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Technology Update

Indian Pediatrics 1999;36: 999-1010

Interventional Pediatric Cardiology

Shyam S. Kothari

From the Cardiothoracic Center, All India Institute of Medical Sciences, New Delhi 110 029, India.
Reprint requests: Dr. Shyam S. Kothari, Cardiothoracic Center, All India Institute of Medical Sciences, New Delhi 110 029, India.

Interventional pediatric cardiology has grown remarkably over the last two decades(1). Catheter based interventional procedures have become the treatment of choice for many cardiac lesions, and these serve as alternatives or as adjuncts to surgical treatment for many other conditions. This treatment modality is available and seems to be growing in India as well. This article briefly overviews the utility and limitations of common interventional cardiac procedures (Table I) for the pediatrician.

Table I__Common Interventional Procedures.







Lesions for which the Interventional therapy is the treatment of choice:

Balloon atrial septostomy*
Valvular pulmonic stenosis
Valvular aortic stenosis
Rheumatic mitral stenosis
Recoarctation of aorta
Pulmonary arterial stenosis
Takayasu's aortoarteritis with narrowing of aorta
Small patent ductus arteriosus
Aortopulmonary collateral embolization
Arteriovenous fistulae (coronary, pulmonary)




Lesions for which interventional therapy is equally efficacious to surgical treatment 

Small to moderate size ASD (selected cases)
Moderate - to large PDA
Native coarctation of aorta beyond early infancy.
* Balloon atrial septostomy is well established procedure and is not discussed in this article.

In general, if the efficacy and safety of an interventional procedure equals the contempo-rary surgical results, the interventional therapy is preferred as it avoids a scar and the psychological trauma of an operation, is associated with shorter hospital stay, a decrease in blood transfusion requirements and other morbidity associated with surgery, and overall reduction in the cost as well.

Valvular Stenosis

An appropriately sized non-compliant balloon, if positioned and inflated across a stenosed valve, exerts circumferential stress leading to tearing of the fused commissures (Fig. 1). Kan et al. in 1982 performed the first successful pulmonary ballon valvotomy(2) and since then the procedure has been widely used to treat any of the stenosed cardiac valves. Improvements in balloon technolgy have made it possible to treat infants and small children safely. In general, significant isolated stenosis of a valve (in the absence of associated regurgitation) is amenable to balloon dilatation. Elective dilatation is not done during an active infection in the body.

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Fig. 1. Pulmonary valvuloplasty. Fig. 1a. Right ventricular angiogram shows pulmonary valve stenosis Fig. 1b. A guide wire is placed across the valve with the help of catheter Fig. 1c. A balloon is threaded on the wire and inflated at appropriate position which opens the stenosed valve.

Valvular Pulmonic Stenosis

Moderate to severe pulmonic stenosis (PS), i.e., Doppler gradients 50 mmHg across the pulmonary valve is an indication for pulmonary valve balloon dilatation (PVBD)(3). Patients commonly are asymptomatic, but may present with severe right sided failure even in infancy. Patients with infundibular stenosis are not candidates for PVBD. Similarly, PVBD is not attempted in patients having coexisting lesions requiring surgical treatment, e.g., large atrial or ventricular septal defects. The pulmonary annulus is measured on echocardiography or on right ventricular angiogram. A balloon 1.2-1.4 times larger than the pulmonary annulus is used to dilate pulmonary valve. The procedure is successful in the vast majority, and result in gradients less than 30 mmHg(4). Complications occur in less than 1% and are inversely related to the age of the patients. Improvement in right ventricular function is the rule and the right ventricular hypertrophy regresses. The procedure results in pulmonic regurgitation that is usually mild, and is well tolerated. Critical PS in infants is more difficult to manage(5). Some of these cases have associated tricuspid valve and right ventricular hypoplasia. The PVBD may be unsuccesful in up to 10% of infants due to inability to cross the pulmonary valve, and complications like death, tamponade, perforations may occur (10%) in these cases. Surgical valvotomy in these cases also carries high risks. With improved skills and availability of the necessary hardwares, majority of infants with critical PS and right ventricular failure can be salvaged by PVBD(5). The relief is long lasting and restenosis does not occur(6). In some cases residual obstruction of more than 30 mmHg may remain. Dysplastic pulmonary valves in patients with Noonan's syndrome also respond less well to balloon dilatation, but PVBD is usually tried with large balloons initially(4). Patients in whom pulmonary valve annulus is very small, or PVBD has not been successful are treated surgically.

