© 2014 Wiley Periodicals, Inc.
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Immediate Postoperative Percutaneous Stenting of Superior Vena Cava Obstruction Following Heart Transplantation in Adult Patients with Pacemaker Leads David Asseff, M.D.,* Ahmad Y. Sheikh, M.D.,y Daniel Sze, M.D., Ph.D.,z Richard Ha,y Lawrence Hofmann, M.D.,z and Pieter J.A. van der Starre, M.D., Ph.D.* *Department of Anesthesiology and Perioperative Medicine, Stanford University School of Medicine, Stanford, California; yDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California; and zDepartment of Interventional Radiology, Stanford University School of Medicine, Stanford, California ABSTRACT Vena cava superior syndrome is a serious complication after heart transplantation, leading to low cardiac output, cerebral edema, and multi-organ dysfunction. We report three adult patients who underwent heart and heart–lung transplantation and required immediate postoperative balloon angioplasty and stent placement by interventional radiology. The observed obstructions were located at sites of intraoperatively removed pacemaker or defibrillator wires. Percutaneous stent placement immediately improved the hemodynamic condition of the patients. Early recognition of the complication and availability of immediate intervention are essential to prevent further deterioration. doi: 10.1111/jocs.12387 (J Card Surg 2014;29:733–
736)
Acute obstruction of the superior vena cava (SVC) following heart transplantation is a serious complication, since it may cause significant impairment of venous return leading to low cardiac output, cerebral edema, and organ failure. We describe three patients with acute, intraoperative occlusion of the SVC following heart transplantation, likely related to removal of previous pacemaker or internal cardiac defibrillator (ICD) leads, successfully treated with immediate postoperative percutaneous stent placement, and discuss the underlying cause, early warning signs, and potentially preventative measures.
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Pieter J.A. van der Starre, M.D., Ph.D., Department of Anesthesiology and Perioperative Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305. Fax: þ1-650-725-8544; e-mail: [email protected]
PATIENT PROFILES Stanford University Institutional Review Board approval was obtained to report this case series. Patient 1 A 31-year-old male patient who had undergone a Mustard-Senning procedure as a child for transposition of the great arteries and pacemaker implantation for AV block five years prior underwent orthotopic heart transplantation (OHT) for severe right heart failure. Surgical technique included bicaval anastomoses1 and removal of the pacemaker wires. Immediately postoperatively, the patient developed clinical signs of SVC syndrome, including edema, and plethora of the face and upper extremities accompanied by hypotension, lactic acidosis, and oliguria. Transesophageal echocardiography (TEE) demonstrated hypovolemia of both the right and left ventricles. There were no signs of tamponade. Subsequent venography confirmed the diagnosis of high-grade SVC obstruction with near
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J CARD SURG 2014;29:733–736
Figure 1. (A) Venogram showing high-grade SVC obstruction with near stasis of flow (!). (B) Recovery of blood flow in the SVC after balloon angioplasty and stent graft placement with a 10 38 mm PTFE-covered balloon-expandable stent (!).
