- Email: [email protected]
Successful removal of massive cardiac neurilemoma with cardiopulmonary bypass
Ann Thorac Surg 1998;66:553–5
from the prior exploratory laparatomy was obtained. Injuries included a through-and-through gunshot wound to both the liver and the stomach, as well as extensive splenic injury. The liver lacerations and through-andthrough gastric wounds were repaired and splenectomy was performed. A 2.5-cm tear in the diaphragm was repaired with interrupted sutures, and a left tube thoracostomy drained 700 mL of blood. A febrile postoperative course complicated the exploratory laparotomy and splenectomy. Results of fluoroscopy of the diaphragm and a liver spleen scan were normal. A left subphrenic abscess was subsequently drained with an uneventful recovery. Thoracic splenosis was not considered in the differential diagnosis of this patient because there was no history of thoracoabdominal trauma. The history, radiologic findings, and results of the CT-guided needle biopsy were inconclusive, and a malignant pulmonary lesion could not be excluded. Suspicion of the true diagnosis was aroused only when multiple dense thoracic adhesions were encountered and the frozen section diagnosis was consistent with lymphoid tissue.
CASE REPORT HASHIMOTO ET AL CARDIAC NEURILEMOMA
553
ranted [6]. This approach may avoid the need for thoracotomy and removing splenic tissue, which may provide protection against sepsis.
References 1. Widmann WD, Laubscher FA. Splenosis: a disease of beneficial condition? Arch Surg 1971;102:152– 8. 2. Pearson HA, Johnston D, Smith KA, Touloukian RJ. The born-again spleen: return of splenic function after splenectomy for trauma. N Engl J Med 1978;298:1389–92. 3. Sass W, Bergholz M, Kehl A, Seifert J, Hamelmann H. Overwhelming infection after splenectomy in spite of some spleen remaining and splenosis. Klin Wochenschr 1983;61: 1075–9. 4. Madjar S, Weissberg D. Thoracic splenosis. Thorax 1994;49: 1020–2. 5. Shaw AFB, Shafi A. Traumatic autoplastic transplantation of splenic tissue in man with observations on the late results of splenectomy in six cases. J Pathol 1937;45:215–35. 6. Roucos S, Tabet G, Jebara VA, Ghossain MA, Biagini J, Saade B. Thoracic splenosis: case report and literature review. J Thorac Cardiovasc Surg 1990;99:361–3. 7. Moncada R, Williams V, Fareed J, Messmore H. Thoracic splenosis. AJR 1985;144:705– 6.
Comment Splenosis describes ectopic implantation of splenic tissue to the peritoneal cavity. It is postulated to provide a protective effect, with respect to sepsis, prompting some authors to suggest it may, in fact, be a beneficial condition [1]. Pearson and associates [2] found splenosis and return of splenic function occurred more frequently than anticipated and postulated it led to lower rates of bacterial sepsis. Other authors have disputed this finding and have reported fatal sepsis in a patient with splenosis [3]. In comparison, thoracic splenosis is rare; to our knowledge, only 22 previously reported cases have been described in the English-language literature [4]. This condition was first reported in 1937 by Shaw and Shafi as an autopsy finding [5]. The patients have a history of thoracoabdominal trauma with splenic injury or splenectomy, with the interval between the initial trauma and discovery of the thoracic splenosis averaging 16 years [6]. Thoracic splenosis typically presents on chest radiographs as an asymptomatic pulmonary mass, either solitary or multiple. Computed tomographic scan usually demonstrates a subpleural mass; however, the CT characteristics are not diagnostic. Our patient had a typical presentation of an asymptomatic pulmonary mass confirmed on CT scan with an inconclusive needle biopsy. Diagnosis of thoracic splenosis can be established with the use of radionuclide scans [7]. The diagnosis of thoracic splenosis frequently is made at the time of operation. Thoracotomy can be avoided if the diagnosis is entertained preoperatively in a patient with a new pulmonary mass and a history of thoracoabdominal trauma, no matter how remote. Appropriate radionuclide studies will confirm the diagnosis, and because the natural history of this entity is thought to be benign, observation with serial chest radiographs is war© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Successful Removal of Massive Cardiac Neurilemoma With Cardiopulmonary Bypass Takehisa Hashimoto, MD, Shoji Eguchi, MD, Takashi Nakayama, MD, Hajime Ohzeki, MD, and Jun-ichi Hayashi, MD Department of Thoracic and Cardiovascular Surgery, Niigata University School of Medicine, Niigata, Japan