Aortic Stenosis

Symptoms of exertional breathlessness, angina, syncope or congestive heart failure in a child indicates severe aortic stenosis (AS) and the need for aortic valve balloon dilatation (AVBD). An aortic valve gradient of more than 50 mmHg on Doppler echocardiography even in the absence of symptoms merits AVBD(7). In an infant with AS and heart failure, AVBD is done irrespective of gradients. Some infants with severe AS and very low cardiac output have very little forward flow and low gradients (e.g., 10-20 mmHg), and these infants may be misdiagnosed as having dilated cardiomyopathy unless AS is appreciated on 2-D echo.

Successful AVBD results in decrease in aortic gradients (Fig. 2) and improvement in left ventricular function and decrease in ventricular hypertrophy. Complications may include death, aortic regurgitation, femoral artery thrombosis, life threatening arrhythmias, blood loss and damage to other cardiac structures. Mild aortic regurgitation is common but severe aortic regurgitation may occur (<5%)(8). Severe regurgitation following AVBD occurs more often in patients with an unicuspid aortic valve as compared to those with a bicuspid aortic valve. Femoral artery thrombosis is now uncommon, and is treatable with intravenous thrombolytic therapy with streptokinase(9). Presence of left ventricular dysfunction, endocardial fibroelastosis, very small left ventricle size and small aortic annulus are other risk factors for mortality during the procedure(10). The procedure carries higher risks than PVBD, and in contrast to PVBD, it is a palliative procedure as restenosis does develop with time. Surgical valvotomy has similar or higher mortality, higher incidence of aortic regurgitation, and high reoperation rates(10). Thus AVBD appears a preferrable first line therapy for infants and children with AS(11) although randomized comparable data are not available. In our experience, ABVD in infants has been very safe and effective procedure(12).

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Fig 2.
Left ventricular and aortic pressure tracings before (left), and after (right), aortic valvuloplasty.Note marked reduction in the gardient across the aortic  valva.

Mitral Stenosis

Rheumatic mitral stenosis in India often presents with severe pulmonary hypertension and heart failure during childhood. Balloon dilatation of mitral valve is very effective in mitral stenosis and has replaced closed mitral valvotomy(13). Severe mitral stenosis, (mitral valve area <1.0 cm2), and significant symptoms of breathlessness (Class III/IV) are indications for dilatation. Presence of left atrial thrombus, more than mild mitral regurgitation, and  calcification of the valve are contraindications for the procedure. The valve morphology is a determinant of success and suboptimal results are expected in patients with severe subvalvar fibrosis and deformity. Cardiac tamponade (during transseptal puncture to reach left atrium from right atrium), and severe mitral regurgita-tion requiring emergency valve replacement occur in less than 1% and 5%, respectively(13). Excellent results are obtained even in young children with rheumatic mitral stenosis with balloon dilatation(14). The benefits of valve dilatation are maintained in the intermediate term, and nearly 10% patients restenose over 3 years(15).

Congenital mitral stenosis results from various pathoanatomic subsets in which commissural fusion is not a dominant mecha-nism of stenosis. The balloon dilatation of congenital mitral stenosis has not been amply successful but the surgical results are also poor in these patients. Triscupid stenosis is rare and usually coexist with rheumatic mitral stenosis. Significant tricuspid stenosis can be dilated with a larger sized balloon than that used for mitral valve(16).

Long term infective endocarditis prophy-laxis is required after balloon dilatation in all patients as usual, since balloon dilatation does not result in normal valves. Similarly, secondary prophylaxis for rheumatic fever is continued as usual.

Coarctation of aorta (CoA)

Surgical treatment of CoA is effective, but is associated with recurrence of coarctation especially in infants, and rarely with complica-tion like ischemic spinal cord damage(17). Repeat surgery in patients with recoarct is difficult and carries higher risks. Recoarctation results from fibrosis and cicatrization of the scar and is well suited for balloon dilatation. Weak femoral pulse, upper body hypertension, an aortic gradient of >20 mmHg across the coarctation are indications of restenosis(18). A balloon equal to the size of aortic isthmus (area just below left subclavian artery) is chosen and results are very satis-factory. Rare cases of dissection of aorta and fatal aortic rupture have occurred(18,19).

