- Email: [email protected]
Congenital Mitral Disease: Anomalous Mitral Arcade in a Young Man
Ann Thorac Surg 2010;89:629 –31
We would like to thank Alexander Filatov, MD, Gabriel Levi, MD, Chunkeun Oh, MD, and Edward Machernis, MD for their contribution in the surgical pathology consultation.
References 1. McDonnell PJ, Mann RB, Bulkley BH. Involvement of the heart by malignant lymphoma. A clinicopathologic study. Cancer 1982;49:944 –51. 2. McAllister HA, Fenoglio JJ. In: Tumors of the cardiovascular system: atlas of tumor pathology, 2nd series, fasicle 15. Washington, DC: Armed Forces Institute of Pathology, 1978: 99 –102. 3. Ceresoli GL, Ferreri AJ, Eraldo B, Ripa C, Ponzoni M, Villa E. Primary cardiac lymphoma in immunocompetent patients: diagnostic and therapeutic management. Cancer 1997;80: 1497–506. 4. Curtsinger CR, Wilson MJ, Yoneda K. Primary cardiac lymphoma. Cancer 1989;64:521–5. 5. Terracciano LM, Mhaweck P, Suess K, et al. Calretinin as a marker for cardiac myxoma. Diagnostic and histogenetic considerations. Am J Clin Pathol 2000;114:754 –9. © 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
629
Congenital Mitral Disease: Anomalous Mitral Arcade in a Young Man Duccio Federici, MD, Elisabetta Palmerini, MD, Matteo Lisi, MD, Luca Centola, MD, Mario Chiavarelli, MD, and Sergio Mondillo, MD Department of Cardiovascular Diseases, University of Siena, Italy
We present the case of a 33-year-old man referred to our institution with a diagnosis of severe mitral valvular stenosis and insufficiency. We realized the valvular disease was due to an “anomalous mitral arcade,” a rare congenital malformation of the mitral tensor apparatus characterized by enlarged papillary muscles connected to mitral leaflets by a typical fibrous tissue bridge. This arrangement creates a fibrous continuity between valvular and subvalvular apparatus. The reported echocardiographic images shows in detail the anatomic and functional features of this rare condition. (Ann Thorac Surg 2010;89:629 –31) © 2010 by The Society of Thoracic Surgeons
A
nomalous mitral arcade is a rare congenital malformation of the mitral valve and of its tensor apparatus that was first described by Layman Edwards [1] in 1967. This anomaly is characterized by enlarged and elongated papillary muscles connected to each other and to the free edge of the anterior mitral leaflet by a bridge of fibrous tissue. The lack of interposition of chordae between the fibrous bridge and anterior leaflet creates a fibrous continuity that restricts valvular motion and prevents normal leaflets apposition. Generally, posterior leaflet chordae arise from the apices of papillary muscles. These may appear as few, short, and dysplastic; however, the posterior leaflet mobility is usually preserved. The natural history of the malformation is characterized by progressive worsening of valvular regurgitation or stenosis, or both. A patient who reaches adulthood usually undergoes mitral valve repair or replacement [2]. A 33-year-old man was admitted to our institution with evidence of effort dyspnea (New York Heart Association functional class II) and atrial fibrillation. We also appreciated an apical systolic murmur (grade 3/6) that had been casually diagnosed when the patient was 12 years old (grade 2/6). There was no history of tonsillitis or rheumatic fever. The first echocardiographic assessment was performed at the age of 20 when the patient was still asymptomatic, and posed the diagnosis of moderate mitral regurgitation associated with a mild grade of stenosis without evidence of rheumatic calcification. At the age of 32, an echocardiogram was repeated because Accepted for publication July 21, 2009. Address correspondence to Dr Federici, University Hospital, “S. Maria alle Scotte” viale Bracci n.2, Siena, 53100, Italy; e-mail: [email protected].
