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Stent Protrusion in Palliative Congenital Heart Disease Interventions: Does it Cause Any Harm?

Haysam Baho, MD¬π, Salem Deraz, MD2, Heba Abouzeid, MD3, Jameel Al-Ata, MD1, Amjad Kouatli, MD1

Keywords
September 2013

Abstract: Background. Protrusion of the patent ductus arteriosus (PDA) stent can occur into the lumen of the main pulmonary artery (MPA) branch, the aorta, or both. This protrusion can vary from trivial to major, causing potential obstruction to the vessel lumen, which may cause flow obstruction or risk of thromboses. As far as we know, no one has followed these patients with protruding stents to see whether they do pose a risk of obstruction or thromboses. Methods. A retrospective, descriptive, cross-sectional study reviewing charts of all included patients who received stents in the MPA branches with residual protrusion into the pulmonary artery branch lumen (total, 87 patients; 34 patients with protruding stents) was performed to determine whether this protrusion caused any undesired effects on flow or coagulation. The patients were divided into two groups: the protruding stents group (group 1); and the non-protruding stent group that served as a control group (group 2). Each group was then categorized into 3 sections according to the stent position, the PDA, the MPA branches, and the Blalock-Taussig shunt. Results. The only risk factor that had statistical significance was the number of stents in the PDA site. Conclusion. Protruding stents do not cause an increased risk of thrombosis in patients on aspirin. Mild protrusion is more likely in PDA stents and severe protrusion is more likely in the MPA branch stents. Severe protrusion is more likely when more stents are used in the PDA location. There is no statistical evidence that protrusion can cause lung perfusion defects from the small numbers we have.   

J INVASIVE CARDIOL 2013;25(9):460-463

Key words: CHD, stent, protrusion

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Bare-metal stents (BMSs) have been used in congenital heart disease (CHD) since the late 1980s with excellent results.1,2 Later, their use progressed to palliative procedures in the management of ductal-dependant CHD. Options for maintaining pulmonary flow currently include stenting the ductus arteriosus, which was first performed in 1992.3 The procedure underwent technical improvements and became a widely accepted option in managing ductal-dependant CHD.4,5 Deploying the stent at exactly the right position can be a challenging task due to the minute distances involved. Occasionally, this procedure leads to the protrusion of one or both ends of the stent into the lumen of the pulmonary artery (PA) branch, the aorta, or both. This protrusion can vary from trivial to major, causing potential obstruction to the vessel lumen, which may cause flow obstruction or risk of thromboses. As far as we know, no one has followed these patients with protruding stents to see whether they do pose a risk of obstruction or thromboses. 

Methods

Study design. A retrospective, descriptive, cross-sectional study reviewing charts of all included patients who received stents in the patent ductus arteriosus (PDA), main pulmonary artery (MPA) branches, or Blalock-Taussig (BT) shunt with residual protrusion into the MPA branch lumen. Our purpose was to study whether this protrusion caused any undesired effects on flow or coagulation by reviewing all the imaging studies and laboratory work that were done before and after the procedure and the anticoagulation/antiplatelet protocol used. The patients were divided into two groups: the protruding stents group (group 1); and the non-protruding stent group that served as a control group (group 2). Each group was then categorized into 3 sections according to the stent position, the PDA, the MPA branches, and the BT shunt.

The protrusion was classified into these 3 categories: 

1. Mild: the stent protruded slightly (Figure 1A).

2. Moderate: the stent protruded significantly, but did not block any vascular lumen (Figure 1B).

3. Severe: the stent blocked at least one vessel so that the blood flow to that vessel was entirely through the stent struts (Figures 1C and 1D).

Inclusion criteria. All patients who had a stent placed in the PDA, any of the PA branches, or BT shunt and were determined to have part of this stent “protruding” into either one of the MPA branches or the aorta during stent placement or by following imaging were included.

Primary endpoints. The primary study endpoints were: (1) The presence of any thrombus in any of the PA branches or the aorta. Initial diagnosis was done by angiography after insertion of the stent. Follow-up studies included echocardiography and, if there was any suspicion, cardiac computed tomography with or without diagnostic cardiac catheterization was done. All cases of PDA or BT shunt stents underwent diagnostic cardiac catheterization before the definitive surgery (Glenn surgery or biventricular repair). (2) The presence of any obstruction to flow in any PA branches or the aorta. 

The following patient data were gathered: biographical information; diagnosis; vital signs; indication; stent size; cardiac catheterization complications; poststent anticoagulation; degree of stent protrusion; the presence of any obstruction to flow based on the poststent angiograms and/or the follow-up echocardiograms or perfusion scans that were done if there was any suspicion of abnormal growth of MPA branches by echocardiography; and the presence of any thrombus. All patients had routine follow-up echocardiograms done as outpatient or inpatient. All angiogram reports performed during the stent placement were reviewed for any obstruction or thrombosis that the stents had caused. All scintigram reports were reviewed, and the percentage of perfusion to each lung was determined.

