superior vena cava syndrome after repeated insertion of transvenous pacemaker

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1014 Yoon et al. October 1993 American Heart Journal Superior vena cava syndrome after repebted ivlsertion elf trzwweno~us pacemaker Jin Yoon, MD, Kwang Kon Koh, MD, FACA, Sang Kyoon Choj MD, Sain SOO Kim, MD, and Sung Hoon Jin, MD Seong Nan, Korea The use of transvenous permanent pacemakers has in- creased in patients with serious bradyarrhythmias and some tachyarrhythmias because of their relative ease of implantation and safety of operatibti. Many of the early limitations related to device size and longevity appear to have been resolved by the development of technology. However, whenever a foreign body is introduced into the heart and central veins and is left there permanently, the risk of thromboembolic complications exists.l There have already been reports of the superior vena cava syndrome resulting from thrombosis around the pacemaker electrode in the right ventricle and superior vena cava.2 The patient reported herein developed superior vena cava thrombosis after repeated insertion of a transvenous pacemaker, and she was thereafter treated by surgical intervention. The patient was a 57-year-old woman who was admitted to our hospital with a l-month history of progressive swelling of the face, neck, arms, and upper chest. Fourteen years earlier she had undergone implantation of a trans- venous VVI pacing system in the right infraclavicular area for symptomatic sick sinus syndrome. Pacemaker revision with transvenous lead implantation was performed via the left subclavian vein 9 years before this admission and the right generator was removed, but the right electrode was firmly adherent to the endocardium and could not be removed. Two years before the generator was replaced by a VVIR type system and the electrode was not changed. Physical examination on admission revealed a body tem- perature of 36.7” C, blood pressure of 100/60 mm Hg, a pulse rate of 8O/min, and a respiratory rate of 20/min. The upper half of the body was swolten. A computed tomogra- phy scan of the chest with injection of contrast medium showed an enlarged superior vena cava and decreased at- tenuation, consistent with intraluminal clot. Through a right subclavian vein catheter, contrast medium was in- jected. Superior venacavography showed extensive clot forniation and total occlusion of the superior vena cava, with multiple collateral veins in the axilla and neck (Fig. 1). From theDivision of Cardiology, Department of Internal Medicine, and”the Department of Thoracic Surgery, Inha Univemity Hospital. Reprint requests: Kwang Non Koh, MD, FACA, Division of Cardiology, Department of Internal Medicine, Inha University Hospital, 3309-327 Tae Pyeong-dong, Seong Nam-shi, Kyunggi-do, 461-192, Korea. AM HEART J 1993;126:1014-1015. Copyright @ 1993 by Mosby-Year Book, Inc. 000%8703/93/$1.00 + .lO 4/4/48524 Fig. 1. Superior venacavogram demonstrated a large fill- ing defect in the superior vena cava tiith marked dilatation of the right internal jugular vein and subclavian vein and complete obstruction of the superior vena cava. Multiple tortuous collateral vessels were noted. Two pacemaker electrodes were found in the right ventricle. Urokinase was administered by continuous infusion of 20,000 units/hr for 3 days. However, the edema did not subside. Two days after discontinuation of the urokinase infusion, surgical intervention was performed. This in- cluded thrombectomy with a Fogarty catheter and supe- rior vena cava reconstruction with pericardium. The elec- trodes in the superior vena cava and right ventricle were removed. Pacemaker revision with epimyocardial lead im- plantation was performed and the lead was positioned at the right ventricle. On pathologic examination, the mate- rial obtained from the superior vena cava showed organized thrombus with calci&tion (Fig. 2). After surgery, the edema subsided. The paiient was discharged without tak- ing &nticoagula.nts. Thrombosis of the superior vena cava is an uncommon but potentially life-threatening complication of trans- venous cardiac pacing. The pathogenesis of venous throm- bosis after implantation of a transvenous permanent pace- maker has not been cleaily determined. Thrombosis in the absence of coexistent stebosis tends to occur early, usually less than 1 year after implantation of a permanent pace- maker. Venous thrombosis that occurs more than 1 year after implantation of a permanent transvenous pacemaker is usuilly associated with underlying venous stenosis. Studies tell us that whenever the electrodes came itito con-

