World Journal for Pediatric and Congenital Heart Surgery http://pch.sagepub.com/
Laubry-Pezzi Syndrome With Aortic Root Dilatation Treated With a Bentall and De Bono Procedure Efrén Martínez-Quintana, Fayna Rodríguez-González and María Jesús López-Gude World Journal for Pediatric and Congenital Heart Surgery 2013 4: 299 DOI: 10.1177/2150135113484160 The online version of this article can be found at: http://pch.sagepub.com/content/4/3/299
Published by: http://www.sagepublications.com
On behalf of:
World Society for Pediatric and Congential Heart Surgery
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Case Report
Laubry-Pezzi Syndrome With Aortic Root Dilatation Treated With a Bentall and De Bono Procedure
World Journal for Pediatric and Congenital Heart Surgery 4(3) 299-301 ª The Author(s) 2013 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/2150135113484160 pch.sagepub.com
Efre´n Martı´nez-Quintana, MD, PhD1, Fayna Rodrı´guez-Gonza´lez, MD2, and Marı´a Jesu´s Lo´pez-Gude, MD3
Abstract Laubry-Pezzi syndrome is a clinical entity in which prolapse of an aortic valve cusp into a subjacent ventricular septal defect (VSD) due to Venturi effect results in progressive aortic valve insufficiency. Aortic valve prolapse is found in over 5% of children with VSDs, most commonly in association with supracristal VSDs, and the risk of development of aortic regurgitation increases during childhood, peaking at 5 to 10 years of age. The VSD closure eliminates the low-pressure zone that is the cause of ongoing aortic valve cusp deformity and, if performed early, prevents the development of aortic regurgitation. However, the management of this rare pathology is still a matter of some debate with respect to indications, operative techniques, and timing. We report the case of a patient with Laubry-Pezzi syndrome, originally operated on at six years of age for VSD closure and plasty between the left and the right aortic cusps. However, in the follow–up the patient developed severe aortic regurgitation and aortic root dilatation. Eventually, a Bentall and De Bono procedure was performed. Keywords Laubry, valvuloplasty, regurgitation, aortic valve, aorta Submitted November 5, 2012; Accepted March 5, 2013.
Introduction In 1921, Laubry and Pezzi described a case of a patient with ventricular septal defect (VSD) and aortic insufficiency due to aortic valve prolapse.1 Anatomically, such findings usually involve the right coronary cusp and sinus in relation to a lack of leaflet support due to a supracristal VSD. Surgical closure of the VSD is indicated in patients with associated progressive aortic regurgitation, because VSD closure eliminates the lowpressure zone that is the cause of ongoing aortic valve cusp deformity and, if performed early, prevents the development of aortic regurgitation. Aortic valvuloplasty can be considered in selected patients with aortic cusp prolapse and regurgitation of moderate or greater degree in an attempt to avoid the need for eventual prosthetic aortic valve implantation.2
Case Report We present the case of a 23-year-old male patient who presented with New York Heart Association functional class III/ IV symptoms and a medical history of arterial hypertension, smoking habit, and Laubry-Pezzi syndrome operated on at six years of age. Findings at the original cardiac surgery included a tricuspid aortic valve with prolapse of the right aortic cusp
through the VSD, which was moderately large and was situated just below the right coronary cusp, extending between the right and the noncoronary cusps in a perimembranous position. There was severe aortic regurgitation and no aortic root dilatation. The VSD was closed with a synthetic patch, and a plasty between the left and the right cusps of the aortic valve was performed without significant aortic regurgitation after the initial repair. When the patient presented at 23 years of age, clinical examination evidenced a holodiastolic murmur in the right parasternal location. Echocardiogram showed bicuspid morphology of the aortic valve, with severe aortic regurgitation and mild stenosis. Computed tomography revealed an asymmetric 1 Complejo Hospitalario Universitario Insular-Materno Infantil, Las Palmas de Gran Canaria, Spain 2 Hospital Universitario de Gran Canaria Dr Negrı´n, Las Palmas de Gran Canaria, Spain 3 Hospital Universitario 12 de Octubre, Madrid, Spain
Corresponding Author: Efre´n Martı´nez-Quintana, Complejo Hospitalario Universitario Insular-Materno Infantil, Alcalde Ramı´rez Bethencourt 10, 3-A, Las Palmas de Gran Canaria 35003, Spain. Email: [email protected]
Downloaded from pch.sagepub.com at MEMORIAL UNIV OF NEWFOUNDLAND on November 25, 2014
300
World Journal for Pediatric and Congenital Heart Surgery 4(3)
Figure 1. A, Axial computed tomography view showing a dilated aortic root with a tricuspid aortic valve with asymmetrical cusps (arrowhead). B, Three-dimensional computed tomographic scan reconstruction of the aorta showing ascending aortic dilatation.