A 46-year-old woman was referred to our hospital because of cardiac enlargement seen on a chest radiograph. Imaging studies showed a massive intrapericardial tumor with a size of 123837 cm. Tumor dissection included inspection of the inner aspect of the superior vena cava with use of cardiopulmonary bypass, because the mass was tightly adherent to both superior vena cava and right atrium. The pathologic diagnosis was neurilemoma. (Ann Thorac Surg 1998;66:553–5) © 1998 by The Society of Thoracic Surgeons
P
rimary neurogenic neoplasms of the heart are extremely uncommon. Neurilemoma, a benign tumor, is among the rarest [1, 2]. To our knowledge, only 7 cases of cardiac neurilemoma have been reported [1–7]. We
Accepted for publication Feb 23, 1998. Address reprint requests to Dr Hashimoto, Department of Thoracic and Cardiovascular Surgery, School of Medicine, Niigata University, 1—751 Asahimachi-dori, Niigata City, 951, Japan.
0003-4975/98/$19.00 PII S0003-4975(98)00473-1
554
CASE REPORT HASHIMOTO ET AL CARDIAC NEURILEMOMA
Fig 1. Computed tomography revealed a solid mass (arrow) measuring 93938 cm located between the right atrium, superior vena cava (SVC), ascending aorta (Ao), and right pulmonary artery (PA).
present the case of a large cardiac neurilemoma, which was removed successfully with use of cardiopulmonary bypass. A 46-year-old woman was admitted to our hospital for investigation of an enlarged cardiac silhouette seen on a chest radiograph. Past surgical history included a uterine myomectomy. Examination on admission revealed slight dilation of both external jugular veins and a grade 2/6 systolic murmur at the left sternal border. The electrocardiography showed regular sinus rhythm. A chest roentgenogram revealed cardiomegaly with a cardiothoracic ratio of 79%. Echocardiography confirmed a mass measuring 738 cm with a location superficial and anterior to the right atrium and an inhomogeneous echo density. Mild mitral and tricuspid regurgitation, and a small pericardial effusion also were evident. Computed tomography (Fig 1) and magnetic resonance imaging revealed a massive solid intrapericardial tumor between the superior vena cava (SVC) and ascending aorta. The caval wall was indented toward the right and increased in
Ann Thorac Surg 1998;66:553–5
thickness. An angiogram showed two feeding arteries originating from both the circumflex and right coronary arteries. A pressure gradient of 7 mm Hg was measured between the SVC and the right atrium. Arrangements were made for immediate operation in anticipation of a malignant tumor or cardiac complication. At operation, we prepared cardiopulmonary bypass in anticipation of tumor invasion of a cardiac chamber or the great vessels. Through a median sternotomy and pericardiotomy, 200 mL of yellowish pericardial fluid was aspirated. Cytologic examination demonstrated no malignant cells. The tumor was located in close relation to the right atrium, SVC, azygos vein, ascending aorta, left atrium, and right pulmonary artery. To avoid phrenic nerve injury, we opened the right pleural space and retracted it. Tight adhesion to the right atrium and SVC necessitated cardiopulmonary bypass. It was easy to cannulate the SVC above this tumor because the SVC was elongated and the space for cannulation was enough. The SVC was divided, and the tumor was dissected carefully with ongoing inspection from the internal aspect of the SVC. The SVC was reconstructed with an end-to-end anastomosis. Macroscopically the tumor was encapsulated, not invasive, and sure to have a benign nature, so a frozen section was not done at the time of the operation. The tumor was surrounded by a thin fibromembranous capsule, measured 12 3 8 3 7 cm, and weighed 360 g. Its cut surface revealed both cream-colored and yellow areas, with secondary degenerative changes such as cystification, calcification, and focal hemorrhage. Microscopic sections showed a mixed proliferation of typical Antoni type A and Antoni B tissue. Immunohistochemical staining was positive for S-100 protein. These findings resulted in a diagnosis of neurilemoma, a benign tumor. The patient had normal phrenic nerve function and rapidly recovered from the operation. A subsequent angiogram showed a smooth internal surface where the SVC had been reconstructed. No evidence of recurrence was noted 2 years after the operation.