Results

From 2002 to 2011, a total of 117 BMSs were placed in 87 patients in the PDA, MPA branch, or BT shunt positions. Due to the small number of protruding stents in the BT position (n = 3), they were not included in the statistical analysis. 

The mean age ranged from 1.05-37 months in group 1, and from 17.68-19 months in group 2. The P-values were .15, .20, and .60 when comparing the stents in the PDA (Figures 2 and 3), MPA branches, and BT shunts, respectively (Figure 4). The mean weight was between 2.3-3.2 kg in group 1, while it was between 5.1-12.4 kg in group 2. The P-values were .09 and .44 when comparing the stents in the PDA and MPA branches. The BT shunts were not included because of the small number. The mean follow-up period was 54 ± 26 months for group 1 and 52 ± 24 months for group 2. The P-values were .40, .48, and .28, respectively. The number of stents ranged from 1.47-1.6 stents in group 1 and 1.16-1.5 stents in group 2. The P-values were .001, .68, and .31, respectively (Table 1). All patients had echocardiograms initially and on follow-up exam. Twelve patients from group 1 had lung nuclear perfusion scan because follow-up echocardiography showed suspicion of abnormal MPA branch growth (Table 4). All patients received anticoagulation in the acute stage, consisting of heparin that was discontinued on discharge and replaced with aspirin for the follow-up.

The total study population included 87 patients. Group 1 included 34 patients, comprised of 17 patients with protruding stent in the PDA, 14 patients with protruding stent in the MPA branches, and only 3 patients with stent protruding in the BT shunt. Group 2 included 53 patients, comprising 19 patients with non-protruding stent in the PDA, 28 patients with stents placed in the PA branches, and 6 patients with stents placed in the BT shunt (Table 2).  There were no thromboses associated with any of the protruding stents based on the imaging studies done. Out of the 34 protruding stents, the degree of protrusion was mild in 20 cases, moderate in 4 cases, and severe in 10 cases. Mild protrusion was more common with the PDA group, whereas severe protrusion was more common in the PA branch group (P<.05) (Table 3). The results of perfusion scans done in 12 out of 34 patients with protruding stents are shown in Table 4. Perfusion scan was done if there was any suspicion of abnormal growth in one the PA branches by echocardiography.

There was no difference in the PA branch growth between both groups based on echocardiogram and perfusion scans, which were done in patient who had any suspicion in echocardiography for abnormal growth of the MPA branches. Comparing, age, weight, and the number of stents used among all sections in every group, the only risk factor that had statistical significance was the number of stents in the PDA site. Using the criteria by Spadone et al6 (35/65%), who had the largest series of scintigrams in patients with pulmonary branch stents, the pulmonary perfusion scans did not conclusively support an adverse effect caused by the protruding stents.

Discussion

Patent ductus arteriosus is a congenital heart abnormality defined as persistent patency in term infants >3 months old. Isolated PDA is found in around 1/2000 full-term infants. A higher prevalence is found in preterm infants, especially those with low birth weight. The female to male ratio is 2:1.7

Stenting of PDA as first-stage palliation in PDA-dependent pulmonary circulation has been advocated as safe and effective procedure in neonates and as an alternative to surgical shunts.8,9

Ductal stenting in neonates with either duct-dependent pulmonary or systemic circulation has become a good alternative for the initial palliation of complex CHD. Changes in stent and catheter technology (eg, low-profile, flexible, premounted stents with good scaffolding), better patient selection and preparation, optimal interventional access, and covering the complete length of the duct have significantly improved results.10

Stent implantation into the arterial duct has been proposed as a non-surgical alternative to aortopulmonary shunt surgery. It offers the potential advantage of eliminating the need for palliative surgery, thus reducing the number of operations required, and optimizing the time of definitive surgical correction.11-14

When choosing a stent, important features are stent length, diameter, and design. The most distal parts of the duct appear to have a remarkable ability to constrict, even when only a few millimeters are left unsupported.15-18

The length of the duct, number of stents required for complete coverage, and technical and procedural complications are significantly related to the orientation of the arterial duct.19

As described by Boucek et al, the majority of the ducts take a leftward orientation (type 1, 65%) with an average length of 17.4 mm. The second most common ductal anatomy is a direct front-to-back orientation (type 2, 27.5%). These ducts are shorter, averaging 15.3 mm. The ducts that take a rightward course are uncommon (type 3, 7.5%) and are short (mean length, 10.9 mm).19

Therefore, great care must be taken to cover the duct completely from the aortic end until well within the pulmonary trunk, without covering the orifice of the PAs. Ideally, the complete duct should be covered by a single stent. In cases of incomplete stenting, an additional stent should be implanted to cover the entire duct. The chosen stent length is thus slightly longer than the length of the duct.5

Conclusion

Protruding stents do not cause an increased risk of thrombosis in patients on aspirin. Mild protrusion is more likely in PDA stents and severe protrusion is more likely in MPA branch stents. Severe protrusion is more likely when more stents are used in the PDA location. There is no statistical evidence that protrusion can cause lung perfusion defects from the small numbers we have. A prospective study with a large number of patients is needed.