The constricting shelf of native CoA can also be safely dilated by the radial forces of balloon. The dilatation works by creating a limited dissection in the aortic intima and media. The results are comparable to surgery and many workers recommend BD as therapy for native CoA(18). However, the rates of restenosis in neonates and infants are even  higher with BD than with surgery. Our own observations(20) indicate that surgery is preferable for coarctation in infants aged less than 3 months. Balloon dilatation, however, can be used as a temporizing measure to improve depressed left ventricular function in some circumstances, when the surgical option is not available or considered as high risk in a moribund infant.

On follow up, aortic aneurysm at the site of CoA may develop in 5% of patients treated surgically or with balloon dilatation(18). Hence, longterm surveillance is required. The inci-dence of persistent hypertension is higher in patients treated later in life. Therefore, elective treatment of CoA is recommended around 1-2 years even in asymptomatic infants(21). We would recommend BD in older children as initial therapy. However, some anatomic features like marked distortion of aorta and significant aortic arch hypoplasia may render CoA not amenable for BD.

Aortic Dilatation in Takayasu's Aortoarteritis

Aortic narrowing in Takayasu's arteritis results in systemic hypertension, increase in systemic after load and consequent ventricular dysfunction(22). The renal arteries are commonly narrowed also and contribute to systemic hypertension. An aortic gradient more than 20 mmHg and narrowing of the lumen >50% are indicators of significant stenosis. The diffuse and widespread nature of the disease make surgical therapy impractical and results are poor(23). Presence of left ventricular dysfunction and severe hypertension are reasons for intervention if suitable anatomic features like short segment tight narrowing of aorta or discrete renal arterial narrowing are present. Highly impressive results in this group of patients have been reported with balloon dilatations of the aorta and the renal

arteries(24,25). Marked improvement in the ventricular function occurs following successful dilatation(24-26). Ongoing active inflammation should be excluded by clinical evaluation and erythrocytic sedimentation rate before the intervention. More recently, lesions that do not respond with balloon dilatation are effectively treated by implanting metallic slotted tubes in the aorta (stents). However, not all lesions are amenable to these forms of treatment.

Pulmonary Arterial Dilatation

Pulmonary arterial stenosis (PAS) may occur in Rubella syndrome, William's syn- drome, Noonan's syndrome, or Alagille's syndrome(27). More commonly, it is associated with complex congenital heart disease and complicates the management. Significant PAS leads to decrease perfusion of corresponding segments of lungs, and that can be quantitated by lung perfusion scan. The results of surgical treatment for PAS are dismal. Even high pressure balloon dilatation is effective in less than 50% of patients(28). Either the lesion requires even higher pressures, or more commonly it recoils after BD. The more recent application of slotted metallic tubes (stents) within the vascular tree has revolutionized the  therapy of this group of patients (Fig. 3)(29). Stenting the pulmonary arteries have made many otherwise inoperable patients with congenital heart disease operable. The stents provide a scaffold which endothelialize in few weeks time. The incidence of restenosis in pulmonary arterial stents is low. However, pulmonary arterial stenting is a complex and technically demanding procedure. Inappropriate placement of stents, stent embolisation, pulmo-nary arterial rupture, side branch occlusions, etc. may occur(29).

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                               Fig. 3a                                                                  Fig 3b

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Fig 3c

Fig. 3. Pulmonary arterial stent. Fig. 3a shows thin right pulmonary artery in which a metallic slotted tube (Fig. 3b) is placed, and the final result (Fig. 3c) shows an adeqaute size right pulmonary artery. All injections are from superior vena cava in a superior vena cava to pulmonary artery anastomosis.