Comment Neurilemoma typically involves the flexor surfaces of extremities, neck, mediastinum, retroperitoneum, posterior spinal roots, or cerebellopontine angle [2]. Although neurogenic tumors make up 33% of mediastinal tumors [8], primary neurogenic neoplasms of the heart are extremely uncommon. To our knowledge, only 7 cases of cardiac neurilemoma have been reported [1–7]. Most of these tumors have been right-sided, arising near the cardiac plexus [1–3, 6, 7], with 2 cases occurring on the left [4, 5]. Primary neurogenic neoplasms of the heart arise from cardiac branches of the vagus nerve and the cardiac plexus [2, 6]. We believe the present lesion originated from the cardiac plexus extending from the right atrial
Ann Thorac Surg 1998;66:555–7
wall to the SVC, ascending aorta, and right pulmonary artery. The massive cardiac neurilemoma seen in our patient compressed the SVC and appeared to increase its thickness; it had no symptoms or signs except for slight jugular venous dilatation and elevation of the SVC pressure. Because benign cardiac neoplasms may compress or occupy the cardiac chambers, their manifestations are not type-specific but rather an effect of their size and location [5, 6]. Cardiovascular symptoms of such a tumor may include chest pain, syncope, heart failure, cardiac tamponade, arrhythmias, and conductive disorders. Chronic obstruction may cause cardiac failure, with intermittent obstruction representing one cause of syncope. A right-sided tumor may produce obstruction of the SVC [6]. Among the reported occurrences of cardiac neurilemoma, two right-sided tumors have produced right ventricular outflow tract obstruction and subsequent dyspnea [3, 6], and a left-sided tumor has caused atrial fibrillation [4]. Clinical differentiation of cardiac neurilemoma from other cardiac tumors is impossible except by histologic examination. In our case the possibilities of sudden death, syncope, heart failure, arrhythmia, and malignant tumor all demanded prompt surgical treatment, and the resected specimen provided the diagnosis. The prognosis of benign cardiac tumor depends on resectability. After complete resection the prognosis is excellent, and adjuvant therapy is not needed. Among reported cases of cardiac neurilemoma, only 3 have required cardiopulmonary bypass [3–5]. Cardiopulmonary bypass provides a stable hemodynamic state and satisfactory visualization to excise the tumor. In our case cardiopulmonary bypass facilitated complete resection of the tumor from the heart and great vessels, particularly the SVC.
References 1. Factor S, Turi G, Biempica L. Primary cardiac neurilemoma. Cancer 1976;37:883–90. 2. Gleason TH, Dillard DH, Gould VE. Cardiac neurilemoma. NY State J Med 1972;72:2435– 6. 3. Kodama M, Aoki M, Sakai K. Primary cardiac neurilemoma. Circulation 1995;92:274–5. 4. Forbes AD, Schmidt RA, Wood DE, Cochran RP, Munkenbeck F, Verrier ED. Schwannoma of the left atrium: diagnostic evaluation and surgical resection. Ann Thorac Surg 1994;57: 743– 6. 5. Monroe B, Federman M, Balogh K. Cardiac neurilemoma. Report of a case with electron microscopic examination. Arch Pathol Lab Med 1984;108:300– 4. 6. Betancourt B, Defendini EA, Johnson C, et al. Severe right ventricular outflow tract obstruction caused by an intracavitary cardiac neurilemoma. Successful surgical removal and postoperative diagnosis. Chest 1979;75:522– 4. 7. Hallman GL, Cooley DA, Webb JA. Primary tumors of the heart: results of surgical treatment in ten patients. J Cardiovasc Surg 1966;7:447–57. 8. Cayten CG, Kastor JA, Park CD. Unusual presentation of © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT PIETSCH ET AL RECOVERY FROM END-STAGE CARDIOMYOPATHY
555
intrathoracic malignant schwannoma. J Thorac Cardiovasc Surg 1973;66:601– 6.