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Page 1: Superior vena cava syndrome after repeated insertion of transvenous pacemaker

1014 Yoon et al. October 1993

American Heart Journal

Superior vena cava syndrome after repebted ivlsertion elf trzwweno~us pacemaker

Jin Yoon, MD, Kwang Kon Koh, MD, FACA, Sang Kyoon Choj MD, Sain SOO Kim, MD, and Sung Hoon Jin, MD Seong Nan, Korea

The use of transvenous permanent pacemakers has in- creased in patients with serious bradyarrhythmias and some tachyarrhythmias because of their relative ease of implantation and safety of operatibti. Many of the early limitations related to device size and longevity appear to have been resolved by the development of technology. However, whenever a foreign body is introduced into the heart and central veins and is left there permanently, the risk of thromboembolic complications exists.l There have already been reports of the superior vena cava syndrome resulting from thrombosis around the pacemaker electrode in the right ventricle and superior vena cava.2 The patient reported herein developed superior vena cava thrombosis after repeated insertion of a transvenous pacemaker, and she was thereafter treated by surgical intervention.

The patient was a 57-year-old woman who was admitted to our hospital with a l-month history of progressive swelling of the face, neck, arms, and upper chest. Fourteen years earlier she had undergone implantation of a trans- venous VVI pacing system in the right infraclavicular area for symptomatic sick sinus syndrome. Pacemaker revision with transvenous lead implantation was performed via the left subclavian vein 9 years before this admission and the right generator was removed, but the right electrode was firmly adherent to the endocardium and could not be removed. Two years before the generator was replaced by a VVIR type system and the electrode was not changed. Physical examination on admission revealed a body tem- perature of 36.7” C, blood pressure of 100/60 mm Hg, a pulse rate of 8O/min, and a respiratory rate of 20/min. The upper half of the body was swolten. A computed tomogra- phy scan of the chest with injection of contrast medium showed an enlarged superior vena cava and decreased at- tenuation, consistent with intraluminal clot. Through a right subclavian vein catheter, contrast medium was in- jected. Superior venacavography showed extensive clot forniation and total occlusion of the superior vena cava, with multiple collateral veins in the axilla and neck (Fig. 1).

From theDivision of Cardiology, Department of Internal Medicine, and”the Department of Thoracic Surgery, Inha Univemity Hospital.

Reprint requests: Kwang Non Koh, MD, FACA, Division of Cardiology, Department of Internal Medicine, Inha University Hospital, 3309-327 Tae Pyeong-dong, Seong Nam-shi, Kyunggi-do, 461-192, Korea.

AM HEART J 1993;126:1014-1015.

Copyright @ 1993 by Mosby-Year Book, Inc. 000%8703/93/$1.00 + .lO 4/4/48524

Fig. 1. Superior venacavogram demonstrated a large fill- ing defect in the superior vena cava tiith marked dilatation of the right internal jugular vein and subclavian vein and complete obstruction of the superior vena cava. Multiple tortuous collateral vessels were noted. Two pacemaker electrodes were found in the right ventricle.

Urokinase was administered by continuous infusion of 20,000 units/hr for 3 days. However, the edema did not subside. Two days after discontinuation of the urokinase infusion, surgical intervention was performed. This in- cluded thrombectomy with a Fogarty catheter and supe- rior vena cava reconstruction with pericardium. The elec- trodes in the superior vena cava and right ventricle were removed. Pacemaker revision with epimyocardial lead im- plantation was performed and the lead was positioned at the right ventricle. On pathologic examination, the mate- rial obtained from the superior vena cava showed organized thrombus with calci&tion (Fig. 2). After surgery, the edema subsided. The paiient was discharged without tak- ing &nticoagula.nts.

