(Circulation. 1999;99:2608-2609.)
© 1999 American Heart Association, Inc.
Editorial |
Stenting the Ductus Arteriosus
A "Wanna-Be" Blalock-Taussig
From the Division of Pediatric Cardiology, Department of Pediatrics (C.E.R.), and the Division Pediatric Cardiac Surgery, Department of Surgery (L.E.B.), Loma Linda University Children's Hospital and Medical Center, Chicago, Ill.
Correspondence to Carlos E. Ruiz, MD, PhD, Director, Pediatric Cardiac Catheterization Laboratories, Professor of Pediatrics, RUSH University Children's Hospital and Heart Center, 1653 West Congress Parkway, Room # MU-736, Chicago, IL.60610.
In 1947, Dr Helen B. Taussig wrote of the aortopulmonary surgical shunt operation that she and Dr Alfred Blalock developed to increase pulmonary artery blood flow, "The essence of the operation is the creation of an artificial ductus arteriosus through which a mixture of arterial and venous blood is directed to the lungs."1 Who could have imagined that 50 years later, some of us would be trying to create an "artificial" Blalock-Taussig shunt through manipulation of the ductus arteriosus.
Our institution has been a pioneer in neonatal cardiac transplantation since 19852 ; hence, the opportunities to explore new ways of extending the survival of the potential recipients awaiting the right donor are many. Our productive combination of a confident pediatric cardiac surgical team with a creative pediatric interventional cardiology department, operating under a Food and Drug Administration–approved protocol, began stenting the ductus arteriosus in patients with hypoplastic left heart syndrome (HLHS) who had evidence of ductal flow restriction while the patients were awaiting heart transplantation.3 It would have been too ambitious to extend the protocol to pathologic conditions other than the medically unresponsive HLHS listed for transplantation because the surgical outcomes for aortopulmonary shunts at our and most other centers have been outstanding.4 In addition, we were uncertain about stent use in general, notwithstanding their use in the ductus arteriosus; for ductus arteriosus use, only animal experience had been reported5 6 7 and, unfortunately, no good animal models for these complex congenital heart malformations exist.
The use of stents to maintain the patency of the ductus arteriosus in neonates with ductal-dependent systemic blood flow and infants with ductal-dependent pulmonary blood flow congenital anomalies, one of the subjects of the present report in Circulation,8 is of particular interest. The authors of the present report have shown the courage and skills required of interventionists to develop the notion of a nonsurgical, artificial, Blalock-Taussig shunt.
We concur with the authors that their long-term results were suboptimal, despite initial technical success. However, we should be cautious about drawing firm conclusions before analyzing these results in context.
Stenting the ductus arteriosus in patients with duct-dependent systemic blood flow, such as those with HLHS, assumes that the patient was not responding to conventional prostaglandin E-1 therapy and that the hemodynamic problem arose from a restrictive duct, not from a restrictive atrial septal defect (ASD). Furthermore, this type of stenting implies that the center where the stent procedure is being contemplated has a successful neonatal transplant program where potential recipients must await a matching donor's heart. Patients being considered for univentricular palliation with Norwood's staged procedures do not need a ductal stent because the sooner those patients undergo surgical reconstruction, the better their outcomes. Thus, the expected duration of the implanted ductal stent before transplant should be relatively short, perhaps only a few months, thereby reducing the impact of restenosis within a correctly placed stent. We further concur with the authors that in this HLHS-type of pathologic condition, controlling pulmonary blood flow is difficult. We believe that the atrial-level left-to-right shunt plays a critical role in regulating pulmonary blood flow. Our approach has been to avoid atrial septectomies or even dilatation of the ASD unless an increased Doppler velocity of >2.5 m/sec across the defect exists. Nevertheless, manipulation of the ASD occasionally becomes essential because patients with highly restricted ASDs tend to experience a more difficult pre- and post-transplant course and higher mortality.
At our institution, we have no experience with stenting the ductus arteriosus in infants with duct-dependent pulmonary blood flow anomalies, largely because the surgical results of placing conventional systemic-pulmonary shunts are superb, even in critically ill neonates. We believe it would be an almost impossible task to win approval for this type of investigation from an Institutional Review Board in North America because of our present limited knowledge of the behavior of stents in ductal tissue. Limited animal experience9 indicates that severe neointimal proliferation occurs within 14 months of the implant. This finding agrees with those reported by Gibbs et al.8 We agree that the placement of stents in infants with ductus-dependent pulmonary blood flow anomalies is far more technically demanding than stenting in infants with ductus-dependant systemic blood flow lesions. For instance, the ductal anatomy in infants with ductus-dependent pulmonary blood flow is longer, more tortuous, and more complex than the anatomy usually seen in HLHS patients. In addition, access to the pulmonary flow–dependent ductus is usually accomplished through a peripheral arterial site, which limits the variety and size of the devices available. Also, the stents available for this application have not been designed with this particular use in mind. They are of a length and diameter designed to cover stenotic, atherosclerotic, arterial lesions and not the ductus arteriosus. Thus, it might frequently be necessary to implant multiple devices to cover all of the ductal tissue, and the diameter needed may not be the one that the stent was designed for. Therefore, we are in full agreement with the conclusion reached by Gibbs et al8 : stenting the ductus in congenital cardiac malformations to ensure adequate pulmonary blood flow should not be universally attempted using the presently available technology. That is not to say that we should abandon further efforts at developing a safe, durable, nonsurgical, artificial, Blalock-Taussig shunt.