(Figure 2). Because the patient had neither congenitally bicuspid aortic valve nor a known connective tissue disease (such as Marfan syndrome), histological studies were not performed on resected aortic wall.
Discussion
Figure 2. Intraoperative image showing a tricuspid aortic valve, rendered functionally bicuspid, in relation to a previous commissural plasty between the right and the left coronary leaflets (arrowhead) with sutures supported on the ventricular septal patch.
tricuspid aortic valve (Figure 1A) and a significant dilation of the aortic root (48 mm) and ascending aorta (43 mm; Figure 1B). Angiography showed normal coronary arteries with no residual VSD and an aortic root diameter of 50 mm. Due to his functional class and the presence of severe aortic regurgitation with dilation of the aortic root, a Bentall and De Bono procedure was performed using a mechanical valved conduit (St Jude Medical, Inc, St Paul, Minnesota). During the operation, a tricuspid aortic valve, which had been rendered functionally bicuspid as a result of the previous commissural plasty, was observed. The previous surgery had resulted in fusion between the right and the left coronary leaflets with sutures supported on the VSD patch. In addition, prolapse of the noncoronary cusp was seen
The Laubry-Pezzi syndrome is characterized by prolapse of an aortic valve cusp into a subjacent VSD due to Venturi effect, resulting in progressive aortic valve insufficiency. Lack of continuity between the ventricular septum and the aortic sinus accounts for the deficiency of support for the aortic valve apparatus. Anatomically, this lack of support beneath the right coronary/noncoronary commissure, seen mostly in the setting supracristal VSDs, allows the adjacent margins of the cusps to prolapse, predisposing to aortic regurgitation. Meanwhile, the restrictive and high-velocity shunting through the VSD creates a low-pressure zone that impacts the adjacent aortic valve cusp, resulting in aortic valve prolapse and subsequent aortic regurgitation, even more if one considers the pronounced form and size asymmetry of the valve cusps found in this syndrome.3,4 One might speculate that loss of continuity between the media and the annulus of the aortic valve may produce inherent weakness of this area, with a tendency for progressive dilatation of the sinus, especially if there are associated factors such as male gender5 or long-standing volume overload in relation to chronic aortic regurgitation. These findings, similar to those described in patients with aneurysms of the sinus of Valsalva (in whom the media of the aortic sinus fails to reach the aortic annulus6) may aggravate the anatomic and functional abnormalities found in this syndrome, which are essentially progressive in nature. In the view of these data, it is plausible to suggest that Laubry-Pezzi syndrome may eventually lead to a malformation
Downloaded from pch.sagepub.com at MEMORIAL UNIV OF NEWFOUNDLAND on November 25, 2014
Martı´nez-Quintana et al
301
that simultaneously combines the anomalies in the truncal (sigmoid valves) and the conal (conal septum or crista supraventricularis) structures with compromise of the ascending aorta as seen in other congenital heart diseases such as the single ventricle, truncus arteriosus communis, transposition of the great arteries, tetralogy of Fallot, bicuspid aortic valve, or the Marfan syndrome, which, in varying degrees, associate aortic media abnormalities and eventual and progressive aortic root dilatation.7,8 In the present case, the initial surgical management of the incompetent aortic valve was somewhat unconventional. Bicuspidization of a tricuspid aortic valve is not a common form of repair, because even extreme prolapse and leaflet stretching can usually be treated by a reduction in the