenko angiographic classification (Figure 1).18 Procedural data collected included percutaneous access and sheath size, direction of wire crossing of the duct (antegrade or retrograde), device type and size. Technical success was defined as device implantation in the appropriate position without complication and with little or no residual flow angiographically at the conclusion of the case or on inpatient echocardiography after the procedure. Procedural success was defined as technical success without an in-hospital complication (death, myocardial infarction (MI), stroke). An unfavourable outcome during follow-up was defined as embolization, persistent haemolysis, residual leak requiring a further procedure or flow impairment in adjacent structures.
Statistical analysis Mean and standard deviation or median and interquartile range, as appropriate, were
6
calculated for continuous variables. Counts and percentages were calculated for categorical variables. Pre and post procedural angiographic measurements and hemodynamic data for continuous variables were compared using the paired t-test and for categorical variables using Fisher’s exact or chi squared tests. All tests were be performed at an alpha of 5%. Statistical analyses were performed using SPSS statistics Version 22 (IBM Corporation, Armonk, NY, USA)
Results We identified one hundred and forty one consecutive adults who had undergone device closure of a PDA at the TCCCA between 2001 and 2017. Patient demographics are presented in Table 1. Mean age (standard deviation) at the time of the procedure was 43±15 years and 24% were male. No patient had undergone previous surgical ligation. Three patients had undergone previous transcatheter PDA closure using coils or a Rashkind device but had significant residual shunting. Approximately half of patients (45%) were symptomatic (dyspnea on exertion, chest pain, palpitations or dizziness) at the time of diagnosis whilst 2.9% presented in heart failure and 0.6% presented with endocarditis. Based on echocardiography performed before the procedure, LV enlargement was evident in 27%. LV dysfunction was present in 10%. Morphology of the duct was A 74%, B 2%, C 5%, D 1%, E 18%. Mean ductal diameter at the PA end was 4.0±1.5mm (range 1-14mm), whilst the mean diameter at the aortic side was 7.8±3.3mm (range 1.5-19mm). The PA diameter was the narrowest dimension in 99% of patients. In 16% of cases, the narrowest PDA diameter was >5mm. Mean PDA length was 10.0± 4.7mm (median 9, range 2-17mm). Mean PA pressure at time of closure was 25±9mmHg (median 23mmHg, range 137
68mmHg); 36% had an elevated mean PA pressure (ie >25mmHg) and 8% had moderate pulmonary hypertension (ie mean PA pressure 35-45mmHg, all with PA systolic:Ao systolic ratio <0.5). One patient had severe pulmonary hypertension (mean PA pressure 68mmHg, PA systolic:Ao systolic ratio 0.9)
Procedural details Aside from two patients who had general anaesthesia, all cases were performed under local anaesthesia. Wire passage across the duct was achieved from the venous side (antegrade from PA) in 85% and from the arterial side (retrograde from aorta) in 15%. The need for a retrograde approach appeared to relate duct size (mean minimal duct diameter smaller in those requiring retrograde wire crossing (2.8±0.9mm versus 3.5±1.3mm, p=0.01). Sizing of the defect was largely performed via angiography. Balloon sizing was only required in 2 cases with large type B defects. Mean device waist diameter was 9.4±1.9mm (range 5-18mm). The device used was ADO1 occluder in 97% (n=136) of cases. ADO1 device sizes included: 5/4 n=2, 6/4 n=7, 8/6 n=50, 10/8 n=52, 12/10 n=25. Other devices used included an AmplatzerTM Muscular VSD device in 3 patients (6mm, 10mm, 18mm), an AmplatzerTM Septal Occluder (ASO) device in 1 (13mm) and an AmplatzerTM Vascular Plug 4 (6mm device) in 1. The Muscular VSD and ASO devices were used in patients with significant pulmonary hypertension and large ducts, where a double disc device was felt to be preferable. Mean fluoroscopy time was 14.3±8.8 minutes (range 4-50). The device was successfully deployed in 100% of patients. Trivial flow was present on aortography after device deployment in 35% of patients. Residual shunting was graded as small (ie. ‘smoke’ or jet <2mm diameter) in all with residual flow. Technical success (stable device and none-trivial residual shunt either 8
angiographically during the case or on echocardiography after the procedure) was achieved in 99% of patients. No major procedural complications were observed (no deaths, no device embolization, no perforation or tamponade, no thrombotic event, no encroachment on aorta or branch pulmonary artery). A minor vascular access complication occurred in one patient who developed a groin hematoma.
