Percutaneous Occlusion of the Patent Ductus Arteriosus with the Amplatzer Device for Atrial Septal Defects

Percutaneous occlusion of the patent ductus arteriosus (PDA) has been performed safely and effectively with different devices over the last years.^1–6 Selection of the closure device is based on the anatomic configuration of the duct and its minimal diameter. The large and short (window-type) ductuses are generally associated with higher rates of incomplete occlusion, device embolization and abandoned procedure failures.^2,3 Also, the procedure can be technically demanding in adults due to suboptimal visualization of the ductal anatomy on angiography, local calcification and the occasional association of pulmonary hypertension.^7–10 We report 2 cases of percutaneous closure of large and short ductuses in adults with mild to moderate pulmonary hypertension with the Amplatzer device (AGA Medical Corp., Golden Valley, Minnesota) designed for atrial septal defect (ASD) occlusion. Case Report. Patient #1. This patient was a 47-year-old man, weighing 95 kg, with a medical history of a cardiac murmur detected in childhood and shortness of breath during moderate activities, which had been ameliorated in the last 2 years after he was started on furosemide. On physical examination, there was a mild ejection murmur at the left mid sternal border and a mild continuous murmur at the left infraclavicular region. The second heart sound was moderately increased in intensity. There was mild cardiomegaly and increased pulmonary vascular markings on chest radiogram, and left ventricular hypertrophy on the electrocardiogram (ECG), with no T-wave or ST-segment changes. Transthoracic color Doppler echocardiography demonstrated a discrete fibromuscular membrane in the left ventricular outflow tract (LVOT) with a maximal instantaneous systolic gradient of 75 mmHg, and a moderate-size PDA. The patient had trivial aortic insufficiency, mild ventricular overload and good qualitative ventricular function. There were signs of pulmonary hypertension on the M-mode of the pulmonary valve. The patient was referred to the catheterization laboratory for possible closure of the PDA and reassessment of the gradient across the LVOT after the procedure or test occlusion. Under local anesthesia, six and 7 French (Fr) sheaths were inserted in the right femoral artery and vein, respectively. Heparin was given (2,500 IU) and right and left standard catheterization showed the following pressures: right atrium (RA), 7 mmHg; right ventricle (RV), 65/10 mmHg; main pulmonary artery (MPA), 65/22 mmHg (m 37); aorta, 130/70 mmHg (m 80); LVOT, 130/15 mmHg; and left ventricle (LV), 180/15 mmHg. The Qp/Qs was 2.8. An angiogram in the descending thoracic aorta with a high-flow pigtail catheter (Cook Cardiology, Bloomington, Indiana) in the lateral projection revealed a large and short type A ductus¹¹ with a shallow aortic ampulla, measuring 6.5 mm at the narrowest point (Figure 1). The ductus was crossed from the pulmonary artery to the descending aorta using a 7 Fr angiographic Berman catheter balloon (Arrow, Reading, Pennsylvania). After balloon inflation and catheter retraction for ductal test occlusion, the pulmonary pressure taken through the side-holes of the catheter located in the pulmonary side decreased to 45/18 mmHg (m 26). Also, there was a decrease in the LVOT gradient: LV, 150/12 mmHg; LVOT, 130/12 mmHg; aorta, 130/80 mmHg (m 90). Due to the size of the patient and non-satisfactory ductal visualization on angiography, a decision was made to determine the “stretched” diameter of the ductus. With the aid of an end-hole right coronary Judkins catheter (Cordis Corporation, Miami, Florida) and a hydrophilic 0.035´´ Roadrunner guidewire (Cook Cardiology), the ductus was crossed from the MPA to the aorta. The hydrophilic wire was then exchanged for a 0.035´´ x 260 cm Amplatz “extra-stiff” wire (Cook Cardiology), which was left in the descending aorta. The Judkins catheter (Cordis Corporation) and the femoral short sheaths were taken out. Over the exchange wire, a 24 mm sizing balloon catheter (AGA Medical Inc.), commonly employed for determination of the stretched ASD diameter, was advanced from the femoral vein to the descending aorta through the ductus. The balloon was then inflated with 10–15 ml of contrast medium and saline in the descending aorta and pulled back, anchoring at the aortic side of the ductus. At this point, the operator felt a little bit of resistance on the catheter. With continuous and gentle traction on the catheter, the balloon was pulled all the way through the ductus to the pulmonary artery. This maneuver was recorded on cine so that the best frame could be chosen for determination of the “stretched” diameter of the ductus at the site of waist formation on the balloon. This measured 7.5 mm using the markers on the catheter for digital calibration. Because it was a large and short, funnel-like ductus with a shallow aortic ampulla, associated with pulmonary hypertension, a decision was made to implant an 8 mm ASD Amplatzer device. Better accommodation and stabilization of the device within the ductus was the rationale for this decision. The sizing balloon was removed and exchanged over the wire for a long, manually pre-shaped 7 Fr sheath (Cook Cardiology), which was advanced to the descending aorta through the ductus. The 8 mm ASD Amplatzer device was loaded in the usual fashion, advanced through the long sheath and implanted in the ductus. The steps of implantation were similar to those used for the Rashkind PDA umbrella (USCI, Billerica, Massachusetts) technique¹ and ASD occlusion.