Recovery From End-Stage Ischemic Cardiomyopathy During LongTerm LVAD Support Lars Pietsch, MD, Horst Laube, MD, Gerd Baumann, MD, PhD, and Wolfgang Konertz, MD, PhD Departments of Cardiac Surgery and Cardiology, Charite´, Humboldt University, Berlin, Germany
A patient with ischemic cardiomyopathy and extremely reduced left ventricular function (left ventricular ejection fraction 5 0.10) presented to our institution for cardiac transplantation. Because of his worsening condition he was placed on the Novacor left ventricular assist device. During 3 months of support his left ventricular function recovered and he successfully underwent percutaneous transluminal coronary angioplasty and minimally invasive direct coronary artery bypass grafting procedures; subsequently he could be weaned from the left ventricular assist device and discharged. The patient is no longer considered for cardiac transplantation. (Ann Thorac Surg 1998;66:555–7) © 1998 by The Society of Thoracic Surgeons
T
here is increasing evidence that some patients’ hearts recover during long-term left ventricular (LV) assist [1]. This has been observed with patients after heterotopic heart transplantation [2], as well as after mechanical circulatory assist. Successful coronary revascularization is highly dependent on the presence of viable myocardium. Tools for discriminating hibernating myocardium from scar and nonviable tissue are not perfect. Currently no technique shows 100% accuracy, especially in extremely dysfunctional hearts [3]. A 54-year-old patient was transferred to our institution with cardiac failure. An intensified medical regimen including diuretics, b-blockers, digitalis, and angiotensin-converting enzyme inhibitors failed to improve his situation. Cardiac catheterization showed two-vessel disease with occlusion of the proximal left anterior descending artery and a 75% stenosis of the circumflex artery. Left ventricular function was extremely reduced, with an LV ejection fraction of 0.10. The LV end-diastolic volume Accepted for publication Feb 25, 1998. Address reprint requests to Dr Pietsch, Universita¨tsklinikum Charite, Klinik fu¨r Herzchirurgie, Schumannstr 20-21, 10717 Berlin, Germany (e-mail: cardiac&rz.charite.hu-berlin.de).
0003-4975/98/$19.00 PII S0003-4975(98)00507-4
from the prior exploratory laparatomy was obtained. Injuries included a through-and-through gunshot wound to both the liver and the stomach, as well as extensive splenic injury. The liver lacerations and through-andthrough gastric wounds were repaired and splenectomy was performed. A 2.5-cm tear in the diaphragm was repaired with interrupted sutures, and a left tube thoracostomy drained 700 mL of blood. A febrile postoperative course complicated the exploratory laparotomy and splenectomy. Results of fluoroscopy of the diaphragm and a liver spleen scan were normal. A left subphrenic abscess was subsequently drained with an uneventful recovery. Thoracic splenosis was not considered in the differential diagnosis of this patient because there was no history of thoracoabdominal trauma. The history, radiologic findings, and results of the CT-guided needle biopsy were inconclusive, and a malignant pulmonary lesion could not be excluded. Suspicion of the true diagnosis was aroused only when multiple dense thoracic adhesions were encountered and the frozen section diagnosis was consistent with lymphoid tissue.
CASE REPORT HASHIMOTO ET AL CARDIAC NEURILEMOMA
553
ranted [6]. This approach may avoid the need for thoracotomy and removing splenic tissue, which may provide protection against sepsis.
References 1. Widmann WD, Laubscher FA. Splenosis: a disease of beneficial condition? Arch Surg 1971;102:152– 8. 2. Pearson HA, Johnston D, Smith KA, Touloukian RJ. The born-again spleen: return of splenic function after splenectomy for trauma. N Engl J Med 1978;298:1389–92. 3. Sass W, Bergholz M, Kehl A, Seifert J, Hamelmann H. Overwhelming infection after splenectomy in spite of some spleen remaining and splenosis. Klin Wochenschr 1983;61: 1075–9. 4. Madjar S, Weissberg D. Thoracic splenosis. Thorax 1994;49: 1020–2. 5. Shaw AFB, Shafi A. Traumatic autoplastic transplantation of splenic tissue in man with observations on the late results of splenectomy in six cases. J Pathol 1937;45:215–35. 6. Roucos S, Tabet G, Jebara VA, Ghossain MA, Biagini J, Saade B. Thoracic splenosis: case report and literature review. J Thorac Cardiovasc Surg 1990;99:361–3. 7. Moncada R, Williams V, Fareed J, Messmore H. Thoracic splenosis. AJR 1985;144:705– 6.