0003-4975/10/$36.00 doi:10.1016/j.athoracsur.2009.07.070
FEATURE ARTICLES
additional point of interest is the identification of a CD20, Ki-67, and CD10 large, B-cell lymphoma with anaplastic cytologic features inside of an atrial myxoma. A B-cell lymphoma presenting as a primary cardiac tumor, and arising in an atrial myxoma has not been previously described. A unique aspect of this case is the intimate association of the malignant lymphoid cells with an atrial myxoma, without cardiac wall invasion. Previous studies have showed that calretinin is a reliable marker for the diagnosis of cardiac myxoma, useful for the differential diagnosis with the most challenging entities, such as mural thrombus with myxoid changes [5]. There are two possible explanations for how this lesion developed. The neoplastic process may have arisen within and remained localized to the previously formed atrial myxoma, with growth and invasion limited by atrial cavity flow. Alternatively, a primary lymphoma remote from the heart and clinically occult seeded an existing atrial myxoma. An extensive subsequent workup failed to demonstrate a distant focus of lymphoma, suggesting the lymphoma arose primarily in the myxoma. Primary cardiac lymphomas in nonimmunocompromised individuals are exceedingly rare. Before 1987 there were only 20 reported cases of primary cardiac lymphomas in the English language literature. Since 1987, there has been a significant increase in the presence of this lesion associated with immunosuppression, both in individuals iatrogenically immunosuppressed for solid organ transplantation and in patients positive for human immunodeficiency virus or acquired immunodeficiency syndrome. Most patients with a primary cardiac lymphoma have an acute clinical course in onset with a rapid demise. Early diagnosis may best be made by echocardiography. Combined chemotherapy and radiation therapy may be appropriate in the early stages. Our patient may have reasonable prognosis due to the early detection of his primary cardiac lymphoma.
CASE REPORT FEDERICI ET AL ANOMALOUS MITRAL ARCADE
630
CASE REPORT FEDERICI ET AL ANOMALOUS MITRAL ARCADE
Fig 1. Transthoracic short-axis view shows the arc-like configuration of both papillary muscles (P) with a fibrous tissue bridge (FB) connecting them with the mitral leaflets. (LV ⫽ left ventricle.)
FEATURE ARTICLES
of the onset of effort dyspnea. This study, performed in another institution, showed severe mitral regurgitation associated with moderate grade of stenosis. At admission to our institution 1 year later, the patient was in atrial fibrillation and was referred for worsening effort dyspnea. The echocardiographic evaluation performed in our department confirmed a severe mitral insufficiency with moderate valvular stenosis and left atrial enlargement without signs of rheumatic degeneration. The subvalvular mitral apparatus showed an “arclike” configuration formed by enlarged papillary muscles and a characteristic fibrous tissue bridge connecting the muscles to each other and to the free edge of the anterior mitral leaflet (Fig 1). The posterior leaflet also showed a fibrous continuity with the fibrous bridge without interposition of chordae (Fig 2); this aspect represents a discordant feature from the usual manifestation of the anomaly. The resulting restriction in the motion of the anterior mitral leaflet caused severe valvular regurgitation by lack of coaptation and moderate degree of stenosis. Therefore, we made the diagnosis of anomalous mitral arcade. The patient was referred to the cardiac surgeon and underwent mitral valve repair after surgical confirmation of echocardiographic diagnosis. The repair consisted of posteromedial papillary splitting, interposition of 2 artiFig 3. Postoperative echocardiographic evaluation in (A) short axis and (B) apical 4-chamber views. The fibrous bridge was removed, the posteromedial papillary muscle (PPM) was split, and 2 artificial polytetrafluoroethylene chordae were positioned at the P1 level (*). A complete mitral annuloplasty ring (AR) completed the repair, with an excellent result. (LA ⫽ left atrium; LV ⫽ left ventricle; P ⫽ papillary muscles.)