stasis of flow (Fig. 1A). The patient underwent balloon angioplasty and stenting of the SVC using a 10 mm 38 mm polytetrafluoroethylene (PTFE)-covered balloon-expandable stent-graft (i-Cast, Atrium Medical Inc., Hudson, NH, USA). His hemodynamic condition improved rapidly with resolution of the SVC syndrome (Fig. 1B). The patient recovered completely, and was discharged from the hospital on postoperative day (POD) 15. Patient 2 A 27-year-old male patient with a history of idiopathic cardiomyopathy, atrial fibrillation, and epicardial lead placement during implantation of an automatic internal cardiac defibrillator (AICD) six years prior underwent OHT for worsening left heart failure. The AICD wires were removed. Immediately after weaning from cardiopulmonary bypass (CPB) the patient developed signs of SVC obstruction, with high central venous pressure (CVP) of up to 60 mmHg, arterial hypotension, and oliguria. The patient was transfered straight from the operating room to the interventional radiology (IR) suite, where occlusion of both the right brachiocephalic vein and SVC was documented by venography (Fig. 2A). After balloon angioplasty of the right brachiocephalic vein and angioplasty and stenting with a 12 mm 60 mm self-expanding nitinol stent of the SVC (SMART stent, Cordis Inc., Miami Lakes, FL, USA) (Fig. 2B), his hemodynamic condition improved instantly, with no signs of neurologic impairment. He was discharged from the hospital on POD 11. Patient 3 A 62-year-old male patient with a history of ischemic cardiomyopathy, coronary artery bypass surgery, AICD
placement eight years prior, and progressive interstitial lung disease underwent heart–lung transplantation, complicated by the inability to remove one of the AICD wires. After sternal closure facial swelling was noted, with concomitant hypotension and progressive lactic acidosis. An attempt at insertion of a pulmonary artery catheter was aborted due to apparent obstruction in the SVC. TEE showed hypovolemia of the right and left ventricles. The patient was transferred to the IR suite, where venography revealed a nearly complete obstruction of the SVC and an extremely dilated azygos vein with retrograde flow (Fig. 3A). After balloon angioplasty and stenting with a 14 mm 40 mm self-expanding stent (SMART stent), blood flow in the SVC normalized (Fig. 3B). Despite improvement of his cardiac output, the patient’s condition deteriorated during the following weeks, mainly due to seizures, multiple strokes, heparin-induced thrombocytopenia, acute kidney injury requiring dialysis, candida sepsis, and adenovirus viremia. He expired on POD 53. DISCUSSION This series of patients with postoperative SVC syndrome following heart and heart–lung transplantation shows that immediate postoperative treatment with percutaneous balloon angioplasty and stenting improves the hemodynamic condition of the patient considerably and quickly. The method appeared to be safe, despite these recently transplanted patients having fresh, unhealed bicaval anastomoses, even with the use of bare (uncovered) stents. In adult patients endovascular stenting of the SVC has been mainly described in the setting of benign SVC syndrome due to pacemaker wire-related thrombosis or chronic indwelling venous access devices.2,3 In a report of two cardiac surgery patients with postoperative SVC syndrome and early stenting, the
J CARD SURG 2014;29:733–736
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Figure 2. (A) Venogram showing occlusion of both the right brachiocephalic vein and SVC (!). (B) Recovery of blood flow after balloon angioplasty of the right brachiocephalic vein, and angioplasty and stenting of the SVC with a 12 60 mm self-expanding nitinol stent (!).
Figure 3. (A) Venogram showing a nearly complete obstruction of the SVC and an extremely dilated azygos vein with retrograde flow (!). (B) Recovery of blood flow after balloon angioplasty and stenting of the SVC with a 14 40 mm self-expanding stent (!).
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obstructions were related to repairs of lacerations during cannulation of the SVC.4 The only earlier reported series of SVC syndrome and stenting in adult patients after heart transplantation involved three patients who underwent both thrombolysis and stenting, but only after POD 8 or later.5 Facial swelling, combined with systemic hypotension, lactic acidosis, and oliguria, is a strong indication for obstruction of the SVC. Failure to insert a balloondirected pulmonary artery catheter through one of the internal jugular veins following the transplantation adds to the diagnosis, in particular when TEE confirms the absence of tamponade. In our series the obstructions in the SVC were located superior to the anastomotic or cannulation sites, clearly related to the former location of AICD or pacemaker wires. They had apparently gradually caused thrombosis and stricture, and after removal during surgery the vena cava collapsed, presumably due to dissection or disruption of the vessel walls. Subsequently, this resulted in low cardiac output, lactic acidosis, and oliguria. This finding excludes the surgical option of open repair, since the location of the obstruction is almost inaccessible, and reopening the sternum would be accompanied by a significantly increased risk of complications. Since AICD insertion for severe heart failure has increased dramatically over the last decade, the risk of development of SVC syndrome following heart transplantation will probably become greater in the coming years.6 It may be recommended to make preoperative computer tomographic (CT) venogram a standard screening procedure in heart transplant recipients
J CARD SURG 2014;29:733–736
with a longstanding AICD in place, to assess the risk of postoperative SVC obstruction. This should be more indicated in patients with a history of congenital abnormalities. It may be worth considering to harvest longer venous pedicles for patients with preexisting pacemaker or AICD wires, and to reconstruct the superior vena cava and brachiocephalic vein of the recipient. Acknowledgments: The authors wish to thank Drs. Ramin Beygui, Philip Oyer, and Michael Dake for their contributions in preparing the manuscript.