Follow-up Clinical follow-up was available in 90% of patients at a mean of 7 months after the procedure (median = 2 months, range 1-144 months) and an echocardiogram available in 61% (n=70) of patients at median of 3 months after the procedure. There was a residual leak in two patients (a small leak across an 11mm window-like PDA closed with a 13mm ASO and a small leak across an ADO1 10/8mm device). There were no cases of endocarditis nor embolization. In the 61% of patients who had a follow up echocardiogram in the first year, there was evidence of LV remodeling with mean LVEDDi 27.5±4.7mm/m2 (LVEDDi 30.3±4.3 pre-procedure, p<0.001) and mean LVESDi 18.3±3.2mm/m2 (LVESDi 19.9±3.6 pre-procedure, p=0.0008). In those with LV dysfunction (n=14), LV function improved to normal in all except one patient. In those patients with pulmonary hypertension present at catheterization pre-closure, the majority had normal pulmonary pressures at follow-up (RVSP was >50mmHg in two patients only).
Discussion
9
In this study, we evaluated the procedural and short-term outcomes of a cohort of adults to have undergone percutaneous PDA closure. The main finding of this singlecentre study is that device PDA closure in adults is a highly effective and very safe procedure. The majority of evidence for PDA device occlusion relates to the paediatric population. In children, coil occlusion is usually very effective, in particular for small PDAs (<3mm diameter). Success rates are high in children (95% occlusion rate was documented at one year in 1258 patients in the European Paediatric Cardiology Registry) with a ‘suboptimal’ outcome (abandoned procedure, persistent hemolysis, residual leak requiring a further procedure, flow impairment in adjacent structures or duct recanalization) occurring in up to 10% of cases. 4 A suboptimal outcome was more likely to occur in larger ducts or tubular shaped ducts in this European registry. Our series is the largest reported series of adults with PDA closure with previous reports in adults ranging from 21 to 69 patients 12-15, 19. The range of duct morphologies and mean minimal duct diameter was similar in our study to the previous series with similar high procedural success rates documented using the AmplatzerTM Duct Occluder (ADO) device. Almost 100% PDA occlusion rate at mid and long-term follow-up has been documented in other series.12, 13, 19
Technique PDA closure in adults is technically feasible and successful in most cases. Imaging of the duct is usually achieved by aortogram at the time of closure, which can be suboptimal in larger ducts or short ducts (eg type B); in these cases, balloon sizing (eg AmplatzerTM sizing balloon) may be useful and also provide information regarding distensibility. A high cineangiographic frame rate may be required to capture the
10
balloon waist if stability of the inflated balloon is an issue. CT aortography before the procedure can be of value in defining the size and characteristics of the duct, and excluding other causes of continuous murmurs including coronary fistula, aortopulmonary collaterals, and anomalous connections between the internal mammary arteries and the lung circulation due to TB or other pulmonary disease. The main challenge of the procedure in adults is crossing the duct with a wire. This can be achieved from the venous aspect in most cases (85% in our series) using a Gensini diagnostic catheter and a straight wire. Otherwise, retrograde crossing from the aorta is usually straight-forward using a JL4 diagnostic catheter; snaring of an exchange length angled GlidewireTM (Terumo Medical, Japan) with an EN SnareTM (Merit Medical, UT, USA) or an AmplatzTM Gooseneck snare (Medtronic, MN, USA) in the branch pulmonary artery allows externalization of the wire and subsequent delivery of a multipurpose catheter from the venous side across the duct to the aorta. Once a multipurpose catheter is positioned across the duct, an AmplatzTM extra-stiff exchange length wire is delivered to the aorta over which the appropriate sized Amplatzer delivery sheath can be delivered (usually 6 or 7 French). Hypotension at this stage of the procedure may relate to severe tricuspid insufficiency due to valve splinting by a stiff wire and sheath (usually resolves once the delivery equipment is withdrawn). The selected device is then deployed in the duct; the anterior border of the trachea in the lateral projection represents a good anatomic landmark to mark the aortic aspect of the duct and guide device deployment. The most commonly used device in adults is the AmplatzerTM ADO1 occluder. It is a versatile device that can be used in all duct morphologies 12, 13, as evidenced in this study where the device was used for 97% of cases. The commonest device sizes employed are 8/6mm and 10/8mm; it can be used to treat ducts up to 12mm in
11
