Following Long-Term Transvenous Pacing
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1 The Incidence of Venous Thrombosis Following Long-Term Transvenous Pacing William S. Stoney, M.D., Ronald B. Addlestone, M.D., William C. Alford, Jr., M.D., George R. Bums, M.D., Robert A. Frist, M.D., and Clarence S. Thomas, Jr., M.D. ABSTRACT Long-term cardiac pacing with permanent transvenous electrodes has achieved wide acceptance with only occasional reports of venous obstruction and edema. To determine the incidence of venous abnormalities associated with transvenous electrodes, 34 venograms were obtained in 32 patients paced 18 months or longer. Eleven venograms demonstrated severe obstruction with collateral circulation communicating with the opposite cervical and innominate venous channels; 7 of these showed total occlusion. Seven venograms revealed no obstruction. The remaining 16 venograms showed venous stenosis without collaterals. It is concluded that venous abnormalities associated with permanent transvenous pacing occur commonly but are not usually associated with arm or facial edema. Permanent cardiac pacing utilizing transvenous electrodes has become one of the most satisfactory cardiac surgical procedures developed in the past fifteen years. Although initially permanent pacemakers were associated with frequent problems and failure related to the electrodes and components, the units available at present are noted for reliability and durability. Complications produced by electrode fracture and displacement, late threshold elevation, and premature battery failure still occasionally occur but have been diminished by improvements in electrode and pacemaker design and in surgical technique. Venous thrombosis of the subclavian or innominate vein containing the permanent electrode has been infrequently described. The actual incidence of venous abnormalities From the Cardiac Surgical Service, St. Thomas Hospital, and the Department of Thoracic Surgery, Vanderbilt University Hospital, Nashville, TN. Presented at the Twelfth Annual Meeting of The Society of Thoracic Surgeons, Jan 26-28, 1976, Washington, DC. Address reprint requests to Dr. Stoney, Suite 501, St. Thomas Medical Building, 4230 Harding Rd, Nashville, TN associated with permanent transvenous pacemaker electrodes has been reported [l, 71 but has received little attention in the English literature. To assess the frequency of venous abnormalities produced by pacemaker electrodes, a group of patients was; evaluated by venograph y. Materials and Methods During a 6-month period, subclavian venograms were obtained in patients with permanent pacemakers who were hospitalized for elective replacement. All electrodes had been functioning for two years or more except 1 which had been in place for 18 months. All patients admitted for pacemaker replacement were studied except those excluded by request of the patient or the referring physician. The permanent pacemaker electrode had been inserted in the external jugular vein in a few patients, but the majority had been placed in the cephalic vein at the deltoid-pectoral junction. Thirty-two patients were stu'died. Two patients had had an electrode in each subclavian vein in the past, and bilateral venograms were obtained. A total of 34 venograms was available for study. The venograms were performed by placing a 16-gauge cannula in a peripheral arm vein on the side to be studied. Using forcejful hand injection, 50 cc of Conray-60 was injected and ten films were exposed at a rate of one frame per second. In 3 patients bilateral siimultaneous injections were made. Results A normal venogram with no obstruction was found in only 7 patients (21%) (Fig 1). Mild obstruction estimated to be less than 50% of the lumen of the innominate or subclavian vein was found in 5 additional patients ('15%). Obstruc- 166
2 167 Stoney et al: Venous Thrombosis after Transvenous Pacing Fig 1. A normal venous system containing a bipolar electrode. (SVC = superior vena cava.) tion involving 50 to 90% of the lumen was seen in patients (440/0) (Fig 2); Of them had cervical collateral venous channels. In 7 patients (21%) total venous obstruction was observed (Fig 3); each Of these patients had developed venous collateral circulation. sion. This suggests that a large bipolar electrode is more likely to produce obstruction than a smaller unipolar electrode. The was commonly located in the central part of the subclavian vein 2 or 3 cm proximal to the cephalic vein, which was the usual site of cannulation. In 7 patients the obstruction was noted in the innominate vein at its junction with the superior vena cava. In no A Ordis Or instance was the superior vena cava involved. electrode had been utilized in 11 patients, and Clinical symptoms and physical findings Partial was Ob- were rare. One patient was hospitalized because served, only 1 patient with a unipolar electrode of sudden onset of pain and edema of the left had The remaining 23 arm after four years of uneventful cardiac patelectrodes were bipolar Medtronic units, and 6 ing. * venogram revealed complete of them were associated with complete occluof the innominate and subclavian veins extend- FigZ. Severestenosis ofthesubclavian vein, which contains a unipolar electrode. There are no collaterals. (SVC = superior vena cava.) ing out to the axillary vein (Fig 4). Following initial arm elevation and intravenous heparinization the acute symptoms subsided, and 3