Ann Thorac Surg 2010;89:629 –31
Fig 2. Transthoracic apical 2-chamber view shows the direct fibrous tissue bridge (FB) continuity between the leaflets and the papillary muscles (P). (LA ⫽ left atrium; LV ⫽ left ventricle.)
ficial polytetrafluoroethylene chordae (Gore-Tex, W. L. Gore and Associates, Flagstaff, AZ) at the P1 level after resection of an anterior papillary head and removal of fibrous tissue, and finally, application of complete mitral annuloplasty ring (Sovering No. 38, Sorin Biomedica, Italy). The procedure was successful. The patient’s postoperative course was uneventful. An echocardiogram on postoperative day 4 showed normal mitral leaflets coaptation and no residual regurgitation (Fig 3). The patient was promptly discharged from the hospital with bisoprolol and warfarin therapy.
Comment Since the first description of this mitral anomaly in 1967, 14 cases have been reported. Most were detected when the patients were aged younger than 3 years. To date, only 3 adult patients have been described [3–5]. In this report we present a 33-year-old man in whom we evidenced the presence of an anomalous mitral arcade characterized by the typical arc-like configuration of subvalvular tensor apparatus causing restrictive motion of mitral leaflets. Of all reported cases to date, only 2 were diagnosed preoperatively by echocardiography; here we present a preoperative echocardiographic eval-
Ann Thorac Surg 2010;89:631–3
References 1. Layman TE, Edwards JE. Anomalous mitral arcade: a type of congenital mitral insufficiency. Circulation 1967;35:389 –95. 2. Castaneda AR, Anderson RC, Edwards JE. Congenital mitral stenosis resulting from anomalous arcade and obstructing papillary muscles: report of correction by use of ball valve prosthesis. Am J Cardiol 1969;24:237– 40. 3. Kim SJ, Shin ES, Park MK, Choi SH, Lee SG. Congenital mitral insufficiency caused by anomalous mitral arcade in an elderly patient. Circ J 2005;69:1560 – 63. 4. Peretz JA, Herzberg AJ, Reimer KA, Bashore TM. Congenital mitral insufficiency secondary to anomalous mitral arcade in an adult. Am Heart J 1987;114:894 –5. 5. Myers ML, Goldbach MM, Sears GA, Silver MD. Anomalous mitral arcade: a rare cause of mitral valve disease in an adult. Can J Cardiol 1987;3:60 –2.
Radical Resection of the Superior Vena Cava Using the Contegra Bovine Jugular Vein Conduit
631
rior vena cava in 2 patients, with demonstrable patency of grafts at 12 months and 7 months postoperatively. (Ann Thorac Surg 2010;89:631–3) © 2010 by The Society of Thoracic Surgeons
R
esection of anterior mediastinal masses involving the superior vena cava (SVC) poses a challenge for the cardiothoracic surgeon. Often, these tumors are regarded as irresectable; however, potentially curative radical resection with SVC replacement is possible in selected patients. The choice of conduit for total SVC replacement is limited, and we describe the use of the Contegra graft (Medtronic Inc, Minneapolis, MN) in this setting.
Case Reports Patient 1 A 48-year-old woman with severe scleroderma and a progressively enlarging anterior mediastinal mass, presumed to be thymoma, was referred for surgical intervention. Infiltration of the mass into the SVC necessitated radical resection, and extended thymectomy was undertaken. Full right atrial to aortic cardiopulmonary bypass was instituted. The left and right brachiocephalic veins and the right atrium proximal to the cavoatrial junction were clamped and the anterior mediastinal mass and SVC excised en bloc. An 18-mm Contegra graft bovine jugular conduit was used for the reconstruction. The patient remains well, with a patent conduit demonstrable on computed tomography (CT) at 12 months.
