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.
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.
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.
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.
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 ³50 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.
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).
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).
Fig. 3a Fig 3b
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.
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.
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.
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).
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.
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.
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