REFERENCES 1. Davies R, Russo R, Morgan J, et al: Standard versus bicaval techniques for orthotopic heart transplantation: An analysis of the United Network for Organ Sharing database. J Thorac Cardiovasc Surg 2010;140:700–708. 2. Borsato G, Rajan D, Simons M, et al: Central venous stenosis associated with pacemaker leads: Short-term results of endovascular interventions. J Vasc Interv Radiol 2012;23:363–367. 3. Rizvi A, Kalra M, Bjarnason H, et al: Benign superior vena cava syndrome: Stenting is now first line of treatment. J Vasc Surg 2008;47:372–380. 4. Garcia-Delgado M, Navarrete-Sanchez I, Colmenero M, et al: Superior vena cava syndrome after cardiac surgery: Early stenting treatment by percutaneous stenting. J Cardiothorac Vasc Anesth 2007;21:417–419. 5. Sze D, Robbins R, Semba C, et al: Superior vena cava syndrome after heart transplantation: Percutaneous treatment of a complication of bicaval anastomoses. J Thorac Cardiovasc Surg 1998;116:253–261. 6. Cheng S: Superior vena cava syndrome: A contemporary review of a historic disease. Cardiol Rev 2009;17:16–23.
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Immediate Postoperative Percutaneous Stenting of Superior Vena Cava Obstruction Following Heart Transplantation in Adult Patients with Pacemaker Leads David Asseff, M.D.,* Ahmad Y. Sheikh, M.D.,y Daniel Sze, M.D., Ph.D.,z Richard Ha,y Lawrence Hofmann, M.D.,z and Pieter J.A. van der Starre, M.D., Ph.D.* *Department of Anesthesiology and Perioperative Medicine, Stanford University School of Medicine, Stanford, California; yDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California; and zDepartment of Interventional Radiology, Stanford University School of Medicine, Stanford, California ABSTRACT Vena cava superior syndrome is a serious complication after heart transplantation, leading to low cardiac output, cerebral edema, and multi-organ dysfunction. We report three adult patients who underwent heart and heart–lung transplantation and required immediate postoperative balloon angioplasty and stent placement by interventional radiology. The observed obstructions were located at sites of intraoperatively removed pacemaker or defibrillator wires. Percutaneous stent placement immediately improved the hemodynamic condition of the patients. Early recognition of the complication and availability of immediate intervention are essential to prevent further deterioration. doi: 10.1111/jocs.12387 (J Card Surg 2014;29:733–
736)
Acute obstruction of the superior vena cava (SVC) following heart transplantation is a serious complication, since it may cause significant impairment of venous return leading to low cardiac output, cerebral edema, and organ failure. We describe three patients with acute, intraoperative occlusion of the SVC following heart transplantation, likely related to removal of previous pacemaker or internal cardiac defibrillator (ICD) leads, successfully treated with immediate postoperative percutaneous stent placement, and discuss the underlying cause, early warning signs, and potentially preventative measures.