Patient 2 A 73-year-old woman presented with superior vena caval obstruction (SVCO) secondary to malignant thymoma. After induction chemoradiation, CT (Fig 1) and magnetic resonance imaging showed a residual 7-cm anterior mediastinal mass filling the entire SVC from the confluence of the left and right brachiocephalic veins to the superior
Elizabeth Belcher, FRCS, PhD, Michael Dusmet, MD, and Mario Petrou, FRCS, PhD Departments of Thoracic Surgery and Adult Cardiac Surgery, Royal Brompton Hospital, London, United Kingdom
Radical resection of the superior vena cava poses a challenge for the cardiothoracic surgeon. The Contegra graft (Medtronic Inc, Minneapolis, MN), a biologic conduit comprising the valved segment of the bovine jugular vein, is established as a right ventricular to pulmonary artery conduit for right ventricular outflow tract repair in the pediatric population. We describe the use of the Contegra graft to facilitate radical resection and reconstruction of the supeAccepted for publication April 6, 2009. Address correspondence to Dr Petrou, Department of Adult Cardiac Surgery, Royal Brompton Hospital, Sydney St, London, SW3 6NP, United Kingdom; e-mail: [email protected].
© 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
Fig 1. Contrast computed tomography scan of the chest shows an anterior mediastinal mass in continuity with the superior vena cava, which has a filling defect (arrow) suggestive of direct tumor invasion or intraluminal thrombus. 0003-4975/10/$36.00 doi:10.1016/j.athoracsur.2009.04.146
FEATURE ARTICLES
uation showing in detail the anatomic and functional characteristics of the anomaly. Therefore, echocardiography is a valuable tool for the diagnosis of this congenital malformation by virtue of its noninvasiveness and easy reproducibility. Echocardiography may also be helpful for the cardiac surgeon in planning the operation mainly for the choice of the best reparative technique. A careful echocardiographic evaluation of mitral leaflets structure is essential in diagnosis of anomalous mitral arcade. In fact, the lack of commissural fusion and calcific degeneration along with the subvalvular arc-like configuration enables the physicians to recognize this anomaly among other causes of mitral disease. In conclusion, in all cases of mitral stenosis or insufficiency, mainly in people who have not a history of rheumatic disease, it would be appropriate to consider the possibility of an anomaly in the development of the mitral arcade.
CASE REPORT BELCHER ET AL CONTEGRA AS SVC CONDUIT
We would like to thank Alexander Filatov, MD, Gabriel Levi, MD, Chunkeun Oh, MD, and Edward Machernis, MD for their contribution in the surgical pathology consultation.
References 1. McDonnell PJ, Mann RB, Bulkley BH. Involvement of the heart by malignant lymphoma. A clinicopathologic study. Cancer 1982;49:944 –51. 2. McAllister HA, Fenoglio JJ. In: Tumors of the cardiovascular system: atlas of tumor pathology, 2nd series, fasicle 15. Washington, DC: Armed Forces Institute of Pathology, 1978: 99 –102. 3. Ceresoli GL, Ferreri AJ, Eraldo B, Ripa C, Ponzoni M, Villa E. Primary cardiac lymphoma in immunocompetent patients: diagnostic and therapeutic management. Cancer 1997;80: 1497–506. 4. Curtsinger CR, Wilson MJ, Yoneda K. Primary cardiac lymphoma. Cancer 1989;64:521–5. 5. Terracciano LM, Mhaweck P, Suess K, et al. Calretinin as a marker for cardiac myxoma. Diagnostic and histogenetic considerations. Am J Clin Pathol 2000;114:754 –9. © 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
629
Congenital Mitral Disease: Anomalous Mitral Arcade in a Young Man Duccio Federici, MD, Elisabetta Palmerini, MD, Matteo Lisi, MD, Luca Centola, MD, Mario Chiavarelli, MD, and Sergio Mondillo, MD Department of Cardiovascular Diseases, University of Siena, Italy
We present the case of a 33-year-old man referred to our institution with a diagnosis of severe mitral valvular stenosis and insufficiency. We realized the valvular disease was due to an “anomalous mitral arcade,” a rare congenital malformation of the mitral tensor apparatus characterized by enlarged papillary muscles connected to mitral leaflets by a typical fibrous tissue bridge. This arrangement creates a fibrous continuity between valvular and subvalvular apparatus. The reported echocardiographic images shows in detail the anatomic and functional features of this rare condition. (Ann Thorac Surg 2010;89:629 –31) © 2010 by The Society of Thoracic Surgeons