free edge of the coronary cusp9 by the placement of plicating sutures in the prolapsing leaflet in combination with closure of the VSD, thus elevating the annulus, reducing the size of the sinus, and restoring competence of the aortic valve.10 It is possible, however, in more advanced cases that secondary changes in the form of thickening, asymmetry (size discrepancy among leaflets), and retraction of the free borders of all three cusps may hamper a conventional correction. Although we might be tempted to suggest that patients with Laubry-Pezzi syndrome with aortic dilatation be subjected to a program of follow-up similar to that which is prescribed for patients with bicuspid aortic valve or patients with aneurysms of the sinus of Valsalva, we recognize that Laubry-Pezzi syndrome represents a distinct clinical entity, for which there is no evidence at the present time of abnormal histology or elastic properties of the ascending aortic wall. Certainly, those who may encounter cases such as ours should be motivated to undertake histologic evaluation of aortic wall and aortic sinus tissue. In addition, we believe that larger scale investigations and longitudinal studies should be undertaken to confirm whether the findings observed in our patient are unique, or whether they have been seen late in the course in other patients who present initially with the combination of VSD and aortic valve prolapse. Authors’ Note This manuscript has not been submitted for publication nor has it been published in whole or in part elsewhere. We attest to the fact that all authors listed on the title page have contributed significantly to the work, have read the manuscript, attest to the validity, and legitimacy of the data and its interpretation. The authors of this manuscript have also certified that they comply with the Principles of Ethical Publishing.
Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Laubry C, Pezzi C. Traite´ des maladies conge´nitales du coeur. Paris: JB Bailliere; 1921. Quoted by Labury C, Routier D, Soulie P. Les souffles de la maladie de Roger. Rev Med Paris. 1933;50: 439-448. 2. Kostolny M, Schreiber C, von Arnim V, Vogt M, Wottke M, Lange R. Timing of repair in ventricular septal defect with aortic insufficiency. Thorac Cardiovasc Surg. 2006;54(8): 512-515. 3. Dykukha SE, Zakharova VV, Osadchiı˘ AI. Anatomical characteristics of the aortic valve in Laubry-Pezzi anomaly. Klin Khir. 1994;(7): 41-44. 4. Tomita H, Arakaki Y, Ono Y, Yamada O, Yagihara T, Echigo S. Impact of noncoronary cusp prolapse in addition to right coronary cusp prolapse in patients with a perimembranous ventricular septal defect. Int J Cardiol. 2005;101(2): 279-283. 5. Sonesson B, La¨nne T, Vernersson E, Hansen F. Sex difference in the mechanical properties of the abdominal aorta in human beings. J Vasc Surg. 1994;20(6): 959-969. 6. Sakakibara S, Konno S. Congenital aneurysrn of the sinus of Valsalva: anatomy and classification. Am Heart J. 1962;63: 405-424. 7. Niwa K, Perloff JK, Bhuta SM, et al. Structural abnormalities of great arterial walls in congenital heart disease. Light and electron microscopic analyses. Circulation. 2001;103(3): 393-400. 8. Bonderman D, Gharehbaghi-Schnell E, Wollenek G, Maurer G, Baumgartner H, Lang IM. Mechanisms underlying aortic dilatation in congenital aortic valve malformation. Circulation. 1999; 99(16): 2138-2143. 9. Brizard C. Surgical repair of infundibular ventricular septal defect and aortic regurgitation. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2006:153-160. 10. Yacoub MH, Khan H, Stavri G, Shinebourne E, Radley-Smith R. Anatomic correction of the syndrome of prolapsing right coronary aortic cusp, dilatation of the sinus of Valsalva, and ventricular septal defect. J Thorac Cardiovasc Surg. 1997;113(2): 253-260; discussion 261.