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Pieter J.A. van der Starre, M.D., Ph.D., Department of Anesthesiology and Perioperative Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305. Fax: þ1-650-725-8544; e-mail: [email protected]
PATIENT PROFILES Stanford University Institutional Review Board approval was obtained to report this case series. Patient 1 A 31-year-old male patient who had undergone a Mustard-Senning procedure as a child for transposition of the great arteries and pacemaker implantation for AV block five years prior underwent orthotopic heart transplantation (OHT) for severe right heart failure. Surgical technique included bicaval anastomoses1 and removal of the pacemaker wires. Immediately postoperatively, the patient developed clinical signs of SVC syndrome, including edema, and plethora of the face and upper extremities accompanied by hypotension, lactic acidosis, and oliguria. Transesophageal echocardiography (TEE) demonstrated hypovolemia of both the right and left ventricles. There were no signs of tamponade. Subsequent venography confirmed the diagnosis of high-grade SVC obstruction with near
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J CARD SURG 2014;29:733–736
Figure 1. (A) Venogram showing high-grade SVC obstruction with near stasis of flow (!). (B) Recovery of blood flow in the SVC after balloon angioplasty and stent graft placement with a 10 38 mm PTFE-covered balloon-expandable stent (!).
stasis of flow (Fig. 1A). The patient underwent balloon angioplasty and stenting of the SVC using a 10 mm 38 mm polytetrafluoroethylene (PTFE)-covered balloon-expandable stent-graft (i-Cast, Atrium Medical Inc., Hudson, NH, USA). His hemodynamic condition improved rapidly with resolution of the SVC syndrome (Fig. 1B). The patient recovered completely, and was discharged from the hospital on postoperative day (POD) 15. Patient 2 A 27-year-old male patient with a history of idiopathic cardiomyopathy, atrial fibrillation, and epicardial lead placement during implantation of an automatic internal cardiac defibrillator (AICD) six years prior underwent OHT for worsening left heart failure. The AICD wires were removed. Immediately after weaning from cardiopulmonary bypass (CPB) the patient developed signs of SVC obstruction, with high central venous pressure (CVP) of up to 60 mmHg, arterial hypotension, and oliguria. The patient was transfered straight from the operating room to the interventional radiology (IR) suite, where occlusion of both the right brachiocephalic vein and SVC was documented by venography (Fig. 2A). After balloon angioplasty of the right brachiocephalic vein and angioplasty and stenting with a 12 mm 60 mm self-expanding nitinol stent of the SVC (SMART stent, Cordis Inc., Miami Lakes, FL, USA) (Fig. 2B), his hemodynamic condition improved instantly, with no signs of neurologic impairment. He was discharged from the hospital on POD 11. Patient 3 A 62-year-old male patient with a history of ischemic cardiomyopathy, coronary artery bypass surgery, AICD
placement eight years prior, and progressive interstitial lung disease underwent heart–lung transplantation, complicated by the inability to remove one of the AICD wires. After sternal closure facial swelling was noted, with concomitant hypotension and progressive lactic acidosis. An attempt at insertion of a pulmonary artery catheter was aborted due to apparent obstruction in the SVC. TEE showed hypovolemia of the right and left ventricles. The patient was transferred to the IR suite, where venography revealed a nearly complete obstruction of the SVC and an extremely dilated azygos vein with retrograde flow (Fig. 3A). After balloon angioplasty and stenting with a 14 mm 40 mm self-expanding stent (SMART stent), blood flow in the SVC normalized (Fig. 3B). Despite improvement of his cardiac output, the patient’s condition deteriorated during the following weeks, mainly due to seizures, multiple strokes, heparin-induced thrombocytopenia, acute kidney injury requiring dialysis, candida sepsis, and adenovirus viremia. He expired on POD 53. DISCUSSION This series of patients with postoperative SVC syndrome following heart and heart–lung transplantation shows that immediate postoperative treatment with percutaneous balloon angioplasty and stenting improves the hemodynamic condition of the patient considerably and quickly. The method appeared to be safe, despite these recently transplanted patients having fresh, unhealed bicaval anastomoses, even with the use of bare (uncovered) stents. In adult patients endovascular stenting of the SVC has been mainly described in the setting of benign SVC syndrome due to pacemaker wire-related thrombosis or chronic indwelling venous access devices.2,3 In a report of two cardiac surgery patients with postoperative SVC syndrome and early stenting, the
J CARD SURG 2014;29:733–736
ASSEFF, ET AL. SUPERIOR VENA CAVA STENTING
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Figure 2. (A) Venogram showing occlusion of both the right brachiocephalic vein and SVC (!). (B) Recovery of blood flow after balloon angioplasty of the right brachiocephalic vein, and angioplasty and stenting of the SVC with a 12 60 mm self-expanding nitinol stent (!).