3 168 The Annals of Thoracic Surgery Vol 22 No 2 August 1976 Fig3. Total venous obstruction of the innominate and subclavian vein with elaborate cervical collaterals. months later the arm had returned to normal size. Several patients were noted to have either a prominent external jugular vein or a conspicuous subcutaneous venous pattern in the pectoral region, and this was usually associated with an abnormal venogram. Other than minimal dependent edema of the hand, the remaining patients were asymptomatic. One additional physical sign of jugular venous obstruction has been observed during ex- Fig4. Total subclavian venous obstruction extending back to the axillary vein with few cervical collaterals. This patient hadsevere arm edema. amination of the supine patient. The absence of a venous pulse in the internal jugular vein on the same side as the pacemaker and electrode, with a prominent cardiac venous pulse in the contralateral jugular system, is suggestive of occlusion on the nonpulsatile side. This physical sign has been observed and confirmed by venography in a single patient and suggests that examination of each jugular system by Doppler ultrasonography could identify veinous obstruction without venography. Comment One of the initial objections to the concept of permanent transvenous cardiac pacing was the
4 169 Stoney et al: Venous Thrombosis after Transvenous Pacing prediction that a significant number of patients would develop thrombosis of the superior vena cava or innominate vein. This prediction was based on the rather frequent occurrence of venous thrombosis associated with central venous catheters introduced through a peripheral vein and the incidence of venous thrombosis following placement of ventriculovenous shunts for hydrocephalus [8]. Surprisingly, venous thrombosis has not been a common problem with long-term transvenous pacing. Only 4 cases of symptomatic superior vena caval obstruction have been documented [5, , and 4 additional reports have been published describing axillary-innominate venous obstruction associated with permanent transvenous electrodes [24, 91. All these patients had sudden onset of edema of the face or arm, and the venous obstruction was documented by venography. On the other hand, two recent reports in the German literature suggest that venous obstruction associated with permanent pacemaker electrodes is more common than has previously been suspected. Balau, Mam, and colleagues [ll obtained venograms in 49 patients who were hospitalized for elective pacemaker replacement and found evidence of innominate and subclavian thrombosis in 14. Six patients had extensive collateral circulation in the region of the obstruction, and 3 had chronic edema of the arm. A year later they reported the findings from venograms in 120 patients with permanent transvenous pacemakers [71; the venograms were obtained both early (10 to 30 days) and late (6 to 36 months). Evidence of venous thrombosis was discovered in 34 patients, 18 of whom had collateral venous circulation at the site of obstruction. Six patients had edema of the arm, 4 of these in the first 30 days after pacemaker implantation. In our study a similar ratio of patients was observed to have abnormalities of the venous system containing the permanent pacemaker electrode (Table). Although venous abnormalities associated with permanent pacemaker electrodes are far more common than previously suspected, only an occasional patient has been noted to have facial or arm edema. It is possible that innominate and subclavian obstruction occurs gradually, allowing an adequate collateral circulation to develop so that edema is unusual. Sudden thrombosis in the first few weeks after implantation would be more likely to produce edema since collaterals would not have formed. Similarly, extension of a previously localized obstruction into the axillary vein could obliterate collaterals and produce late symptoms. It was suspected that our single symptomatic patient may have had such progression of thrombosis. Pulmonary embolism has been observed as a rare complication of both temporary and permanent transvenous electrodes [61. In the majority of reported cases the embolus originated in the right atrium