diameter (using the 16/14mm device). It is suggested that the device waist diameter (at aorta) should be > 2mm larger than the minimum duct diameter; we would recommend assuming that the true ductal diameter is usually larger than the angiographic measurement (ductal spasm may contribute for example), thus one should select the next size up from that which would be selected based on minimum duct diameter plus 2mm (Figure 2). The Occlutech OccluderTM (Occlutech, Germany) was recently introduced with some potential advantages including: wider core at pulmonary aspect and longer lengths for better stability; prominent screw attachment at pulmonary end to facilitate easy snaring if need be and absence of distal clamp at aortic end. It is available up to 24/18mm (diameter) and 16mm length. The CeraTM occluder device (Lifetech Scientific, Shenzen, China) is also useful for larger ducts (available up to 26/24mm)19. The use of AmplatzerTM Muscular VSD devices is also described for larger ducts (Figure 3), in particular in the setting of pulmonary hypertension, where the double disc design can prevent embolization20, 21. These devices are symmetrical and can also be delivered from the aortic side, which has been associated with shorter procedure times and lower radiation exposure22. Other devices available include the ADO2 device (can treat ducts <5.5mm diameter) and vascular plugs (such as AmplatzerTM vascular plugs 2 and 4, which some have advocated as being suitable for long, tubular ducts, in particular ductal types C, D, or E) 23; the role of these devices in adults is likely in smaller ducts that may be difficult to cross antegrade from the pulmonary artery as they can easily be delivered in a retrograde fashion from the aorta.
Complications
12
Complications of device closure in adults were rare in this study and others 12, 13, 15, 19, 24
. Obstruction of the aorta or branch pulmonary arteries is rarely an issue in adults. A
residual leak is uncommon but can be seen in irregular and calcified ducts where there may not be adequate conformation of device. Haemolysis can occur due to residual leak in very large ducts, but usually settles with time5. Transient left ventricular systolic dysfunction has been reported after PDA closure, in particular with large shunts and pre-existing LV dysfunction or pulmonary hypertension; this may relate to preload reduction with a sudden afterload increase25, 26, but rarely translates into pulmonary oedema post closure and pre-procedure diuretic use is rarely required. Device embolization is very uncommon in adults, likely relating to the ability to generously oversize devices without fear of obstruction of the LPA or aorta. A chest x-ray and transthoracic echocardiogram are performed after the procedure to ensure stable device position and document any residual shunting. Patients with no residual shunt, normal LV size and function with normal pulmonary pressures do not warrant follow-up beyond 6 months. Otherwise, review 1 to 3 yearly is reasonable. Persistent LV systolic dysfunction was reported in approximately 10% of patients in a study of 45 adults to undergo PDA closure in a South Korean study by Jeong et al. 27 In that study, pre-closure LVEF was the best index to predict late LVEF after closure.
Indications for closure Indications for PDA closure are largely similar in adults and children. Closure is indicated in all patients with evidence of LV volume overload (LV dilation ± dysfunction) and in those with pulmonary hypertension (without evidence for Eisenmenger physiology). Expert opinion is largely in favor of device closure of small PDAs that are audible (continuous murmur) without evidence of a
13
haemodynamically significant shunt (ie normal LV size and normal pulmonary pressures) to avoid PDA-related complications, such as endarteritis (10% lifetime risk) and pulmonary hypertension. In adults, duct closure is reasonable in the presence of a systolic murmur only if there exists any LV enlargement or elevation of pulmonary pressures. A ‘clinically silent’ small duct is likely best managed conservatively, however, a small risk of endarteritis remains. One issue that requires consideration on occasion is what severity of pulmonary hypertension represents a contra-indication to closure. In general, closure is safe as long as there is a residual left-to-right shunt and no features of Eisenmenger physiology. Zabal et al. studied 168 selected patients (mean age 10±14 years) with a PDA and elevated systolic pressure (>50mmHg, mean PASP 64±16mmHg, mean PVR 3.7±2.1 Wood units); device closure using AmplatzerTM devices (ADO1 86%, muscular VSD device 11%, ASO device 2%) was safe with an immediate drop in pulmonary artery pressures, which continued to decline over time (PASP 30±8mmHg at median of 30 months post closure).28 Zhang et al. reported findings after test occlusion of the PDA in 137 patients with severe pulmonary hypertension. They described an approach of observing haemodynamics post device deployment but before release (rather than test occlusion using a balloon); an invasively derived ratio of PA systolic pressure to aortic systolic pressure of greater than 0.5 after trial occlusion (using the device) reliably predicted the presence of late pulmonary hypertension.29
Limitations
14
This was a retrospective study where information was mostly extracted from paper and electronic medical records. The follow-up duration was relatively short and echocardiographic assessment at follow-up incomplete.