References

  1. Latson LA. Pulmonary artery stents — on target, but still ‘‘off label.” Catheter Cardiovasc Interv. 2010;75(5):765-766. 
  2. Shaffer KM, Mullins CE, Grifka RG, et al. Intravascular stents in congenital heart disease: short- and long-term results from a large single-center experience. J Am Coll Cardiol. 1998;31(3):661-667.
  3. Gibbs JL, Rothman MT, Rees MR, Parsons JM, Blackburn ME, Ruiz CE. Stenting of the arterial duct: a new approach to palliation for pulmonary atresia. Br Heart J. 1992;67(3):240-245. 
  4. Schneider M, Zartner P, Sidiropoulos A, Konertz W, Hausdorf G. Stent implantation of the arterial duct in newborns with duct-dependent circulation. Eur Heart J. 1998;19(9):1401-1409. 
  5. Gewillig M, Boshoff DE, Dens J, Mertens L, Benson LN. Stenting the neonatal arterial duct in duct-dependent pulmonary circulation: new techniques, better results. J Am Coll Cardiol. 2004;43(1):107-112.
  6. Spadoni I, Giusti S, Bertolaccini P, Maneschi A, Kraft G, Carminati M. Long-term follow-up of stents implanted to relieve peropheral pulmonary arterial stenosis. Card Young. 1999;9(6):585-591.
  7. Forsey JT, Elmasry OA, Martin RP. Patent arterial duct. Orphanet J Rare Dis. 2009;4:17.
  8. Alwi M, Choo KK, Latiff HA, Kandavello G, Samion H, Mulyadi MD. Initial results and medium-term follow-up of stent implantation of patent ductus arteriosus in duct-dependent pulmonary circulation. J Am Coll Cardiol. 2004;44(2):438-445. 
  9. Mahesh K, Kannan BR, Vaidyanathan B, Kamath P, Anil SR, Kumar RK. Stenting the patent arterial duct to increase pulmonary blood flow. Indian Heart J. 2005;57(6):704-708.
  10. Boshoff DE, Michel-Behnke I, Schranz D, Gewillig M. Stenting the neonatal arterial duct. Expert Rev Cardiovasc Ther. 2007;5(5):893-901.
  11. Coe J, Olley P. A novel method to maintain ductus arteriosus patency. J Am Coll Cardiol. 1991;18(3):837-841.  
  12. Rosenthal E, Qureshi S, Kakadekar A, et al. Comparison of balloon dilatation and stent implantation to maintain patency of the neonatal duct in lambs. Am J Cardiol. 1993;71(15):1373-1376. 
  13. Rosenthal E, Qureshi S, Tynan M. Percutaneous pulmonary valvotomy and arterial duct stenting in neonates with right ventricular hypoplasia. Am J Cardiol. 1994;74(3):304-306.
  14. Gibbs J, Rothman M, Rees M, Parsons J, Blackburn M, Ruiz C. Stenting of the arterial duct: a new approach to palliation for pulmonary atresia. Br Heart J. 1992;67(3):240-245.
  15. Schneider M, Zartner P, Sidiropoulos A, Konertz W, Hausdorf G. Stent implantation of the arterial duct in newborns with duct-dependent circulation. Eur Heart J.1998;19(9):1401-1409. 
  16. Abrams SE, Walsh KP. Arterial duct morphology with reference to angioplasty and stenting. Int J Cardiol.1993;40(1):27-33.
  17. Elzenga NJ, Gittenberger-de Groot AC. The ductus arteriosus and stenoses of the pulmonary arteries in pulmonary atresia. Int J Cardiol.1986;11(2):195-208. 
  18. Rosenthal E, Qureshi SA. Editorial: stent implantation in congenital heart disease. Br Heart J. 1992;67(3):211-212.
  19. Boucek MM, Mashburn C, Kunz E, Chan KC. Ductal anatomy. A determinant of successful stenting in hypoplastic left heart syndrome. Pediatr Cardiol. 2005;26(2):200-205. 

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From the 1Cardiovascular Department, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia, 2Department of Pediatrics, Menoufia University, Shebin El-Koum, Egypt, and ³Department of Pediatrics, Zagazig University, Zagazig, Egypt.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted March 21, 2013, provisional acceptance given April 26, 2013, final version accepted May 24, 2013.

Address for correspondence: Salem Deraz, MD, Department of Pediatrics, Faculty of Medicine, Menoufia University, Shebin El Koum, Egypt; or King Faisal Specialist Hospital – Jeddah – Saudi Arabia, Pediatric Cardiology Section, PO Box 40047, Jeddah 21499, MBC J 39. Email: drsderaz@hotmail.com.


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