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Balloon Angioplasty in a 1200-Gram Premature Infant with Critical Aortic Coarctation
Letters to the Editor
7. Butera G, De Rosa G, Chessa M, Piazza L, Delogu A, Frigiola A, et al. Transcatheter closure of the persistent arterial duct with the Amplatzer duct ocludder in very young symptomatic children. Heart. 2004;90:1467-70. 8. Hijaji ZM, Lloyd TR, Beekman RH, Geggel RL. Transcatheter closure with single or multiple Gianturco coil of patent ductus arteriosus in infants weighing <8 Kg: retrograde versus anterograde approach. Am Heart J. 1996;132:827-35. 9. Haneda N, Kato F, Kim S-H. Coil closure of a large patent arterial duct in a low-birthweight infant. Pediatr Int. 2002;44:317-20. 10. Thukaram R, Suarez WA, Sundararaghavan S. Transcateheter closure of the patent arterial duct using the flipper coil in a premature infant weighing 1,400 g: A case report. Catheter Cardiovasc Interv. 2005;66:18-20.
Balloon Angioplasty in a 1200-Gram Premature Infant With Critical Aortic Coarctation To the Editor, Figure 2. Endoscopic image prior to release. Note transthoracic echocardiographic monitoring (*) and normally positioned device, with 3 coils in the ductal ampulla (1) and 1 on the pulmonary side (2).
recommendation is to resort to surgical closure of PDA when medical treatment has failed or is contraindicated,1,2 there are warnings about the possible negative impact of surgery on the status of a critically ill preterm infant.2-4 Thus, less invasive techniques have been developed5 and devices for percutaneous closure have been designed.7,8,10 In our opinion, although patient selection is of the utmost importance, we feel that percutaneous closure should be considered as an alternative in the treatment of PDA in the preterm newborn infant. Fernando Rueda Núñez, Alejandro Ávila Álvarez, José Luis Fernández Trisac, and César Abelleira Pardeiro
Unidad de Cardiopatías Congénitas, Servicio de Pediatría, Complejo Hospitalario Universitario de A Coruña, A Coruña, Spain.
references
1. Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation. 2006;114:1873-82. 2. Bose CL, Laughon MM. Patent ductus arteriosus: lack of evidence for common treatments. Arch Dis Child Fetal Neonatal Ed. 2007;92:F498-502. 3. Clyman RI, Chorne N. Patent ductus arteriosus: evidence for and against treatment. J Pediatr. 2007;150:216-9. 4. Roberts P, Adwani S, Archer N, Wilson N. Catheter closure of the arterial duct in preterm infants. Arch Dis Child Fetal Neonatal Ed. 2007;92:F248-50. 5. Porstmann W, Wierney L, Warnke H. Closure of the persistent arterial duct without thoracotomy. Ger Med Mon. 1967;12:259-61. 6. Galal MO, Hussain A, Arfi A. Do we still need the surgeon to close the persistently patent arterial duct? Cardiol Young. 2006;16:522-36.
Neonatal aortic coarctation is a serious condition. It is characterized by signs of heart failure and cardiogenic shock. We report the case of a premature twin, born at the gestational age of 32 weeks, with intrauterine growth retardation, referred to our hospital at the age of 17 days with severe heart failure. Echocardiography revealed severe left ventricular dysfunction (Figure 1A); the dimensions of left ventricle in M mode were 19 mm and 13 mm in diastole and systole, respectively. The aortic arch showed severe coarctation (Figure 1B), with a gradient of 40 mmHg diastolic extension (Figure 1C). Treatment was begun with prostaglandin E1, diuretics and inotropic agents. He also required mechanical ventilation. When he was 24 days old and weighed 1200 g, angioplasty was performed using the Seldinger technique, involving a 3-F introducer in the left carotid artery (Figure 2A). The aortic arch, the region of the coarctation and descending aorta measured 3.5 mm, 1.5 mm, and 5 mm in diameter, respectively. A 4 mm × 20 mm Tyshak Mini® balloon catheter (NuMED, Hopkinton, NY, USA) (Figure 2B) was utilized. Following angioplasty, the coarcted segment increased in diameter to 4 mm (Figure 2C). The initial gradient of 35 mmHg disappeared completely. The fluoroscopy time was 7 minutes. After the procedure, the administration of prostaglandins and inotropic agents was discontinued. Starting at 30 days of life, a progressive aortic recoarctation was observed, although it was well tolerated clinically. At the age of 61 days, with a body weight of 2200 grams, the infant underwent a second angioplasty procedure with access via the right femoral artery. The angiography revealed severe recoarctation (Figures 2D and 2E); in addition, Rev Esp Cardiol. 2010;63(6):740-50 741
Letters to the Editor
Figure 1. Echocardiography prior to angioplasty (access via carotid artery). A: M mode, showing left ventricular dysfunction. B: coarcted aortic arch. C: Doppler ultrasound with gradient of 40 mmHg and diastolic extension. D: aortic arch following second angioplasty (at 6 months of age).