Comment Splenosis describes ectopic implantation of splenic tissue to the peritoneal cavity. It is postulated to provide a protective effect, with respect to sepsis, prompting some authors to suggest it may, in fact, be a beneficial condition [1]. Pearson and associates [2] found splenosis and return of splenic function occurred more frequently than anticipated and postulated it led to lower rates of bacterial sepsis. Other authors have disputed this finding and have reported fatal sepsis in a patient with splenosis [3]. In comparison, thoracic splenosis is rare; to our knowledge, only 22 previously reported cases have been described in the English-language literature [4]. This condition was first reported in 1937 by Shaw and Shafi as an autopsy finding [5]. The patients have a history of thoracoabdominal trauma with splenic injury or splenectomy, with the interval between the initial trauma and discovery of the thoracic splenosis averaging 16 years [6]. Thoracic splenosis typically presents on chest radiographs as an asymptomatic pulmonary mass, either solitary or multiple. Computed tomographic scan usually demonstrates a subpleural mass; however, the CT characteristics are not diagnostic. Our patient had a typical presentation of an asymptomatic pulmonary mass confirmed on CT scan with an inconclusive needle biopsy. Diagnosis of thoracic splenosis can be established with the use of radionuclide scans [7]. The diagnosis of thoracic splenosis frequently is made at the time of operation. Thoracotomy can be avoided if the diagnosis is entertained preoperatively in a patient with a new pulmonary mass and a history of thoracoabdominal trauma, no matter how remote. Appropriate radionuclide studies will confirm the diagnosis, and because the natural history of this entity is thought to be benign, observation with serial chest radiographs is war© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Successful Removal of Massive Cardiac Neurilemoma With Cardiopulmonary Bypass Takehisa Hashimoto, MD, Shoji Eguchi, MD, Takashi Nakayama, MD, Hajime Ohzeki, MD, and Jun-ichi Hayashi, MD Department of Thoracic and Cardiovascular Surgery, Niigata University School of Medicine, Niigata, Japan
A 46-year-old woman was referred to our hospital because of cardiac enlargement seen on a chest radiograph. Imaging studies showed a massive intrapericardial tumor with a size of 123837 cm. Tumor dissection included inspection of the inner aspect of the superior vena cava with use of cardiopulmonary bypass, because the mass was tightly adherent to both superior vena cava and right atrium. The pathologic diagnosis was neurilemoma. (Ann Thorac Surg 1998;66:553–5) © 1998 by The Society of Thoracic Surgeons
P
rimary neurogenic neoplasms of the heart are extremely uncommon. Neurilemoma, a benign tumor, is among the rarest [1, 2]. To our knowledge, only 7 cases of cardiac neurilemoma have been reported [1–7]. We
Accepted for publication Feb 23, 1998. Address reprint requests to Dr Hashimoto, Department of Thoracic and Cardiovascular Surgery, School of Medicine, Niigata University, 1—751 Asahimachi-dori, Niigata City, 951, Japan.
0003-4975/98/$19.00 PII S0003-4975(98)00473-1
554
CASE REPORT HASHIMOTO ET AL CARDIAC NEURILEMOMA
Fig 1. Computed tomography revealed a solid mass (arrow) measuring 93938 cm located between the right atrium, superior vena cava (SVC), ascending aorta (Ao), and right pulmonary artery (PA).