Coil Embolization

An unwanted arteriovenous communication can be occluded by embolizing few steel coils laced with dacron threads (to enhance their thrombogenicity) to the particular site(30). Special catheters help in reaching difficult sites, and coils approximately twice the site of vascular lumen to be occluded are placed (Fig. 4). Platinum microcoils, Silicon balloons, gel foam particles, Ivalon, etc. have also been used as occluding agents depending on the lesion(31). Coronary arteriovenous fistula(32), pulmonary arteriovenous fistula(33), aortopul-monary collaterals(34), and bronchial arterial branches (for hemoptysis)(35) have been occluded using catheter techniques. Geneally, these lesions are difficult to treat by operative techniques. The occlusion is effective and permanent if the target site can be reached. However, sometimes arteriovenous fistulae may recur from other tributaries.

4a1005.jpg (7121 bytes) 4b1005.jpg (7339 bytes)                       Fig. 4a                                                                               Fig. 4b
Fig. 4. Pulmonary arteriovenous fistula (Fig 4a) in an infant occluded with coils (Fig 4b).

Small Patent Ductus Arteriosus (PDA)

Conventionally, closure of even small PDA is advised to avoid life time risks of infective endocarditis, as the surgery for PDA is a simple closed heart operation(36). Coil occlusion of small PDA (<3-4 mm) in selected cases is effective(37) and avoids a scar. Majority of small PDAs may be closed by embolization with one or more coils placed through transvenous, or transarterial route even in small children (Fig. 5). The success rate was 77% in a large series(37). However, failure to implant a coil in 5%, coil embolization to lungs or systemic arteries in 16% occured. Flow disturbances in the left pulmonary artery have been observed due to the loop of a protruding coil into it, but these are usually mild and are not associated with significant obstruction. Rarely, severe hemolysis has been reported due to the jet of blood traversing the coil in cases with persistent PDA flow despite the coil implantation(38). Large PDAs and some anatomic types of short length small PDAs are not suitable for coil closure.  Wide application of echocardiography have discovered some tiny PDAs that are not apparent on clinical examination. There does not appear enough justification to advocate closure in these cases(39). Long term benefits of coil occlusion of PDA have not been established. An isolated report has shown some cases of recanalization of PDA after successful occlusion(40), but more studies are required.

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                          Fig 5a                                                 Fig 5b
An aottogram showing a small patent ductus arteiosus (Fig5a), closed by a coil placed in the ductus (Fig 5b) .Th other catheter is in the pulmonary artery.

Device Closure

Closing an intracardiac defect without surgery has long been cherished by the cardiologists. Due to persistent efforts of investigators, there are now at least five types of devices available for atrial septal defect (ASD) closure(41). These differ in various technical aspects. Amplatzer device, clamshell double umbrella, Sideris button device, Das-angel wings and Babic ASDOS system, have been used in humans, each in nearly a thousand patients. However, Amplatzer device and clamshell double umbrella are currently the preferred devices. The ASD should be centrally placed (ASD secundum defect) and should have at least 5 mm of rim of tissues for device to anchor and separate it safely from important structures like atrioventricular valves, pulmo-nary veins, systemic caval veins, and coronary sinus(42). The defects are sized using an occluding balloon size and appropriate sized device is deployed. Best results are obtained in small to moderate sized ASD that has good rims all around (Fig. 6). However, larger defects (>30 mm size) may also be amenable to device closure. It is estimated that nearly half of the secundum ASDs may be anatomically suited for device closure(43).   6a1007.jpg (6007 bytes)   6b1007.jpg (7818 bytes)
                           Fig 6a                                                              Fig 6b  
A transophageal echocardiogram showing an artial septal defect (Fig 6a).An amplatzer   ASD-device is placed across the defect (Fig 6b)RA - right artium, LA - left artium.

Antiplatelets agents (Aspirin) are admini-stered for 3 months and by that time the raw surface of device is expected to be fully covered by endothelium. The procedure is usually done under general anesthesia as it requires transe- sophageal echocardiographic guidance. Device embolization requiring surgery for retrieval and cerebrovascular accidents have rarely occured. The device is relatively expensive, but short hospital stay, no scar, blood transfusions, or other morbidity associated with surgery have made the procedure atractive. Long term follow up data are not yet available, but are expected to be encouraging. Similarly, moderate to large sized PDAs have been closed using Rashkind occluder(44), Amplatzer PDA occluder(45) (Fig. 7) or Sideris device(46). Large PDAs associated with congestive heart failure can be closed even in small children by these devices. PDA with high pulmonary arterial pressures and bidirectional shunt (Eisenmenger syn- drome) obviously should not be closed.