Conclusion Transcatheter PDA closure using the AmplatzerTM Duct Occluder is very effective in adults across all duct morphologies and associated with a very low complication rate.
15
Disclosures
Eric Horlick is a consultant for Abbott Structural Heart Disease and is supported by the Peter Munk Chair in Structural Heart Disease Intervention. Mark D. Osten is a consultant for Abbott Structural Heart. The Peter Munk Cardiac Centre receives unrestricted research and educational grants from Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
16
References
1. Hammerman C. Patent ductus arteriosus. Clinical relevance of prostaglandins and prostaglandin inhibitors in PDA pathophysiology and treatment. Clin Perinatol. 1995;22:457-79. 2. Stout KK, Daniels CJ, Aboulhosn JA, Bozkurt B, Broberg CS, Colman JM, Crumb SR, Dearani JA, Fuller S, Gurvitz M, Khairy P, Landzberg MJ, Saidi A, Valente AM and Van Hare GF. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology. 2019;73:1494-1563. 3. Porstmann W, Wierny L and Warnke H. [The closure of the patent ductus arteriosus without thoractomy. (preliminary report)]. Thoraxchir Vask Chir. 1967;15:199-203. 4. Magee AG, Huggon IC, Seed PT, Qureshi SA, Tynan M and Association for European C. Transcatheter coil occlusion of the arterial duct; results of the European Registry. European heart journal. 2001;22:1817-21. 5. Pass RH, Hijazi Z, Hsu DT, Lewis V and Hellenbrand WE. Multicenter USA Amplatzer patent ductus arteriosus occlusion device trial: initial and one-year results. Journal of the American College of Cardiology. 2004;44:513-9. 6. Faella HJ and Hijazi ZM. Closure of the patent ductus arteriosus with the amplatzer PDA device: immediate results of the international clinical trial. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2000;51:50-4. 7. Tometzki AJ, Arnold R, Peart I, Sreeram N, Abdulhamed JM, Godman MJ, Patel RG, Kitchiner DJ, Bu'Lock FA and Walsh KP. Transcatheter occlusion of the patent ductus arteriosus with Cook detachable coils. Heart. 1996;76:531-5. 8. Jang GY, Son CS, Lee JW, Lee JY and Kim SJ. Complications after transcatheter closure of patent ductus arteriosus. Journal of Korean medical science. 2007;22:484-90. 9. Wang JK, Wu MH, Lin MT, Chiu SN, Chen CA and Chiu HH. Transcatheter closure of moderate-to-large patent ductus arteriosus in infants using Amplatzer duct occluder. Circulation journal : official journal of the Japanese Circulation Society. 2010;74:361-4. 10. Ghasemi A, Pandya S, Reddy SV, Turner DR, Du W, Navabi MA, Mirzaaghayan MR, Kiani A, Sloan K and Forbes TJ. Trans-catheter closure of patent ductus arteriosus-What is the best device? Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2010;76:687-95. 11. Brunetti MA, Ringel R, Owada C, Coulson J, Jennings JM, Hoyer MH and Everett AD. Percutaneous closure of patent ductus arteriosus: a multiinstitutional registry comparing multiple devices. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2010;76:696-702.