Downloaded from pch.sagepub.com at MEMORIAL UNIV OF NEWFOUNDLAND on November 25, 2014
Laubry-Pezzi Syndrome With Aortic Root Dilatation Treated With a Bentall and De Bono Procedure Efrén Martínez-Quintana, Fayna Rodríguez-González and María Jesús López-Gude World Journal for Pediatric and Congenital Heart Surgery 2013 4: 299 DOI: 10.1177/2150135113484160 The online version of this article can be found at: http://pch.sagepub.com/content/4/3/299
Published by: http://www.sagepublications.com
On behalf of:
World Society for Pediatric and Congential Heart Surgery
Additional services and information for World Journal for Pediatric and Congenital Heart Surgery can be found at: Email Alerts: http://pch.sagepub.com/cgi/alerts Subscriptions: http://pch.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav
>> Version of Record - Jul 3, 2013 What is This?
Downloaded from pch.sagepub.com at MEMORIAL UNIV OF NEWFOUNDLAND on November 25, 2014
Case Report
Laubry-Pezzi Syndrome With Aortic Root Dilatation Treated With a Bentall and De Bono Procedure
World Journal for Pediatric and Congenital Heart Surgery 4(3) 299-301 ª The Author(s) 2013 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/2150135113484160 pch.sagepub.com
Efre´n Martı´nez-Quintana, MD, PhD1, Fayna Rodrı´guez-Gonza´lez, MD2, and Marı´a Jesu´s Lo´pez-Gude, MD3
Abstract Laubry-Pezzi syndrome is a clinical entity in which prolapse of an aortic valve cusp into a subjacent ventricular septal defect (VSD) due to Venturi effect results in progressive aortic valve insufficiency. Aortic valve prolapse is found in over 5% of children with VSDs, most commonly in association with supracristal VSDs, and the risk of development of aortic regurgitation increases during childhood, peaking at 5 to 10 years of age. The VSD closure eliminates the low-pressure zone that is the cause of ongoing aortic valve cusp deformity and, if performed early, prevents the development of aortic regurgitation. However, the management of this rare pathology is still a matter of some debate with respect to indications, operative techniques, and timing. We report the case of a patient with Laubry-Pezzi syndrome, originally operated on at six years of age for VSD closure and plasty between the left and the right aortic cusps. However, in the follow–up the patient developed severe aortic regurgitation and aortic root dilatation. Eventually, a Bentall and De Bono procedure was performed. Keywords Laubry, valvuloplasty, regurgitation, aortic valve, aorta Submitted November 5, 2012; Accepted March 5, 2013.
Introduction In 1921, Laubry and Pezzi described a case of a patient with ventricular septal defect (VSD) and aortic insufficiency due to aortic valve prolapse.1 Anatomically, such findings usually involve the right coronary cusp and sinus in relation to a lack of leaflet support due to a supracristal VSD. Surgical closure of the VSD is indicated in patients with associated progressive aortic regurgitation, because VSD closure eliminates the lowpressure zone that is the cause of ongoing aortic valve cusp deformity and, if performed early, prevents the development of aortic regurgitation. Aortic valvuloplasty can be considered in selected patients with aortic cusp prolapse and regurgitation of moderate or greater degree in an attempt to avoid the need for eventual prosthetic aortic valve implantation.2
Case Report We present the case of a 23-year-old male patient who presented with New York Heart Association functional class III/ IV symptoms and a medical history of arterial hypertension, smoking habit, and Laubry-Pezzi syndrome operated on at six years of age. Findings at the original cardiac surgery included a tricuspid aortic valve with prolapse of the right aortic cusp
through the VSD, which was moderately large and was situated just below the right coronary cusp, extending between the right and the noncoronary cusps in a perimembranous position. There was severe aortic regurgitation and no aortic root dilatation. The VSD was closed with a synthetic patch, and a plasty between the left and the right cusps of the aortic valve was performed without significant aortic regurgitation after the initial repair. When the patient presented at 23 years of age, clinical examination evidenced a holodiastolic murmur in the right parasternal location. Echocardiogram showed bicuspid morphology of the aortic valve, with severe aortic regurgitation and mild stenosis. Computed tomography revealed an asymmetric 1 Complejo Hospitalario Universitario Insular-Materno Infantil, Las Palmas de Gran Canaria, Spain 2 Hospital Universitario de Gran Canaria Dr Negrı´n, Las Palmas de Gran Canaria, Spain 3 Hospital Universitario 12 de Octubre, Madrid, Spain
Corresponding Author: Efre´n Martı´nez-Quintana, Complejo Hospitalario Universitario Insular-Materno Infantil, Alcalde Ramı´rez Bethencourt 10, 3-A, Las Palmas de Gran Canaria 35003, Spain. Email: [email protected]
Downloaded from pch.sagepub.com at MEMORIAL UNIV OF NEWFOUNDLAND on November 25, 2014
300
World Journal for Pediatric and Congenital Heart Surgery 4(3)
Figure 1. A, Axial computed tomography view showing a dilated aortic root with a tricuspid aortic valve with asymmetrical cusps (arrowhead). B, Three-dimensional computed tomographic scan reconstruction of the aorta showing ascending aortic dilatation.