Figure 2. A, B, and C: first aortic angioplasty, access via carotid artery. D, E, and F: aortic angioplasty, access via femoral artery: note (E) the permeability of the left carotid artery utilized in the previous procedure.
742 Rev Esp Cardiol. 2010;63(6):740-50
Letters to the Editor
permeability of the left common carotid artery utilized in the previous procedure was observed (Figure 2E). With the aid of a 4-F introducer, a 5 mm × 20 mm Tyshak Mini® balloon catheter was used (Figure 2F), followed by another measuring 6 mm × 20 mm. The initial gradient of 40 mmHg was reduced to 7 mmHg. At the age of 6 months, the infant was asymptomatic and showed adequate weight gain, with a body weight of 5600 grams; echocardiography demonstrated the absence of a gradient in the aortic arch, with a normal color flow Doppler ultrasound (Figure 1D). The treatment of severe coarctation in premature infants requires prolonged infusion of prostaglandins to maintain perfusion in the abdomen and lower extremities. Both surgery and angioplasty prove to be effective in the treatment of native coarctation, but the latter is associated over the long term with more complications, such as recoarctation and the formation of aneurysms.1 Despite the improvement in the results of the surgical treatment of coarctation, prematurity is perceived as a risk factor for morbidity and mortality; in 2 different studies,2,3 the rate of acute mortality was reported to be 5.5% to 12.5%, whereas late mortality ranged between 8.3% and 11%. Moreover, the authors observed recoarctation in 29% and 44% of the treated patients. Experience with angioplasty in premature infants is limited. In a review4 dealing with premature infants weighing less than 1500 grams, four of them with coarctation required six procedures, and two had to undergo surgery to treat recoarctation. There was one death that was not related to the procedure. Other articles involve case reports5,6; the smaller of the 2 children described to was a premature infant weighing 460 grams. Both cases were treated successfully, but neither of them involved access via the carotid artery, as we performed in our patient. Angioplasty in premature infants with aortic coarctation is, in our opinion, a treatment that can improve the serious clinical condition of these patients. We consider that access via the carotid artery not only permits easy vascular access, but is a safe technique as well. Fredy Prada, Juan Carretero, Carlos Mortera, and Daniel Velasco
Servicio de Cardiología, Hospital Sant Joan de Deu, Barcelona, Spain
references
1. Fiore AC, Fischer LK, Schwartz T, Jureidini S, Balfour I, Carpenter D, et al. Comparison of angioplasty and surgery for neonatal aortic coarctation. Ann Thorac Surg. 2005;80:165964. 2. Bacha EA, Almodovar M, Wessel DL, Zurakowski D, Mayer JE Jr, Jonas RA, et al. Surgery for coarctation of the aorta in infants weighing less than 2 kg. Ann Thorac Surg. 2001;71:1260-4.