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Fig 7a                                                                        Fig 7b    
An aortogram which is occluded by an Amplatzer PDA occluder.
Note the device in the ductal ampulla.

Ventricular septal defects are the common-est congenital lesions. It has been amply proven that small VSD which is associated with less than 1:5:1 shunt and normal pulmonary arterial pressure need not be closed surgically(47). Most of the VSD are perimem-branous in location and as yet unsuitable for closure by a device, even if required. Device closure of VSD has been done in cases of muscular VSD or postoperative residual de-fects, mostly using clamshell occluder(48). This procedure is technically demanding and yet considered experimental. With continuous advances in interventional technology, devices tailor made for VSD closure would be available in the near future.


The interventional procedures continue to find other innovative applications. Some of these are not yet widely practised. Pulmonary valve dilatation in tetralogy of fallot with small pulmonary arteries(49), treatment of pulmonary valvar atresia by perforating the valve(50) with a guide wire or laser energy/radiofrequency energy catheters; stenting the PDA to keep it open in duct dependent lesions in neonates(51), and creating an atrial septal defect by balloon dilatation of interatrial septum in patients of primary pulmonary hypertension(52) are some of the examples.


1. Mullins CE. History of pediatric interventional catheterizations: Pediatric therapeutic cardiac             catheterization. Pediatr Cardiol 1998; 19: 3-7.

2. Kan JS, White RIJ, Mitchell SE, Gardner TJ. Percentaneous balloon valvuloplasty: A new method      for treating congenital pulmonary valve stenosis. N Engl J Med 1982; 307: 540-542.

3. Hayes CJ, Gersony WM, Driscoll DJ, Keane JF, Kidd L, O'Fallon WM, et al. Second natural      history study of congenital heart defects: Results of treatment of patients with pulmonary valve
    stenosis. Circulation 1993; 87: [Suppl I] I: 28-37.

4. Stanger P, Cassidy SC, Girod DA, Kan JS, Lababidi Z, Shapiro SR. Balloon pulmonary                valvuloplasty: Results of the valvuloplasty and angioplasty of congenital anomalies registry. Am J Cardiol 1990; 65: 775-783.

5. Gournay V, Piechaud J, Delogu A, Sidi D, Kachaner J. Balloon valvotomy for critical stenosis or       atresia of pulmonary valve in newborns. J Am Coll Cardiol 1995; 26: 1725-1731.

6. Mc Crindle BW. For VACA Registry investigators. Independent predictors of long term results      after balloon pulmonary valvulo-plasty. Circulation 1994; 89: 1751-1759.

7. Keane JF, Driscoll DJ, Gersony WM, Hayes CJ, Kidd L, O'Fallon M, et al. Second natural          history of congenital heart defects. Circulation 1993; 87 [Suppl I): 16-27.

8. Rocchini AP, Beekman RH, Shachor GB, Benson L, Schwartz D, Kan JS. Balloon aortic             valvuloplasty: Results of valvuloplasty and angioplasy of congenital anomalies Registry. Am J Cardiol 1990; 65: 784-789.

9. Kothari SS, Kumar RK, Varma S, Saxena A, Wasir HS. Thrombolytic therapy in infants for femoral arterial thrombosis after cardiac catheterization. Indian Heart J 1996; 48: 246-248.

10. Rao PS. Balloon valvuloplasty for aortic stenosis. In: Transcatheter Therapy in Pediatric Cardiology. New York, Wiley - Liss Inc, 193; pp 105-128.

11. Lock FAB, Joffe HS, Jordan SC. Martin RP. Balloon dilatation (Valvuloplasty) as first line treatment for severe stenosis of the aortic valve in early infancy: Medium term results and determinant of survival. Br Heart J 1993; 70: 546-553.

12. Kothari SS, Mishra S, Juneja R, Reddy SCB, Saxena A. Aortic valve balloon dilatation in infants with critical aortic stenosis. Indian Heart J 1998; 50: 520-522.

13. Arora R, Nair M, Kalra GS, Nigam M, Khalillulah M. Immediate and long term results  of balloon and surgical closed mitral valvotomy: A randomized comparative study. Am Heart J 1993; 125: 1091-1094.