(Figure 2). Because the patient had neither congenitally bicuspid aortic valve nor a known connective tissue disease (such as Marfan syndrome), histological studies were not performed on resected aortic wall.
Discussion
Figure 2. Intraoperative image showing a tricuspid aortic valve, rendered functionally bicuspid, in relation to a previous commissural plasty between the right and the left coronary leaflets (arrowhead) with sutures supported on the ventricular septal patch.
tricuspid aortic valve (Figure 1A) and a significant dilation of the aortic root (48 mm) and ascending aorta (43 mm; Figure 1B). Angiography showed normal coronary arteries with no residual VSD and an aortic root diameter of 50 mm. Due to his functional class and the presence of severe aortic regurgitation with dilation of the aortic root, a Bentall and De Bono procedure was performed using a mechanical valved conduit (St Jude Medical, Inc, St Paul, Minnesota). During the operation, a tricuspid aortic valve, which had been rendered functionally bicuspid as a result of the previous commissural plasty, was observed. The previous surgery had resulted in fusion between the right and the left coronary leaflets with sutures supported on the VSD patch. In addition, prolapse of the noncoronary cusp was seen
The Laubry-Pezzi syndrome is characterized by prolapse of an aortic valve cusp into a subjacent VSD due to Venturi effect, resulting in progressive aortic valve insufficiency. Lack of continuity between the ventricular septum and the aortic sinus accounts for the deficiency of support for the aortic valve apparatus. Anatomically, this lack of support beneath the right coronary/noncoronary commissure, seen mostly in the setting supracristal VSDs, allows the adjacent margins of the cusps to prolapse, predisposing to aortic regurgitation. Meanwhile, the restrictive and high-velocity shunting through the VSD creates a low-pressure zone that impacts the adjacent aortic valve cusp, resulting in aortic valve prolapse and subsequent aortic regurgitation, even more if one considers the pronounced form and size asymmetry of the valve cusps found in this syndrome.3,4 One might speculate that loss of continuity between the media and the annulus of the aortic valve may produce inherent weakness of this area, with a tendency for progressive dilatation of the sinus, especially if there are associated factors such as male gender5 or long-standing volume overload in relation to chronic aortic regurgitation. These findings, similar to those described in patients with aneurysms of the sinus of Valsalva (in whom the media of the aortic sinus fails to reach the aortic annulus6) may aggravate the anatomic and functional abnormalities found in this syndrome, which are essentially progressive in nature. In the view of these data, it is plausible to suggest that Laubry-Pezzi syndrome may eventually lead to a malformation
Downloaded from pch.sagepub.com at MEMORIAL UNIV OF NEWFOUNDLAND on November 25, 2014
Martı´nez-Quintana et al
301
that simultaneously combines the anomalies in the truncal (sigmoid valves) and the conal (conal septum or crista supraventricularis) structures with compromise of the ascending aorta as seen in other congenital heart diseases such as the single ventricle, truncus arteriosus communis, transposition of the great arteries, tetralogy of Fallot, bicuspid aortic valve, or the Marfan syndrome, which, in varying degrees, associate aortic media abnormalities and eventual and progressive aortic root dilatation.7,8 In the present case, the initial surgical management of the incompetent aortic valve was somewhat unconventional. Bicuspidization of a tricuspid aortic valve is not a common form of repair, because even extreme prolapse and leaflet stretching can usually be treated by a reduction in the free edge of the coronary