present the case of a large cardiac neurilemoma, which was removed successfully with use of cardiopulmonary bypass. A 46-year-old woman was admitted to our hospital for investigation of an enlarged cardiac silhouette seen on a chest radiograph. Past surgical history included a uterine myomectomy. Examination on admission revealed slight dilation of both external jugular veins and a grade 2/6 systolic murmur at the left sternal border. The electrocardiography showed regular sinus rhythm. A chest roentgenogram revealed cardiomegaly with a cardiothoracic ratio of 79%. Echocardiography confirmed a mass measuring 738 cm with a location superficial and anterior to the right atrium and an inhomogeneous echo density. Mild mitral and tricuspid regurgitation, and a small pericardial effusion also were evident. Computed tomography (Fig 1) and magnetic resonance imaging revealed a massive solid intrapericardial tumor between the superior vena cava (SVC) and ascending aorta. The caval wall was indented toward the right and increased in
Ann Thorac Surg 1998;66:553–5
thickness. An angiogram showed two feeding arteries originating from both the circumflex and right coronary arteries. A pressure gradient of 7 mm Hg was measured between the SVC and the right atrium. Arrangements were made for immediate operation in anticipation of a malignant tumor or cardiac complication. At operation, we prepared cardiopulmonary bypass in anticipation of tumor invasion of a cardiac chamber or the great vessels. Through a median sternotomy and pericardiotomy, 200 mL of yellowish pericardial fluid was aspirated. Cytologic examination demonstrated no malignant cells. The tumor was located in close relation to the right atrium, SVC, azygos vein, ascending aorta, left atrium, and right pulmonary artery. To avoid phrenic nerve injury, we opened the right pleural space and retracted it. Tight adhesion to the right atrium and SVC necessitated cardiopulmonary bypass. It was easy to cannulate the SVC above this tumor because the SVC was elongated and the space for cannulation was enough. The SVC was divided, and the tumor was dissected carefully with ongoing inspection from the internal aspect of the SVC. The SVC was reconstructed with an end-to-end anastomosis. Macroscopically the tumor was encapsulated, not invasive, and sure to have a benign nature, so a frozen section was not done at the time of the operation. The tumor was surrounded by a thin fibromembranous capsule, measured 12 3 8 3 7 cm, and weighed 360 g. Its cut surface revealed both cream-colored and yellow areas, with secondary degenerative changes such as cystification, calcification, and focal hemorrhage. Microscopic sections showed a mixed proliferation of typical Antoni type A and Antoni B tissue. Immunohistochemical staining was positive for S-100 protein. These findings resulted in a diagnosis of neurilemoma, a benign tumor. The patient had normal phrenic nerve function and rapidly recovered from the operation. A subsequent angiogram showed a smooth internal surface where the SVC had been reconstructed. No evidence of recurrence was noted 2 years after the operation.
Comment Neurilemoma typically involves the flexor surfaces of extremities, neck, mediastinum, retroperitoneum, posterior spinal roots, or cerebellopontine angle [2]. Although neurogenic tumors make up 33% of mediastinal tumors [8], primary neurogenic neoplasms of the heart are extremely uncommon. To our knowledge, only 7 cases of cardiac neurilemoma have been reported [1–7]. Most of these tumors have been right-sided, arising near the cardiac plexus [1–3, 6, 7], with 2 cases occurring on the left [4, 5]. Primary neurogenic neoplasms of the heart arise from cardiac branches of the vagus nerve and the cardiac plexus [2, 6]. We believe the present lesion originated from the cardiac plexus extending from the right atrial
Ann Thorac Surg 1998;66:555–7
wall to the SVC, ascending aorta, and right pulmonary artery. The massive cardiac neurilemoma seen in our patient compressed the SVC and appeared to increase its thickness; it had no symptoms or signs except for slight jugular venous dilatation and elevation of the SVC pressure. Because benign cardiac neoplasms may compress or occupy the cardiac chambers, their manifestations are not type-specific but rather an effect of their size and location [5, 6]. Cardiovascular symptoms of such a tumor may include chest pain, syncope, heart failure, cardiac tamponade, arrhythmias, and conductive disorders. Chronic obstruction may cause cardiac failure, with intermittent obstruction representing one cause of syncope. A right-sided tumor may produce obstruction of the SVC [6]. Among the reported occurrences of cardiac neurilemoma, two right-sided tumors have produced right ventricular outflow tract obstruction and subsequent dyspnea [3, 6], and a left-sided tumor has caused atrial fibrillation [4]. Clinical differentiation of cardiac neurilemoma from other cardiac tumors is impossible except by histologic examination. In our case the possibilities of sudden death, syncope, heart failure, arrhythmia, and malignant tumor all demanded prompt surgical treatment, and the resected specimen provided the diagnosis. The prognosis of benign cardiac tumor depends on resectability. After complete resection the prognosis is excellent, and adjuvant therapy is not needed. Among reported cases of cardiac neurilemoma, only 3 have required cardiopulmonary bypass [3–5]. Cardiopulmonary bypass provides a stable hemodynamic state and satisfactory visualization to excise the tumor. In our case cardiopulmonary bypass facilitated complete resection of the tumor from the heart and great vessels, particularly the SVC.