14. Kothari SS, Kamath P, Juneja R, Bahl VK, Airan B. Percutaneous transverse mitral commissurotomy using Inoue balloon in children less than 12 years. Cathet Cardiovasc Diagn 1998; 43: 408-411.

15. Chen C, Cheng TO, Chen JY, Hirang YG, Huang T, Zhang TB. Long term results of percutaneous balloon mitral valvuloplasty for mitral stenosis: A follow up study to 11 years in 202 patients. Cathet Cardiovasc Diagn 1998; 43: 132-139.

16. Bahl VK, Chandra S, Sharma S. Combined dilatation of rheumatic mitral and tricuspid stenosis with Inoue balloon catheter. Int J Cardiol 1993; 42: 178-181.

17. Kirklin JW, Barrat Boyes BG. Coarctation of aorta and interupted aortic arch. In: Cardiac Surgery. New York, Churchill Livingstone, 1992; pp 1263-1325.

18. Ovaert C, Benson UN, Nykanen D, Freedom RM. Transcatheter treatment of coarctation of the aorta: A review. Pediatr Cardiol 1998; 19: 27-44.

19. Rao PS. Aortic rupture after balloon angioplasty of aortic coarctation. Am Heart J 1993; 125: 1205-1206.

20. Kothari SS, Juneja R, Saxena A, Reddy SCB, Sharma S. Balloon dilatation of simple aortic coarctation in neonates and infants, Indian Heart J 1998; 50: 187-192.

21. Waldman JD, Karp PB. How should we treat coarctation of the aorta? Circulation 1993; 87: 1043-1045.

22. Shrivastava S, Rajani M, Chopra P, Malaviya AN, Tandon R. Systemic hypertension and aortic obstruction in children. Eur J Pediatr 1981; 135: 281-289.

23. Kimoto S. The history and present status of aortic surgery in Japan particularly for the aortitis syndrome. J Cardiovasc Surg 1979; 20: 107-126.

24. Tyagi S, Kaul UA, Nair M, Sethi KK, Arora R, Khalilulah M. Balloon angioplasty of the aorta

in Takayasu's arteritis. Initial and long term results. Am Heart J 1992; 124: 876-882.

25. Sharma S, Thatai D, Saxena A, Kothari SS, Guleria S, Rajani M. Renovascular hyper-tension from non-specific aortoarteritis in children: Midterm results of percutaneous transluminal angioplasty and predictors of restenosis. Am J Roentg 1996; 166: 157-162.

26. Talwar KK, Prabhakaran D, Mohan B, Ramamurthy S, Sharma S, Kamath P, et al. Improvement of left ventricular function following balloon aortoplasty in patients of Takayasu's arteritis. Indian Heart J 1998; 50: 633.

27. Rochini AP, Emmanouilides GC. Peripheral pulmonic stenosis: Management. In: Moss and Adam's Heart Disease in Infants, Children and Adolescent Including the Fetus and Young Adult, 5th edn. Eds. Emmanouilides GC, Riemenschneider TA, Allen HD, Gutgesell HP. Baltimore, Williams and Wilkins, 1995; p 955.

28. Gentles TL, Lock JE, Perry SB. High pressure balloon angioplasty for branch pulmonary artery stenosis: Early experience. J Am Coll Cardiol 1993; 22: 867-877.

29. O' Laughlin MP, Slack MC, Grifka RF, Perry SB, Lock JE, Mullins CE. Implantation and intermediate-term follow up of stents in congenital heart disease. Circulation 1993; 88: 605-614.

30. Gainturco C, Anderson JH, Wallace S. Mechanical devices for arterial occlusion. AJR 1975; 124: 428-435.

31. Rothman A. Pediatric Cardiovascular embolization therapy. Pediatr Cardiol 1998; 19: 74-84.

32. Shrivastava S, Kothari SS, Sharma S. Transcatheter embolization of a coronary artery fistula. Indian Heart J 1993; 45: 201-203.

33. Kothari SS, Sharma M, Sharma S. Transcatheter embolization of pulmonary arteriovenous fistula. Indian Pediatr 1996; 33: 1044-1047.