or right ventricle. The innominate-subclavian system should also be closely evaluated as a possible source if pulmonary embolization occurs in a patient with a temporary or permanent pacemaker. If a permanent pacing catheter fails and the same site is to be used for replacement, a preliminary venogram should be considered since complete or partial stenosis of the innominatesubclavian drainage is likely. In 1 of our patients venography showed both innominate veins to be completely occluded; successful pacing was reestablished utilizing myocardial electrodes. Reports of Venograms in Patients with Permanent Pacemaker Electrodes, Excluding Single Case Reports No. of Venous Obstruction Arm or Report Venograms No. Abnormal with Collaterals Facial Edema Balau et a1 [l] Marx et a1 [7] This report (29%) 6 (12%) (28%) 18 (15%) (44%) 7 (21%) 3 (6%) 6 (5%) 1(3%) Total (31%) 31 (15%) 10 (5%)
5 170 The Annals of Thoracic Surgery Vol 22 No 2 August 1976 These findings lead to the conclusion that occult venous obstruction occurs in a significant number of patients with transvenous electrodes. This may have therapeutic implications should pulmonary embolization occur, and it may also affect surgical management if a catheter requires removal with replacement through the same innominate venous system. References 1. Balau J, Buysch KH, Mam E, et al: Thrombose der Vena subclavia nach transvenoser Schrittmacher Implantation. Radiologe 11:50, Girardier J, Sow M, Bouhey J, et al: Thrombose axillo-sous-claviere apres implantation par voie veineuse d un stimulateur cardiaque. Lyon Chir 68:211, Griepp RB, Daily PO, Shumway NE: Subclavian-axillary vein thrombosis following implantation of a pacemaker catheter in the internal jugular vein. J Thorac Cardiovasc Surg 60:889, Gschnitzer F: Thrombose der Vena subclavia und axillaris nach Herzschrittmacher Implantation. Wien Klin Wochenschr 84:393, Kaulbach MG, Krukonis EE: Pacemaker electrode-induced thrombosis in the superior vena cava with pulmonary embolization. Am J Cardiol 26:205, London AR, Runge PJ, Balsam RF, et al: Large right atrial thrombi surrounding permanent transvenous pacemakers. Circulation 49:661, Marx NE, Schulte HD, Balau J, et al: Phlebographische und klinische friih und spatbefiinde bei transvenos implantierten Schrittmacherelektroden. Z Kreislaufforsch 61:115, Nugent GR, Lucas R, Judy M, et al: Thromboembolic complications of ventriculo-atrial shunts. J Neurosurg 24:34, Pereira W, Mershon JC: Permanent transvenous pacemakers: non-electrical complications and hazards. J Kans Med SOC 74:450, Sethi GK, Bhayana JH, Stewart SM: Innominate venous thrombosis: a rare complication of transvenous pacemaker electrodes. Am Heart J 87:770, Wertheimer M, Hughes RK, Castle CH: Superior vena cava syndrome: complications of permanent transvenous endocardia1 cardiac pacing. JAMA 224:1172, Williams DR, Demos NJ: Thrombosis of superior vena cava caused by pacemaker wire and managed with streptokinase. J Thorac Cardiovasc Surg 68:134, 1974 Discussion DR. SEYMOUR FURMAN (Bronx, NY): A review of our patients shows 5 who have had some kind of symptomatic thrombophlebitis or edema of the arm on the side of implantation out of approximately 1,600 patients who have received a transvenous cardiac pacemaker. One patient was quickly found to have an associated carcinoma of the pancreas. No abnormality was discovered in the second, and the edema receded spontaneously within approximately ten days. The remaining 3 had immediate postimplantation edema; in 2 it receded promptly, but in the third it has persisted at a very mild level for more than a year and has necessitated specific therapy. While the occurrence of embolization from this site should call attention to the possible thoracic venous origin of pulmonary emboli, so few instances of pulmonary embolism have been reported in the medical literature that it remains an unusual complication of transvenous pacer therapy. Perhaps the most significant finding of Dr. Stoney s report, our review of our own patients, and the descriptions in the literature is the benign and even asymptomatic nature of what seems to be radiologically significant venous thrombosis. Three patients with partially or totally occluded venous systems were detected only during investigation and were totally asymptomatic, indicating that the thrombosed vein is a far less significant lesion than the roentgenogram suggests. DR. STONEY: I thank Dr. Furman for his remarks. I believe he has summarized the essence of this discussion: that although venous abnormalities occur frequently, they are almost never a clinical problem. Our findings are not intended in any way to denigrate the transvenous electrode as a primary technique in cardiac pacing, and of course we use it as our technique of choice.
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