3. Sudarshan CD, Cochrane AD, Jun ZH, Soto R, Brizard CP. Repair of coarctation of the aorta in infants weighing less than 2 kilograms. Ann Thorac Surg. 2006;82:158-63. 4. Sutton N, Lock JE, Geggel RL. Cardiac catheterization in infants weighing less than 1,500 grams. Catheter Cardiovasc Interv. 2006;68:948-56. 5. McMahon CJ, Alromani A, Nihill MR. Balloon angioplasty of critical coarctation in a 970-gram premature infant. Cardiol Young. 2001;11:468-71. 6. Schamberger MS, Lababidi ZA. Successful balloon angioplasty of a coarctation in an infant <500 g. Pediatr Cardiol. 1998;19:418-9.
Giant Coronary Artery Fistula Between the Left Main Coronary and the Superior Vena Cava Complicated by Coronary Artery Dissection To the Editor, Coronary fistulas are connections between the coronary arteries and another cavity. They are generally congenital and are due to a defect in the compacting of the myocardium during embryonic development. This persistent primitive vascular pattern can connect the coronary arteries with the ventricular cavities or other vascular structures. The most common type is that which originates in the right coronary artery and drains into the right-sided chambers, followed by fistulas between branches of the left coronary artery and the pulmonary artery.1 These conditions are rare and are mainly associated with a risk of myocardial ischemia (steal phenomenon), heart failure (volume overload, pulmonary hypertension), rupture or dissection, endocarditis and arrhythmias.2 The patient was a 41-year-old man with no known cardiovascular risk factors or family history of heart disease. He was admitted with tightness in the middle of his chest that appeared with moderate exertion, accompanied by other characteristic symptoms of physical discomfort affecting vegetative functions (pallor, perspiration, nausea/vomiting, etc). The electrocardiogram revealed an inferior subepicardial lesion with ST segment depression in right precordial leads and aVL. The administration of sublingual nitroglycerine relieved the pain. Emergency coronary angiography revealed a giant coronary fistula (12 mm in diameter) connecting the origin of the left main coronary artery (LMCA) with superior vena cava prior to its entry into the right atrium. There was highly developed dilation of the LMCA and circumflex artery, with a lesion of 60% in the distal obtuse marginal branch. The ejection fraction was 75%. The observation of a translucent Rev Esp Cardiol. 2010;63(6):740-50 743
7. Butera G, De Rosa G, Chessa M, Piazza L, Delogu A, Frigiola A, et al. Transcatheter closure of the persistent arterial duct with the Amplatzer duct ocludder in very young symptomatic children. Heart. 2004;90:1467-70. 8. Hijaji ZM, Lloyd TR, Beekman RH, Geggel RL. Transcatheter closure with single or multiple Gianturco coil of patent ductus arteriosus in infants weighing <8 Kg: retrograde versus anterograde approach. Am Heart J. 1996;132:827-35. 9. Haneda N, Kato F, Kim S-H. Coil closure of a large patent arterial duct in a low-birthweight infant. Pediatr Int. 2002;44:317-20. 10. Thukaram R, Suarez WA, Sundararaghavan S. Transcateheter closure of the patent arterial duct using the flipper coil in a premature infant weighing 1,400 g: A case report. Catheter Cardiovasc Interv. 2005;66:18-20.
Balloon Angioplasty in a 1200-Gram Premature Infant With Critical Aortic Coarctation To the Editor, Figure 2. Endoscopic image prior to release. Note transthoracic echocardiographic monitoring (*) and normally positioned device, with 3 coils in the ductal ampulla (1) and 1 on the pulmonary side (2).
recommendation is to resort to surgical closure of PDA when medical treatment has failed or is contraindicated,1,2 there are warnings about the possible negative impact of surgery on the status of a critically ill preterm infant.2-4 Thus, less invasive techniques have been developed5 and devices for percutaneous closure have been designed.7,8,10 In our opinion, although patient selection is of the utmost importance, we feel that percutaneous closure should be considered as an alternative in the treatment of PDA in the preterm newborn infant. Fernando Rueda Núñez, Alejandro Ávila Álvarez, José Luis Fernández Trisac, and César Abelleira Pardeiro
Unidad de Cardiopatías Congénitas, Servicio de Pediatría, Complejo Hospitalario Universitario de A Coruña, A Coruña, Spain.