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12. Hong TE, Hellenbrand WE, Hijazi ZM and Amplatzer I. Transcatheter closure of patent ductus arteriosus in adults using the Amplatzer duct occluder: initial results and follow-up. Indian Heart J. 2002;54:384-9. 13. Behjati-Ardakani M, Rafiei M, Behjati-Ardakani MA, Vafaeenasab M and Sarebanhassanabadi M. Long-term Results of Transcatheter Closure of Patent Ductus Arteriosus in Adolescents and Adults with Amplatzer Duct Occluder. N Am J Med Sci. 2015;7:208-11. 14. Bonhoeffer P, Borghi A, Onorato E and Carminati M. Transfemoral closure of patent ductus arteriosus in adult patients. Int J Cardiol. 1993;39:181-6. 15. Bentham JR, Thomson JD and Gibbs JL. Transcatheter closure of persistent ductus arteriosus in adults. J Interv Cardiol. 2012;25:501-4. 16. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, del Nido P, Fasules JW, Graham TP, Jr., Hijazi ZM, Hunt SA, King ME, Landzberg MJ, Miner PD, Radford MJ, Walsh EP, Webb GD, Smith SC, Jr., Jacobs AK, Adams CD, Anderson JL, Antman EM, Buller CE, Creager MA, Ettinger SM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Page RL, Riegel B, Tarkington LG, Yancy CW, American College of C, American Heart Association Task Force on Practice G, American Society of E, Heart Rhythm S, International Society for Adult Congenital Heart D, Society for Cardiovascular A, Interventions and Society of Thoracic S. 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. Journal of the American College of Cardiology. 2008;52:e143-263. 17. Silversides CK, Salehian O, Oechslin E, Schwerzmann M, Vonder Muhll I, Khairy P, Horlick E, Landzberg M, Meijboom F, Warnes C and Therrien J. Canadian Cardiovascular Society 2009 Consensus Conference on the management of adults with congenital heart disease: complex congenital cardiac lesions. Can J Cardiol. 2010;26:e98-117. 18. Krichenko A, Benson LN, Burrows P, Moes CA, McLaughlin P and Freedom RM. Angiographic classification of the isolated, persistently patent ductus arteriosus and implications for percutaneous catheter occlusion. Am J Cardiol. 1989;63:877-80. 19. P S, Jose J and George OK. Contemporary outcomes of percutaneous closure of patent ductus arteriosus in adolescents and adults. Indian Heart J. 2018;70:308-315. 20. Fernando R, Koranne K, Loyalka P, Kar B and Gregoric I. Patent ductus arteriosus closure using an Amplatzer() ventricular septal defect closure device. Experimental and clinical cardiology. 2013;18:e50-4. 21. Eicken A, Balling G, Gildein HP, Genz T, Kaemmerer H and Hess J. Transcatheter closure of a non-restrictive patent ductus arteriosus with an Amplatzer muscular ventricular septal defect occluder. Int J Cardiol. 2007;117:e40-2. 22. Liddy S, Oslizlok P and Walsh KP. Comparison of the results of transcatheter closure of patent ductus arteriosus with newer Amplatzer devices. 18
Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2013;82:253-9. 23. Gillespie MJ, Golden A, Sivarajan VB and Rome JJ. Transcatheter closure of patent ductus venosus with the Amplatzer vascular plug in twin brothers. Pediatric cardiology. 2006;27:142-5. 24. Al-Hamash SM, Wahab HA, Khalid ZH and Nasser IV. Transcatheter closure of patent ductus arteriosus using ado device: retrospective study of 149 patients. Heart Views. 2012;13:1-6. 25. Galal MO, Arfi MA, Nicole S, Payot M, Hussain A and Qureshi S. Left ventricular systolic dysfunction after transcatheter closure of a large patent ductus arteriosus. J Coll Physicians Surg Pak. 2005;15:723-5. 26. Tilahun B and Tefera E. Transient left ventricular systolic dysfunction following surgical closure of large patent ductus arteriosus among children and adolescents operated at the cardiac centre, Ethiopia. J Cardiothorac Surg. 2013;8:139. 27. Jeong YH, Yun TJ, Song JM, Park JJ, Seo DM, Koh JK, Lee SW, Kim MJ, Kang DH and Song JK. Left ventricular remodeling and change of systolic function after closure of patent ductus arteriosus in adults: device and surgical closure. Am Heart J. 2007;154:436-40. 28. Zabal C, Garcia-Montes JA, Buendia-Hernandez A, Calderon-Colmenero J, Patino-Bahena E, Juanico-Enriquez A and Attie F. Percutaneous closure of hypertensive ductus arteriosus. Heart. 2010;96:625-9. 29. Zhang DZ, Zhu XY, Lv B, Cui CS, Han XM, Sheng XT, Wang QG and Zhang P. Trial occlusion to assess the risk of persistent pulmonary arterial hypertension after closure of a large patent ductus arteriosus in adolescents and adults with elevated pulmonary artery pressure. Circ Cardiovasc Interv. 2014;7:473-81.