A
nomalous mitral arcade is a rare congenital malformation of the mitral valve and of its tensor apparatus that was first described by Layman Edwards [1] in 1967. This anomaly is characterized by enlarged and elongated papillary muscles connected to each other and to the free edge of the anterior mitral leaflet by a bridge of fibrous tissue. The lack of interposition of chordae between the fibrous bridge and anterior leaflet creates a fibrous continuity that restricts valvular motion and prevents normal leaflets apposition. Generally, posterior leaflet chordae arise from the apices of papillary muscles. These may appear as few, short, and dysplastic; however, the posterior leaflet mobility is usually preserved. The natural history of the malformation is characterized by progressive worsening of valvular regurgitation or stenosis, or both. A patient who reaches adulthood usually undergoes mitral valve repair or replacement [2]. A 33-year-old man was admitted to our institution with evidence of effort dyspnea (New York Heart Association functional class II) and atrial fibrillation. We also appreciated an apical systolic murmur (grade 3/6) that had been casually diagnosed when the patient was 12 years old (grade 2/6). There was no history of tonsillitis or rheumatic fever. The first echocardiographic assessment was performed at the age of 20 when the patient was still asymptomatic, and posed the diagnosis of moderate mitral regurgitation associated with a mild grade of stenosis without evidence of rheumatic calcification. At the age of 32, an echocardiogram was repeated because Accepted for publication July 21, 2009. Address correspondence to Dr Federici, University Hospital, “S. Maria alle Scotte” viale Bracci n.2, Siena, 53100, Italy; e-mail: [email protected].
0003-4975/10/$36.00 doi:10.1016/j.athoracsur.2009.07.070
FEATURE ARTICLES
additional point of interest is the identification of a CD20, Ki-67, and CD10 large, B-cell lymphoma with anaplastic cytologic features inside of an atrial myxoma. A B-cell lymphoma presenting as a primary cardiac tumor, and arising in an atrial myxoma has not been previously described. A unique aspect of this case is the intimate association of the malignant lymphoid cells with an atrial myxoma, without cardiac wall invasion. Previous studies have showed that calretinin is a reliable marker for the diagnosis of cardiac myxoma, useful for the differential diagnosis with the most challenging entities, such as mural thrombus with myxoid changes [5]. There are two possible explanations for how this lesion developed. The neoplastic process may have arisen within and remained localized to the previously formed atrial myxoma, with growth and invasion limited by atrial cavity flow. Alternatively, a primary lymphoma remote from the heart and clinically occult seeded an existing atrial myxoma. An extensive subsequent workup failed to demonstrate a distant focus of lymphoma, suggesting the lymphoma arose primarily in the myxoma. Primary cardiac lymphomas in nonimmunocompromised individuals are exceedingly rare. Before 1987 there were only 20 reported cases of primary cardiac lymphomas in the English language literature. Since 1987, there has been a significant increase in the presence of this lesion associated with immunosuppression, both in individuals iatrogenically immunosuppressed for solid organ transplantation and in patients positive for human immunodeficiency virus or acquired immunodeficiency syndrome. Most patients with a primary cardiac lymphoma have an acute clinical course in onset with a rapid demise. Early diagnosis may best be made by echocardiography. Combined chemotherapy and radiation therapy may be appropriate in the early stages. Our patient may have reasonable prognosis due to the early detection of his primary cardiac lymphoma.
CASE REPORT FEDERICI ET AL ANOMALOUS MITRAL ARCADE
630
CASE REPORT FEDERICI ET AL ANOMALOUS MITRAL ARCADE
Fig 1. Transthoracic short-axis view shows the arc-like configuration of both papillary muscles (P) with a fibrous tissue bridge (FB) connecting them with the mitral leaflets. (LV ⫽ left ventricle.)