References 1. Factor S, Turi G, Biempica L. Primary cardiac neurilemoma. Cancer 1976;37:883–90. 2. Gleason TH, Dillard DH, Gould VE. Cardiac neurilemoma. NY State J Med 1972;72:2435– 6. 3. Kodama M, Aoki M, Sakai K. Primary cardiac neurilemoma. Circulation 1995;92:274–5. 4. Forbes AD, Schmidt RA, Wood DE, Cochran RP, Munkenbeck F, Verrier ED. Schwannoma of the left atrium: diagnostic evaluation and surgical resection. Ann Thorac Surg 1994;57: 743– 6. 5. Monroe B, Federman M, Balogh K. Cardiac neurilemoma. Report of a case with electron microscopic examination. Arch Pathol Lab Med 1984;108:300– 4. 6. Betancourt B, Defendini EA, Johnson C, et al. Severe right ventricular outflow tract obstruction caused by an intracavitary cardiac neurilemoma. Successful surgical removal and postoperative diagnosis. Chest 1979;75:522– 4. 7. Hallman GL, Cooley DA, Webb JA. Primary tumors of the heart: results of surgical treatment in ten patients. J Cardiovasc Surg 1966;7:447–57. 8. Cayten CG, Kastor JA, Park CD. Unusual presentation of © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT PIETSCH ET AL RECOVERY FROM END-STAGE CARDIOMYOPATHY
555
intrathoracic malignant schwannoma. J Thorac Cardiovasc Surg 1973;66:601– 6.
Recovery From End-Stage Ischemic Cardiomyopathy During LongTerm LVAD Support Lars Pietsch, MD, Horst Laube, MD, Gerd Baumann, MD, PhD, and Wolfgang Konertz, MD, PhD Departments of Cardiac Surgery and Cardiology, Charite´, Humboldt University, Berlin, Germany
A patient with ischemic cardiomyopathy and extremely reduced left ventricular function (left ventricular ejection fraction 5 0.10) presented to our institution for cardiac transplantation. Because of his worsening condition he was placed on the Novacor left ventricular assist device. During 3 months of support his left ventricular function recovered and he successfully underwent percutaneous transluminal coronary angioplasty and minimally invasive direct coronary artery bypass grafting procedures; subsequently he could be weaned from the left ventricular assist device and discharged. The patient is no longer considered for cardiac transplantation. (Ann Thorac Surg 1998;66:555–7) © 1998 by The Society of Thoracic Surgeons
T
here is increasing evidence that some patients’ hearts recover during long-term left ventricular (LV) assist [1]. This has been observed with patients after heterotopic heart transplantation [2], as well as after mechanical circulatory assist. Successful coronary revascularization is highly dependent on the presence of viable myocardium. Tools for discriminating hibernating myocardium from scar and nonviable tissue are not perfect. Currently no technique shows 100% accuracy, especially in extremely dysfunctional hearts [3]. A 54-year-old patient was transferred to our institution with cardiac failure. An intensified medical regimen including diuretics, b-blockers, digitalis, and angiotensin-converting enzyme inhibitors failed to improve his situation. Cardiac catheterization showed two-vessel disease with occlusion of the proximal left anterior descending artery and a 75% stenosis of the circumflex artery. Left ventricular function was extremely reduced, with an LV ejection fraction of 0.10. The LV end-diastolic volume Accepted for publication Feb 25, 1998. Address reprint requests to Dr Pietsch, Universita¨tsklinikum Charite, Klinik fu¨r Herzchirurgie, Schumannstr 20-21, 10717 Berlin, Germany (e-mail: cardiac&rz.charite.hu-berlin.de).
0003-4975/98/$19.00 PII S0003-4975(98)00507-4