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Tables Table 1. Patient characteristics Table 2. Imaging parameters
Figures Figure 1. Krichenko classification
Figure 2. Case – 24 year old with shortness of breath and a continuous murmur. LV dilatation is evident on echocardiography with a PDA. a. Aortogram demonstrates a type A PDA with a minimum diameter of ~6mm (Black arrow). White arrow indicates anterior border of trachea, which serves as a marker for the aortic aspect of the PDA (in the lateral projection) b. Successful Device closure was performed using a 12/10 ADO1 device deployed from the pulmonary artery (minimum diameter + 2mm is 8mm, therefore one size larger is selected). Compression of device waist evident.
Figure 3. 42 year old female with dyspnea and a large PDA with associated LV dilatation, moderate pulmonary hypertension a. CT aortogram demonstrating type B ‘window-like’ duct (8 x 10mm) b. Successful device closure using a 10mm muscular VSD device deployed from the pulmonary artery. Minor residual leak post deployment with haemolysis thereafter, which settled over the following weeks.
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Table 1. Patient baseline characteristics Characteristic Age (years), mean ±SD Male, n (%) BMI (kg/m2), mean ±SD Down syndrome, mean (%) Co-morbidities, n (%) Atrial fibrillation Hypertension Pacemaker Coronary fistula Diabetes Stroke Other congenital heart conditions ASD VSD AS (moderate) Previous cardiac surgery (VSD)
n = 141 42.8 ± 15.4 34 (24) 25.2 ± 5.2 3 (2) 6 (4) 6 (4) 2 (1) 2 (1) 3 (2) 2 (1) 2 (1) 3 (2) 1 (1) 2 (1)
Prior endocarditis 1 AS = aortic stenosis; ASD = atrial septal defect; BMI = body mass index; VSD = ventricular septal defect
Characteristic Age (years), median (range) Male, n (%) BMI (kg/m2), median (range) Down syndrome, mean (%) Co-morbidities, n (%) Atrial fibrillation Hypertension Pacemaker Coronary fistula Diabetes Stroke Other congenital heart conditions ASD VSD AS (moderate)
n = 141 41 (18-82) 34 (24) 24 (15-49) 3 (2) 6 (4) 6 (4) 2 (1) 2 (1) 3 (2) 2 (1) 2 (1) 3 (2) 1 (1)
Previous cardiac surgery (VSD)
2 (1)
Prior endocarditis
1
Table 2. Imaging parameters
n = 141, Median (range) Echocardiogram pre closure LVEDDi LVESDi LVEF RVSP Aortogram pre/at time of closure PDA diameter at PA (mm) PDA diameter at aorta (mm) PDA length (mm)
30 (19-44) 20 (14-34) 62 (33-74) 31(14-74) 4.0 ± 1.5mm (1-14) 7 (1.5-19) 9 (2-17)
Pulmonary hypertension Systolic PA pressure (mmHg) Mean PA pressure (mmHg)
36% 32 (18-105) 23 (13-68)
PA systolic:Aorta systolic PCWP (mmHg) Coronary disease
0.3 (0.2-0.9) 13 (6-29) Nil
LVEDDi = Left ventricular end-diastolic diameter (indexed); LVEF = left ventricular ejection fraction; LVESDi = left ventricular end-systolic diameter (indexed); LVSP = Left ventricular systolic pressure; PA = pulmonary artery; PCWP = pulmonary capillary wedge pressure; RVSP = right ventricular systolic pressure.