references
1. Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation. 2006;114:1873-82. 2. Bose CL, Laughon MM. Patent ductus arteriosus: lack of evidence for common treatments. Arch Dis Child Fetal Neonatal Ed. 2007;92:F498-502. 3. Clyman RI, Chorne N. Patent ductus arteriosus: evidence for and against treatment. J Pediatr. 2007;150:216-9. 4. Roberts P, Adwani S, Archer N, Wilson N. Catheter closure of the arterial duct in preterm infants. Arch Dis Child Fetal Neonatal Ed. 2007;92:F248-50. 5. Porstmann W, Wierney L, Warnke H. Closure of the persistent arterial duct without thoracotomy. Ger Med Mon. 1967;12:259-61. 6. Galal MO, Hussain A, Arfi A. Do we still need the surgeon to close the persistently patent arterial duct? Cardiol Young. 2006;16:522-36.
Neonatal aortic coarctation is a serious condition. It is characterized by signs of heart failure and cardiogenic shock. We report the case of a premature twin, born at the gestational age of 32 weeks, with intrauterine growth retardation, referred to our hospital at the age of 17 days with severe heart failure. Echocardiography revealed severe left ventricular dysfunction (Figure 1A); the dimensions of left ventricle in M mode were 19 mm and 13 mm in diastole and systole, respectively. The aortic arch showed severe coarctation (Figure 1B), with a gradient of 40 mmHg diastolic extension (Figure 1C). Treatment was begun with prostaglandin E1, diuretics and inotropic agents. He also required mechanical ventilation. When he was 24 days old and weighed 1200 g, angioplasty was performed using the Seldinger technique, involving a 3-F introducer in the left carotid artery (Figure 2A). The aortic arch, the region of the coarctation and descending aorta measured 3.5 mm, 1.5 mm, and 5 mm in diameter, respectively. A 4 mm × 20 mm Tyshak Mini® balloon catheter (NuMED, Hopkinton, NY, USA) (Figure 2B) was utilized. Following angioplasty, the coarcted segment increased in diameter to 4 mm (Figure 2C). The initial gradient of 35 mmHg disappeared completely. The fluoroscopy time was 7 minutes. After the procedure, the administration of prostaglandins and inotropic agents was discontinued. Starting at 30 days of life, a progressive aortic recoarctation was observed, although it was well tolerated clinically. At the age of 61 days, with a body weight of 2200 grams, the infant underwent a second angioplasty procedure with access via the right femoral artery. The angiography revealed severe recoarctation (Figures 2D and 2E); in addition, Rev Esp Cardiol. 2010;63(6):740-50 741
Letters to the Editor
Figure 1. Echocardiography prior to angioplasty (access via carotid artery). A: M mode, showing left ventricular dysfunction. B: coarcted aortic arch. C: Doppler ultrasound with gradient of 40 mmHg and diastolic extension. D: aortic arch following second angioplasty (at 6 months of age).
Figure 2. A, B, and C: first aortic angioplasty, access via carotid artery. D, E, and F: aortic angioplasty, access via femoral artery: note (E) the permeability of the left carotid artery utilized in the previous procedure.