Figure 3. (A) Venogram showing a nearly complete obstruction of the SVC and an extremely dilated azygos vein with retrograde flow (!). (B) Recovery of blood flow after balloon angioplasty and stenting of the SVC with a 14 40 mm self-expanding stent (!).
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obstructions were related to repairs of lacerations during cannulation of the SVC.4 The only earlier reported series of SVC syndrome and stenting in adult patients after heart transplantation involved three patients who underwent both thrombolysis and stenting, but only after POD 8 or later.5 Facial swelling, combined with systemic hypotension, lactic acidosis, and oliguria, is a strong indication for obstruction of the SVC. Failure to insert a balloondirected pulmonary artery catheter through one of the internal jugular veins following the transplantation adds to the diagnosis, in particular when TEE confirms the absence of tamponade. In our series the obstructions in the SVC were located superior to the anastomotic or cannulation sites, clearly related to the former location of AICD or pacemaker wires. They had apparently gradually caused thrombosis and stricture, and after removal during surgery the vena cava collapsed, presumably due to dissection or disruption of the vessel walls. Subsequently, this resulted in low cardiac output, lactic acidosis, and oliguria. This finding excludes the surgical option of open repair, since the location of the obstruction is almost inaccessible, and reopening the sternum would be accompanied by a significantly increased risk of complications. Since AICD insertion for severe heart failure has increased dramatically over the last decade, the risk of development of SVC syndrome following heart transplantation will probably become greater in the coming years.6 It may be recommended to make preoperative computer tomographic (CT) venogram a standard screening procedure in heart transplant recipients
J CARD SURG 2014;29:733–736
with a longstanding AICD in place, to assess the risk of postoperative SVC obstruction. This should be more indicated in patients with a history of congenital abnormalities. It may be worth considering to harvest longer venous pedicles for patients with preexisting pacemaker or AICD wires, and to reconstruct the superior vena cava and brachiocephalic vein of the recipient. Acknowledgments: The authors wish to thank Drs. Ramin Beygui, Philip Oyer, and Michael Dake for their contributions in preparing the manuscript.
REFERENCES 1. Davies R, Russo R, Morgan J, et al: Standard versus bicaval techniques for orthotopic heart transplantation: An analysis of the United Network for Organ Sharing database. J Thorac Cardiovasc Surg 2010;140:700–708. 2. Borsato G, Rajan D, Simons M, et al: Central venous stenosis associated with pacemaker leads: Short-term results of endovascular interventions. J Vasc Interv Radiol 2012;23:363–367. 3. Rizvi A, Kalra M, Bjarnason H, et al: Benign superior vena cava syndrome: Stenting is now first line of treatment. J Vasc Surg 2008;47:372–380. 4. Garcia-Delgado M, Navarrete-Sanchez I, Colmenero M, et al: Superior vena cava syndrome after cardiac surgery: Early stenting treatment by percutaneous stenting. J Cardiothorac Vasc Anesth 2007;21:417–419. 5. Sze D, Robbins R, Semba C, et al: Superior vena cava syndrome after heart transplantation: Percutaneous treatment of a complication of bicaval anastomoses. J Thorac Cardiovasc Surg 1998;116:253–261. 6. Cheng S: Superior vena cava syndrome: A contemporary review of a historic disease. Cardiol Rev 2009;17:16–23.