The restenosis observed after stent implantation in the ductus arteriosus requires some comments. The ductus arteriosus is unique when compared with other vascular structures. Although the media of the great vessels is composed primarily of elastic tissue, that of the ductus arteriosus consists mostly of muscular fibers. In this unique vascular media, cylindrical layers of smooth muscle cells spiral in opposing directions, encircling the ductal channel. The intima is thicker than that in the contiguous arteries, and it consists primarily of an endothelial layer and loose connective tissue. The responsive behavior of the ductal cell layers to different stimuli is like that of no other vessel. The reactivity and anatomical closure of the ductus requires that normally quiescent luminal endothelial cells and medial smooth muscle cells migrate into the subendothelial space, forming intimal mounts that eventually coalesce and occlude the vessel. This migratory process requires the presence of multiple integrin receptors. Prenatally, both the smooth muscle cells and endothelial cells lack many of these receptors. However, both types of cells change their phenotype in the immediate postnatal period and express a full repertoire of integrins10 that trigger physiological remodeling. Thus, the vascular remodeling of the ductus differs from that observed in other arteries or veins subjected to traumatic insult. Moreover, this response to injuries may be different in ductus-dependent systemic blood flow as opposed to ductus-dependent pulmonary blood flow.
Nevertheless, the idea of stenting the ductus arteriosus to regulate pulmonary blood flow remains intriguing. It would be highly desirable if we could conquer the obstacles that face us at the present time, as reported by Gibbs et al.8 Ideally, a catheter-directed approach would provide a more natural distribution of blood flow to the pulmonary vasculature. It might avoid surgical injury to the pulmonary arteries, a complication known to increase the risk during further, more definitive surgery. Beyond this, some form of ductal stenting could adjust ductal flow to match the growing physiological requirements. This could potentially be accomplished by further manipulation of the prosthesis. We strongly support continued laboratory investigations into controlling the responses of ductal tissue to exiting stent technology and into technical alternatives to the present devices, such as covered stents. Inevitably, it will require the precious resources of human ingenuity, scientific judgment, and close collaboration with industry to achieve this goal. It would clearly be desirable to provide these young patients, most of whom are destined to have further corrective surgeries, with a safe alternative to the operative Blalock-Taussig shunt. Until then, we should refrain from the elective use of stents to maintain ductal patency whenever a surgical alternative ensures better results.
Footnotes
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
References
1. Taussig HB. Medical aspects of the surgical correction of congenital pulmonary stenosis. In: Congenital Malformations of the Heart. New York: The Commonwealth Fund; 1947:553.
2. Bailey LL, Nehlsen-Cannarella SL, Doroshow RW, Jacobson JG, Martin RD, Allard MW, Hyde MR, Dang Bui RH, Petry EL. Cardiac allotransplantation in newborns as therapy for hypoplastic left heart syndrome. N Engl J Med. 1986;315:949–951.[Medline] [Order article via Infotrieve]
3.
Ruiz CE, Gamra H, Garcia EJ, Boucek MM. Stenting of
the ductus arteriosus as a bridge to cardiac transplantation in infants
with hypoplastic left heart syndrome. N Engl J
Med. 1993;328:1605–1608.
4. Tsai KT, Chang CH, Lin PJ. Modified Blalock-Taussig shunt: statistical analysis of potential factors influencing shunt outcomes. J Cardiovasc Surg (Torino). 1996;37:149–152.[Medline] [Order article via Infotrieve]
5. Coe JY, Olley PM. A novel method to maintain ductus arteriosus patency. J Am Coll Cardiol. 1991;18:837–841.[Abstract]
6. Rosenthal E, Qureshi SA, Kakadekar AP, Tabatabaie AH, Baker EJ, Tynan M. Comparison of stent implantation with balloon dilatation for maintenance of ductus arteriosus patency. J Am Coll Cardiol. 1992;19(suppl A):25A. Abstract.
7. Houde C, Zahn EM, Benson LN, Freedom RM. Stent implantation to maintain ductus arteriosus patency in piglets. Circulation. 1992;86(suppl I):I-632. Abstract.
8.
Gibbs JL, Uzun O, Blackburn MEC, Wren C, Hamilton JRL,
Watterson KG. Fate of the stented arterial duct.
Circulation.. 1999;99:2621–2625.
9. Rosenthal E, Qureshi SA, Tabatabaie AH, Persaud D, Kakadekar AP, Baker EJ, Tynan M. Medium-term results of experimental stent implantation into the ductus arteriosus. Am Heart J. 1996;132:657–663.[Medline] [Order article via Infotrieve]
10. Clyman RI, Goetzman BW, Chen YQ, Mauray F, Kramer RH, Pytela R, Schnapp LM. Changes in endothelial cell and smooth muscle cell integrin expression during closure of the ductus arteriosus: an immunohistochemical comparison of the fetal, preterm newborn and full-term newborn rhesus monkey ductus. Pediatr Res.. 1996;40:198–208.[Medline] [Order article via Infotrieve]
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