FEATURE ARTICLES
of the onset of effort dyspnea. This study, performed in another institution, showed severe mitral regurgitation associated with moderate grade of stenosis. At admission to our institution 1 year later, the patient was in atrial fibrillation and was referred for worsening effort dyspnea. The echocardiographic evaluation performed in our department confirmed a severe mitral insufficiency with moderate valvular stenosis and left atrial enlargement without signs of rheumatic degeneration. The subvalvular mitral apparatus showed an “arclike” configuration formed by enlarged papillary muscles and a characteristic fibrous tissue bridge connecting the muscles to each other and to the free edge of the anterior mitral leaflet (Fig 1). The posterior leaflet also showed a fibrous continuity with the fibrous bridge without interposition of chordae (Fig 2); this aspect represents a discordant feature from the usual manifestation of the anomaly. The resulting restriction in the motion of the anterior mitral leaflet caused severe valvular regurgitation by lack of coaptation and moderate degree of stenosis. Therefore, we made the diagnosis of anomalous mitral arcade. The patient was referred to the cardiac surgeon and underwent mitral valve repair after surgical confirmation of echocardiographic diagnosis. The repair consisted of posteromedial papillary splitting, interposition of 2 artiFig 3. Postoperative echocardiographic evaluation in (A) short axis and (B) apical 4-chamber views. The fibrous bridge was removed, the posteromedial papillary muscle (PPM) was split, and 2 artificial polytetrafluoroethylene chordae were positioned at the P1 level (*). A complete mitral annuloplasty ring (AR) completed the repair, with an excellent result. (LA ⫽ left atrium; LV ⫽ left ventricle; P ⫽ papillary muscles.)
Ann Thorac Surg 2010;89:629 –31
Fig 2. Transthoracic apical 2-chamber view shows the direct fibrous tissue bridge (FB) continuity between the leaflets and the papillary muscles (P). (LA ⫽ left atrium; LV ⫽ left ventricle.)
ficial polytetrafluoroethylene chordae (Gore-Tex, W. L. Gore and Associates, Flagstaff, AZ) at the P1 level after resection of an anterior papillary head and removal of fibrous tissue, and finally, application of complete mitral annuloplasty ring (Sovering No. 38, Sorin Biomedica, Italy). The procedure was successful. The patient’s postoperative course was uneventful. An echocardiogram on postoperative day 4 showed normal mitral leaflets coaptation and no residual regurgitation (Fig 3). The patient was promptly discharged from the hospital with bisoprolol and warfarin therapy.
Comment Since the first description of this mitral anomaly in 1967, 14 cases have been reported. Most were detected when the patients were aged younger than 3 years. To date, only 3 adult patients have been described [3–5]. In this report we present a 33-year-old man in whom we evidenced the presence of an anomalous mitral arcade characterized by the typical arc-like configuration of subvalvular tensor apparatus causing restrictive motion of mitral leaflets. Of all reported cases to date, only 2 were diagnosed preoperatively by echocardiography; here we present a preoperative echocardiographic eval-
Ann Thorac Surg 2010;89:631–3
References 1. Layman TE, Edwards JE. Anomalous mitral arcade: a type of congenital mitral insufficiency. Circulation 1967;35:389 –95. 2. Castaneda AR, Anderson RC, Edwards JE. Congenital mitral stenosis resulting from anomalous arcade and obstructing papillary muscles: report of correction by use of ball valve prosthesis. Am J Cardiol 1969;24:237– 40. 3. Kim SJ, Shin ES, Park MK, Choi SH, Lee SG. Congenital mitral insufficiency caused by anomalous mitral arcade in an elderly patient. Circ J 2005;69:1560 – 63. 4. Peretz JA, Herzberg AJ, Reimer KA, Bashore TM. Congenital mitral insufficiency secondary to anomalous mitral arcade in an adult. Am Heart J 1987;114:894 –5. 5. Myers ML, Goldbach MM, Sears GA, Silver MD. Anomalous mitral arcade: a rare cause of mitral valve disease in an adult. Can J Cardiol 1987;3:60 –2.