¹² After advancing the delivery cable and opening the distal disc, the whole system was brought back as a unit, anchoring at the aortic side of the ductus. Maintaining gentle traction on the delivery cable, the long sheath was retracted over the cable, allowing for reconfiguration of the central waist in the duct and the proximal disc in the pulmonary artery. Test injections in the descending aorta helped to correctly place the device. Nevertheless, there was significant and high-velocity residual shunt through the upper aspect of the device. Because of this, we decided to change the device for a larger one. The long sheath was advanced over the delivery cable, recapturing the device, and left in the descending aorta. The 8 mm device was removed and a 10 mm device was implanted in a similar fashion. A new angiogram before the final release demonstrated good device position and a mild residual shunt through the upper part of the right disc. The device was then released in the usual fashion with counterclockwise rotation of the delivery cable. An angiogram performed 5 minutes after the final release demonstrated the same mild and low velocity residual shunt as before (Figure 2). New hemodynamic assessment revealed similar pressures in the LVOT after ductal test occlusion. The patient was discharged home uneventfully on the same day. On the following morning, a transthoracic color Doppler echocardiography demonstrated complete closure of the ductus and an unobstructive flow pattern in the aortic arch and in the left pulmonary artery. Also, there was a gradient reduction across the LVOT to 35 mmHg. A decision was then made to manage the patient conservatively, with serial echocardiographic assessments (every 6–12 months) focusing on gradient progression across the LVOT and possible deterioration of the aortic valve function. Patient #2. This patient was a 55-year-old woman, weighing 50 kg, with shortness of breath during moderate activities. On physical examination, there was a mild, continuous murmur at the left upper sternal border. The second heart sound was mildly increased in intensity. Mild cardiomegaly and increased pulmonary vascular markings were seen on chest radiogram, and ECG showed left ventricular hypertrophy. Transthoracic color Doppler echocardiography demonstrated a moderate-size PDA with left ventricular overload and qualitatively good ventricular function. On the M-mode of the pulmonary valve, there were signs of pulmonary hypertension. The patient was referred to the catheterization laboratory for possible closure of the defect. Under local anesthesia, six and 7 Fr sheaths were inserted in the right femoral artery and vein, respectively. Heparin was given (2,500 IU) and right and left standard catheterization showed the following pressures: RA, 5 mmHg (mean); RV, 50/8 mmHg; MPA, 50/18 mmHg (m 30); aorta, 120/70 mmHg (m 80); and LV, 120/14 mmHg. The Qp/Qs was 2.0. An angiogram in the descending thoracic aorta with a high-flow pigtail catheter in the lateral projection revealed a short, window-type ductus (or type B according to the Toronto Classification System),¹² measuring 4 mm at the narrowest point (Figure 3). Attempts to cross the ductus from the pulmonary artery to the aorta were unsuccessful. Therefore, the ductus was crossed retrogradely with the aid of a 5 Fr right coronary Judkins catheter (Cordis Corporation) and a 0.014´´ coronary wire (Choice PT, Boston Scientific/Scimed, Inc., Maple Grove, Minnesota). The right coronary Judkins catheter was exchanged for a 6 Fr, end-hole balloon-tipped catheter (Arrow) over the wire, which was then advanced from the aorta to the main pulmonary artery. The balloon was inflated and the catheter withdrawn, anchoring at the pulmonary side of the ductus for test occlusion. The pulmonary artery pressure decreased to 35/16 mmHg (m 22). For better assessment of the size of the ductus, we again determined its “stretched” diameter in a similar fashion as described above. The 0.014´´ wire was snared in the main pulmonary artery into a long, 7 Fr, braided Shuttle sheath (Cook Cardiology), which had been manually shaped, and the end-hole catheter balloon was subsequently advanced over the wire into the long sheath. In this way, there was enough support for the long sheath to be advanced across the ductus over the 0.014´´ wire and the balloon-tipped catheter, reaching the descending aorta. The 0.014´´ wire and the catheter were taken out and a long, 0.035´´ x 260 cm, extra-stiff wire was positioned in the distal descending aorta through the long sheath. After removal of the long sheath, the “stretched” diameter was determined as described above, measuring 4.8 mm (Figure 4). Because it was a classic window-type ductus associated with pulmonary hypertension (albeit mild), a decision was made to implant a 5 mm ASD Amplatzer device using similar rationale to Patient #1. Following the same technical steps, the device was implanted at the first attempt in this case. Angiogram performed 5 minutes after final release demonstrated good device position and trivial and low velocity residual shunt through the wire mesh of the device (Figure 5). Pressures in the main and left pulmonary artery were 35/15 mmHg (m 22) after the procedure. The patient was discharged home uneventfully on the same day. Transthoracic color Doppler echocardiography revealed complete occlusion of the defect on the following morning and unobstructive flow pattern in the aortic arch and in the left pulmonary artery. Discussion. Surgical treatment of the patent ductus arteriosus in adults may be associated with some technical difficulties and hazards. The common findings of calcification, short length and friability of the ductal tissue in adulthood may hinder ductal division. Because laceration and significant bleeding may occur, brief periods of cardiopulmonary bypass may be required.