cusp9 by the placement of plicating sutures in the prolapsing leaflet in combination with closure of the VSD, thus elevating the annulus, reducing the size of the sinus, and restoring competence of the aortic valve.10 It is possible, however, in more advanced cases that secondary changes in the form of thickening, asymmetry (size discrepancy among leaflets), and retraction of the free borders of all three cusps may hamper a conventional correction. Although we might be tempted to suggest that patients with Laubry-Pezzi syndrome with aortic dilatation be subjected to a program of follow-up similar to that which is prescribed for patients with bicuspid aortic valve or patients with aneurysms of the sinus of Valsalva, we recognize that Laubry-Pezzi syndrome represents a distinct clinical entity, for which there is no evidence at the present time of abnormal histology or elastic properties of the ascending aortic wall. Certainly, those who may encounter cases such as ours should be motivated to undertake histologic evaluation of aortic wall and aortic sinus tissue. In addition, we believe that larger scale investigations and longitudinal studies should be undertaken to confirm whether the findings observed in our patient are unique, or whether they have been seen late in the course in other patients who present initially with the combination of VSD and aortic valve prolapse. Authors’ Note This manuscript has not been submitted for publication nor has it been published in whole or in part elsewhere. We attest to the fact that all authors listed on the title page have contributed significantly to the work, have read the manuscript, attest to the validity, and legitimacy of the data and its interpretation. The authors of this manuscript have also certified that they comply with the Principles of Ethical Publishing.
Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Laubry C, Pezzi C. Traite´ des maladies conge´nitales du coeur. Paris: JB Bailliere; 1921. Quoted by Labury C, Routier D, Soulie P. Les souffles de la maladie de Roger. Rev Med Paris. 1933;50: 439-448. 2. Kostolny M, Schreiber C, von Arnim V, Vogt M, Wottke M, Lange R. Timing of repair in ventricular septal defect with aortic insufficiency. Thorac Cardiovasc Surg. 2006;54(8): 512-515. 3. Dykukha SE, Zakharova VV, Osadchiı˘ AI. Anatomical characteristics of the aortic valve in Laubry-Pezzi anomaly. Klin Khir. 1994;(7): 41-44. 4. Tomita H, Arakaki Y, Ono Y, Yamada O, Yagihara T, Echigo S. Impact of noncoronary cusp prolapse in addition to right coronary cusp prolapse in patients with a perimembranous ventricular septal defect. Int J Cardiol. 2005;101(2): 279-283. 5. Sonesson B, La¨nne T, Vernersson E, Hansen F. Sex difference in the mechanical properties of the abdominal aorta in human beings. J Vasc Surg. 1994;20(6): 959-969. 6. Sakakibara S, Konno S. Congenital aneurysrn of the sinus of Valsalva: anatomy and classification. Am Heart J. 1962;63: 405-424. 7. Niwa K, Perloff JK, Bhuta SM, et al. Structural abnormalities of great arterial walls in congenital heart disease. Light and electron microscopic analyses. Circulation. 2001;103(3): 393-400. 8. Bonderman D, Gharehbaghi-Schnell E, Wollenek G, Maurer G, Baumgartner H, Lang IM. Mechanisms underlying aortic dilatation in congenital aortic valve malformation. Circulation. 1999; 99(16): 2138-2143. 9. Brizard C. Surgical repair of infundibular ventricular septal defect and aortic regurgitation. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2006:153-160. 10. Yacoub MH, Khan H, Stavri G, Shinebourne E, Radley-Smith R. Anatomic correction of the syndrome of prolapsing right coronary aortic cusp, dilatation of the sinus of Valsalva, and ventricular septal defect. J Thorac Cardiovasc Surg. 1997;113(2): 253-260; discussion 261.
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