34. Sharma S, Kothari SS, Krishna Kumar R, Saxena A, Sharma R, Taneja K. Systemic to pulmonary collaterals vessels and surgical shunts in patients with cyanotic congenital heart disease; preoperative treatment by transcatheter embolisation. Amer J Roent 1995; 164: 1505-1510.

35. Sharma S, Kothari SS, Rajani M, Venugopal P. Life threatening arterial hemorrhage: Results of treatment with transcatheter embolisation with home made coils. Clin Radiol 1994; 49: 251-255.

36. Brook MM, Heymann MA. Patent ductus arteriosus. In: Moss and Adam's Heart Disease in Infants, Children and Adolescents Including the Fetus and Young Adult, 5th edn. Eds. Emmanouilides GC, Riemenschneider TA, Allen HD, Gutgesell HP. Baltimore, Williams and Wilkins, 1995; p 760.

37. Shim D, Beekman RH. Transcatheter management of patent ductus arteriosus. Pediatr Cardiol 1998; 19: 67-71.

38. Shim D, Wechsler DS, Lloyd TR, Beekman RH. Hemolysis following coil embolization of a patent ductus arteriosus. Cath Cardiovasc Diagn 1996; 39: 287-290.

39. Lloyd TR, Beekman RH. Clinically silent patent ductus arterosus. Am Heart J 1994; 127: 1664.

40. Daniels CJ, Cassidy SC, Teske DW, Wheller JJ, Allen HD. Reopening after successful coil occlusion for patent ductus arteriosus. J Am Coll Cardiol 1998; 31: 444-450.

41. Rao PS. Trans catheter closure of atrial septal defect: Are we there yet? J Am Coll Cardiol 1998; 31: 1117-1119.

42. Masura J, Gavora P, Formanek A, Hijazi ZM. Transcatheter closure of secundum atrial septal defects using the new self-centering Amplatzer septal occluder: Initial human experience. Cathet Cardiovasc Diagn 1997; 42: 388-393.

43. Ferreira MGA, Ho SY, Anderson RH. Morphologic study of defects of the atrial septum within the oval fossa: Implications for trans catheter closure of left to right shunt. Br Heart J 1992; 67: 316-320.

44. Rashkind WS, Mullins CE, Hellenbrand WE, Tait MF. Non-surgical closure of patent ductus arteriosus: Clinical applications of Rashkind PDA occluder system. Circulation 1987; 75: 583-593.

45. Masura J, Hijazi ZH. Catheter closure of moderate to large sized patent ductus arteriosus using the New Amplatzer duct occluder: Immediate and short term results. J Am Coll Cardiol 1998; 31: 878-882.

46. Rao PS, Sideris EB, Haddad J, Rey C, Hausdorf G, Wilson AD, et al. Transcatheter occlusion of patent ductus arteriosus with an adjustable button device: Initial clinical experience. Circulation 1993; 88: 1119-1126.

47. Backer CL, Winters RC, Zales VR. Restrictive ventricular septal defect: How small is too small to close? Ann Thorac Surg 1993; 56: 1014-1019.

48. Lock JE, Block SC, Mc Kay RG, Baim DS, Keane JF. Trancatheter closure of ventricular septal defects. Circulation 1988; 78: 361- 368.

49. Kreutzer J, Perry S, Jones RA, Mayer JE, Castaneda AR, Lock JE. Tetralogy of Fallot with diminutive pulmonary arteries: Preoperative pulmonary valve dilatation and transcatheter rehabilitation of pulmonary arteries. J Am Coll Cardiol 1996; 27: 1741-1747.

50. Justo RN, Nykanen DG, Williamsk WG, Freedom RM, Benson LN. Transcatheter performation of the right ventricular outflow tract as initial therapy for pulmonary valve atresia and intact ventricular septum in the newborn. Cath Cardiovasc Diag 1997; 40: 408-413.

51. Gibbs J. Stenting the arterial duct. Arch Dis Child 1995; 72: 196.

52. Nihill MR, O' Laughlin MP, Mullins CE. Effects of atrial septostomy in patients with terminal cor pulmonale due to pulmonary vascular disease. Cath Cardiovasc Diagn 1991; 24: 116-172.


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