Thrombosis of the superior vena cava is an uncommon but potentially life-threatening complication of trans- venous cardiac pacing. The pathogenesis of venous throm- bosis after implantation of a transvenous permanent pace- maker has not been cleaily determined. Thrombosis in the absence of coexistent stebosis tends to occur early, usually less than 1 year after implantation of a permanent pace- maker. Venous thrombosis that occurs more than 1 year after implantation of a permanent transvenous pacemaker is usuilly associated with underlying venous stenosis. Studies tell us that whenever the electrodes came itito con-

Page 2: Superior vena cava syndrome after repeated insertion of transvenous pacemaker

Volume 126, Number 4

American Heart Journal Yoon et al. 1015

Fig. 2. Om pathologic examination, the material extracted from the superior vena cava showed organized thrombus with calcification.

tact with the vascular endothelial lining, the electrodes were incorporated into the vessel or endocardium and were overgrown by fibrous tissue and endothelium.3*4 The development of venous collaterals may further decrease flow in the stenotic venous segment. Consequently, exten- sion of thrombosis and subsequent venous occlusion occur. The long-term presence of permanent pacemaker elec- trodes in the central vein may also act as a continuing ni- dus for thrombus formation. The presence of multiple transvenous pacemaker leads also increases the risk of thrombosis. 2, 4 Symptomatic thrombosis of the central veins attributed to permanent transvenous pacemaker leads is uncommon; it affects.from 1% to 3% of patients with permanent transvenous pacemaker electrodes. Most patients with chronic venous thrombosis remain asymp- tomatic because the gradual formation of a thrombus facilitates the development of an adequate venous collat- eral circulation. Symptomatic pacemaker-induced venous thrombosis generally implies either acute venous throm- bosis or extension of previously localized thrombus that occludes venous collaterals. Pacemaker-induced superior vena cava syndrome is rare and occurs from 1 month to 15 years after implantation of a pacemaker. Most cases are-the result of thrombosis in the superior vena cava, but several cases involve fibrotic stenosis of the superior vena cava without thrombosis. In addition, propagation of thrombus from peripheral veins to the superior vena cava has also been n0ted.l

The initial therapy for early electrode-induced superior vena cava syndrome is bed rest and anticoagulation with heparin and subs,equently with warfarin. Thrombolytic therapy has been used for the initial management of elec- trode-induced acute thrombosis plus chronic thrombosis and for patients in whom anticoagulation fails. Successful thrombolysis usually occurs when thrombus has been

present for less than 7 to 10 days; in certain cases, however, thrombolytic theraipy results in resolution of the clinical symptoms 3 weeks after their onset.2 In instances in which superior vena cava obstruction induced by endocardial pacing electrodes requires urgent relief, surgical decom- pression is preferred. Thrombotic occlusion of the major venous tributaries may be relieved by thrombectomy with a Fogarty venous catheter, and patching or replacement of the diseased segment of the superior vena cava or the stenotic area of the superior vena cava can be corrected by angioplasty.5, 6 Our case is the result of thrombosis without fibrotic stenosis of the superior vena cava. In our patient surgical repair and thrombectomy with a Fogarty catheter were performed because the thrombotic segment failed to recanalize with thrombolytic therapy and symptoms were progressive.

REFERENCES

1. Peter CS, David LH. Venous complications after insertion of a transvenous pacemaker. Mayo Clin Proc 1992;67:258-65.

2. Blackburn T, Dunn M. Pacemaker-induced superior vena cava syndrome: consideration of management. AM HEART J 1988;116:893-6.

3. Huang TY, Baba N. Cardiac pathology of transvenous pace- makers. Ai HEART J 1972;83:469-74.--

4. Friedman SA. Berger N. Cerruti MM. Kosmoski J. Venous thrombosis &d nirrnaent cardiac iacing. AM HEART J 1973;85:531-53. -

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5. Yakirevich V, Alagem D, Papo J, Vidne BA. Fibrotic stenosis of the superior vena cava obstruction with widespread throm- botic occlusion of its major tributaries: an unusual complica- tion of hansvenous cardiac pacing. J Thorac Cardiovasc Surg 1983; 85:632-4.

6. Sunder SK, Ekong EA, Sivalingam K, Kumar A. Superior vena cava thrombosis due to pacing electrodes: successful treat- ment with combined thrombolysis and angioplasty. AM HEART J 1992;123:790-2.