Radical Resection of the Superior Vena Cava Using the Contegra Bovine Jugular Vein Conduit
631
rior vena cava in 2 patients, with demonstrable patency of grafts at 12 months and 7 months postoperatively. (Ann Thorac Surg 2010;89:631–3) © 2010 by The Society of Thoracic Surgeons
R
esection of anterior mediastinal masses involving the superior vena cava (SVC) poses a challenge for the cardiothoracic surgeon. Often, these tumors are regarded as irresectable; however, potentially curative radical resection with SVC replacement is possible in selected patients. The choice of conduit for total SVC replacement is limited, and we describe the use of the Contegra graft (Medtronic Inc, Minneapolis, MN) in this setting.
Case Reports Patient 1 A 48-year-old woman with severe scleroderma and a progressively enlarging anterior mediastinal mass, presumed to be thymoma, was referred for surgical intervention. Infiltration of the mass into the SVC necessitated radical resection, and extended thymectomy was undertaken. Full right atrial to aortic cardiopulmonary bypass was instituted. The left and right brachiocephalic veins and the right atrium proximal to the cavoatrial junction were clamped and the anterior mediastinal mass and SVC excised en bloc. An 18-mm Contegra graft bovine jugular conduit was used for the reconstruction. The patient remains well, with a patent conduit demonstrable on computed tomography (CT) at 12 months.
Patient 2 A 73-year-old woman presented with superior vena caval obstruction (SVCO) secondary to malignant thymoma. After induction chemoradiation, CT (Fig 1) and magnetic resonance imaging showed a residual 7-cm anterior mediastinal mass filling the entire SVC from the confluence of the left and right brachiocephalic veins to the superior
Elizabeth Belcher, FRCS, PhD, Michael Dusmet, MD, and Mario Petrou, FRCS, PhD Departments of Thoracic Surgery and Adult Cardiac Surgery, Royal Brompton Hospital, London, United Kingdom
Radical resection of the superior vena cava poses a challenge for the cardiothoracic surgeon. The Contegra graft (Medtronic Inc, Minneapolis, MN), a biologic conduit comprising the valved segment of the bovine jugular vein, is established as a right ventricular to pulmonary artery conduit for right ventricular outflow tract repair in the pediatric population. We describe the use of the Contegra graft to facilitate radical resection and reconstruction of the supeAccepted for publication April 6, 2009. Address correspondence to Dr Petrou, Department of Adult Cardiac Surgery, Royal Brompton Hospital, Sydney St, London, SW3 6NP, United Kingdom; e-mail: [email protected].
© 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
Fig 1. Contrast computed tomography scan of the chest shows an anterior mediastinal mass in continuity with the superior vena cava, which has a filling defect (arrow) suggestive of direct tumor invasion or intraluminal thrombus. 0003-4975/10/$36.00 doi:10.1016/j.athoracsur.2009.04.146
FEATURE ARTICLES
uation showing in detail the anatomic and functional characteristics of the anomaly. Therefore, echocardiography is a valuable tool for the diagnosis of this congenital malformation by virtue of its noninvasiveness and easy reproducibility. Echocardiography may also be helpful for the cardiac surgeon in planning the operation mainly for the choice of the best reparative technique. A careful echocardiographic evaluation of mitral leaflets structure is essential in diagnosis of anomalous mitral arcade. In fact, the lack of commissural fusion and calcific degeneration along with the subvalvular arc-like configuration enables the physicians to recognize this anomaly among other causes of mitral disease. In conclusion, in all cases of mitral stenosis or insufficiency, mainly in people who have not a history of rheumatic disease, it would be appropriate to consider the possibility of an anomaly in the development of the mitral arcade.
CASE REPORT BELCHER ET AL CONTEGRA AS SVC CONDUIT