^13–15 Therefore, percutaneous occlusion has been regarded as the preferred method of treatment of the PDA in adults at several centers.^1,2,7–10 Nevertheless, this approach can also be challenging for the interventionalist.^7–10 Even using large amounts of contrast medium injected through high-flow catheters, clear and detailed demonstration of the ductal anatomy may not always be possible. Due to the large size of the patient, inadequate x-ray penetration and dilution of the contrast medium usually occur. This may result in inaccurate measurements, misinterpretation of ductal anatomy, improper device selection, failure to implant the device, higher rates of incomplete occlusion and embolization. To minimize these problems in this age group, we feel that one should determine the “stretched” diameter of the ductus with a sizing balloon. Because these sizing balloons are highly compliant, they are easily deformed when inflated up against more rigid structures, such as the ductus arteriosus. In this regard, the ductus has histologic layers that are similar to those found in the arteries,¹⁶ which are thicker and less compliant than veins and the interatrial septum. Therefore, when the sizing balloon was inflated and pulled across the ductus, it was immediately deformed by the more rigid ductal wall with little “stretch” effect. As a result, waist formation was readily seen on the screen. Since ductal spasm may follow catheter manipulation through the ductus,² the aortic angiogram, in spite of its pitfalls, should be obtained before determining the “stretched” diameter of the ductus. Although the Amplatzer duct occluder works well for closing the vast majority of PDAs, with high rates of complete closure,^4–6 we feel that satisfactory stabilization of the device may not be achieved in the large and short ductus, with shallow or no aortic ampulla. We believe that this anatomic pattern is better dealt with a double-disc type of device, such as the old Rashkind umbrellas,¹ the CardioSEAL/Starflex device (Nitinol, Boston, Massachusetts) and the Amplatzer ASD device. In addition, the presence of pulmonary hypertension may further jeopardize adequate device stabilization if the device has no disc at the pulmonary end of the ductus. Embolization of an Amplatzer duct occluder into the descending aorta in a patient with Down syndrome, a large PDA and severe pulmonary hypertension has been reported, resulting in catastrophic outcomes.⁶ Therefore, the selection of an Amplatzer ASD device to close the PDAs with their unique anatomic features in our patients seemed to be appropriate. The presence of the 2 discs, one on each side of the ductus, and the short distance between them has resulted in optimal device stabilization. We arbitrarily selected an ASD device that was similar to or 1 mm larger than the “stretched” diameter of the ductus. In patient #1, in spite of the good position of the device, there was a large and high-velocity residual shunt through the upper portion, which prompted us to change it for a larger device. It is possible that the first device might have been sufficient for complete closure after its final release. Disadvantages of using an ASD Amplatzer device to close a PDA are higher costs and possible protrusion of the proximal disc into the left pulmonary artery, especially in infants. This was not the case in our patients, since they were adults. The implantation technique was straightforward and easy for operators who are familiar with Amplatzer devices and percutaneous PDA occlusion. Due to the marked anatomic variation encountered in different situations in interventional cardiology for congenital heart disease, each case must be individualized. Because of their versatile characteristics, the Amplatzer devices have been employed to close a variety of defects with optimal adaptation to the underlying anatomy and excellent outcomes.^17–19 Finally, we would like to make a comment on the observation of gradient reduction across the LVOT after PDA closure in patient #1. This had been well documented in patients with aortic valvar stenosis and PDA, in whom the correct estimation of the transaortic gradient could only be determined after ductal test or interventional closure.^20,21 This is of paramount importance, since it may defer surgical or catheter intervention to the aortic valve. The concept of referring patients with subaortic stenosis to surgical treatment at the moment of the diagnosis, regardless of the degree of the gradient across the LVOT, is not universally accepted as standard practice.²² Indeed, there are some patients, such as ours, in whom the disease may show a more “benign” and insidious course, with no significant gradient progression and deterioration of aortic valve function over the years. In addition, due to the possibility of recurrence after surgical resection and other postoperative complications, we adopted a more conservative approach in our patient. Of course, serial echocardiographic reassessment is mandatory to monitor progression of obstruction and valve malfunction. In conclusion, adult patients with large and short PDAs, with shallow or no aortic ampulla, may benefit from percutaneous occlusion with an Amplatzer ASD device, especially when there is associated pulmonary hypertension. Addendum. After the completion of this report, we performed 1 additional procedure using the same technique in an adult with hypertensive, type B PDA with excellent outcomes.

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