742 Rev Esp Cardiol. 2010;63(6):740-50
Letters to the Editor
permeability of the left common carotid artery utilized in the previous procedure was observed (Figure 2E). With the aid of a 4-F introducer, a 5 mm × 20 mm Tyshak Mini® balloon catheter was used (Figure 2F), followed by another measuring 6 mm × 20 mm. The initial gradient of 40 mmHg was reduced to 7 mmHg. At the age of 6 months, the infant was asymptomatic and showed adequate weight gain, with a body weight of 5600 grams; echocardiography demonstrated the absence of a gradient in the aortic arch, with a normal color flow Doppler ultrasound (Figure 1D). The treatment of severe coarctation in premature infants requires prolonged infusion of prostaglandins to maintain perfusion in the abdomen and lower extremities. Both surgery and angioplasty prove to be effective in the treatment of native coarctation, but the latter is associated over the long term with more complications, such as recoarctation and the formation of aneurysms.1 Despite the improvement in the results of the surgical treatment of coarctation, prematurity is perceived as a risk factor for morbidity and mortality; in 2 different studies,2,3 the rate of acute mortality was reported to be 5.5% to 12.5%, whereas late mortality ranged between 8.3% and 11%. Moreover, the authors observed recoarctation in 29% and 44% of the treated patients. Experience with angioplasty in premature infants is limited. In a review4 dealing with premature infants weighing less than 1500 grams, four of them with coarctation required six procedures, and two had to undergo surgery to treat recoarctation. There was one death that was not related to the procedure. Other articles involve case reports5,6; the smaller of the 2 children described to was a premature infant weighing 460 grams. Both cases were treated successfully, but neither of them involved access via the carotid artery, as we performed in our patient. Angioplasty in premature infants with aortic coarctation is, in our opinion, a treatment that can improve the serious clinical condition of these patients. We consider that access via the carotid artery not only permits easy vascular access, but is a safe technique as well. Fredy Prada, Juan Carretero, Carlos Mortera, and Daniel Velasco
Servicio de Cardiología, Hospital Sant Joan de Deu, Barcelona, Spain
references
1. Fiore AC, Fischer LK, Schwartz T, Jureidini S, Balfour I, Carpenter D, et al. Comparison of angioplasty and surgery for neonatal aortic coarctation. Ann Thorac Surg. 2005;80:165964. 2. Bacha EA, Almodovar M, Wessel DL, Zurakowski D, Mayer JE Jr, Jonas RA, et al. Surgery for coarctation of the aorta in infants weighing less than 2 kg. Ann Thorac Surg. 2001;71:1260-4.
3. Sudarshan CD, Cochrane AD, Jun ZH, Soto R, Brizard CP. Repair of coarctation of the aorta in infants weighing less than 2 kilograms. Ann Thorac Surg. 2006;82:158-63. 4. Sutton N, Lock JE, Geggel RL. Cardiac catheterization in infants weighing less than 1,500 grams. Catheter Cardiovasc Interv. 2006;68:948-56. 5. McMahon CJ, Alromani A, Nihill MR. Balloon angioplasty of critical coarctation in a 970-gram premature infant. Cardiol Young. 2001;11:468-71. 6. Schamberger MS, Lababidi ZA. Successful balloon angioplasty of a coarctation in an infant <500 g. Pediatr Cardiol. 1998;19:418-9.
Giant Coronary Artery Fistula Between the Left Main Coronary and the Superior Vena Cava Complicated by Coronary Artery Dissection To the Editor, Coronary fistulas are connections between the coronary arteries and another cavity. They are generally congenital and are due to a defect in the compacting of the myocardium during embryonic development. This persistent primitive vascular pattern can connect the coronary arteries with the ventricular cavities or other vascular structures. The most common type is that which originates in the right coronary artery and drains into the right-sided chambers, followed by fistulas between branches of the left coronary artery and the pulmonary artery.1 These conditions are rare and are mainly associated with a risk of myocardial ischemia (steal phenomenon), heart failure (volume overload, pulmonary hypertension), rupture or dissection, endocarditis and arrhythmias.2 The patient was a 41-year-old man with no known cardiovascular risk factors or family history of heart disease. He was admitted with tightness in the middle of his chest that appeared with moderate exertion, accompanied by other characteristic symptoms of physical discomfort affecting vegetative functions (pallor, perspiration, nausea/vomiting, etc). The electrocardiogram revealed an inferior subepicardial lesion with ST segment depression in right precordial leads and aVL. The administration of sublingual nitroglycerine relieved the pain. Emergency coronary angiography revealed a giant coronary fistula (12 mm in diameter) connecting the origin of the left main coronary artery (LMCA) with superior vena cava prior to its entry into the right atrium. There was highly developed dilation of the LMCA and circumflex artery, with a lesion of 60% in the distal obtuse marginal branch. The ejection fraction was 75%. The observation of a translucent Rev Esp Cardiol. 2010;63(6):740-50 743