Electrophysiology Corner

A Unique Pacemaker Complication of Thrombus Formation in the Right Internal Jugular Vein Due to Unusual Migration of an Atrial P

Thomas S. Faber, MD, Andreas Grom, MD, Manfred Zehender, MD
Thomas S. Faber, MD, Andreas Grom, MD, Manfred Zehender, MD
Common complications of permanent endocardial pacing systems include infection of the generator pocket, the wire track, increase in pacing threshold or complete exit block due to fibrosis at the myocardial contact site, dislocation or (rarely) intravascular migration of the electrode.1 Although phlebothrombosis of upper major veins, such as the superior vena cava and the subclavian vein, occasionally complicates placement of transvenous endocardial leads,2–4 clinical manifestation is uncommon or mild; it includes edema of the upper extremities or cervical venous engorgement due to the vena cava syndrome.4–6 Intravascular migration of a pacing lead and subsequent thrombosis of the right internal jugular vein, a combination of two rarely occurring complications during permanent pacemaker therapy, were observed in the following case report. Case Report. A 64-year-old woman with a 5-year history of permanent dual chamber pacemaker treatment (generator: Siemens 2016T; atrial lead: Osypka KYII67; ventricular lead: Medtronic 4081) due to sinus node dysfunction was admitted to our hospital because of irregular, painless contractions of the right-sided cervical muscles during the previous four months. The patient’s history did not reveal any other disease or neurological symptoms. During the otherwise normal physical examination, frequent right-sided cervical muscle contractions were observed in certain head positions, disappearing completely when the position was changed. The routine surface electrocardiogram showed atrial fibrillation (mean ventricular rate, 85 beats/minutes) with regular non-capturing pacing artifacts at a rate of 60 beats/minute, synchronously to the cervical muscle contractions. The pacemaker test revealed normal function of the unipolar ventricular lead, while the unipolar atrial electrode could not be tested during atrial fibrillation. However, when the highest sensitivity of 0.5 mV was programmed to the atrial lead, the pacing spikes could be reproducibly inhibited by manipulation in the cranial area of the right internal jugular vein. Subsequent posterior-anterior x-ray of the chest and cervical area showed a displaced atrial pacemaker wire as the cause of the intermittent clinical and electrocardiographic phenomenon (Figure 1). Additionally, duplex-ultrasound of the jugular vein revealed a clinically asymptomatic, non-occlusive, floating thrombus formation at the tip of the displaced lead (Figure 2). After diagnosis, surgical extraction of the displaced lead was discussed. However, because of the floating thrombus formation, it was decided to leave the patient on warfarin (INR 2-3), which was previously initiated about 6 months prior because of atrial fibrillation. Finally, the atrial lead was programmed off. When the patient was readmitted 4 weeks later, duplex ultrasound revealed a small, organized and non-floating thrombus formation at the tip of the pacing lead. During the follow-up period of 12 months, there was no evidence for progression and the patient was clinically doing very well. At that point, the patient refused surgical intervention for removal of the dislodged lead. Consequently, therapeutic anticoagulation and frequent duplex ultrasound assessment of the right internal jugular vein were felt to be sufficient to treat this rare complication. Discussion. Phlebothrombosis and displacement of electrodes from the initial contact point are occasional complications of permanent pacemaker therapy. Insertion of endocardial pacemaker leads predisposes to occlusive or non-occlusive thrombosis, mostly involving the lead-containing axillary, subclavian veins or the superior vena cava.2–6 The venographically and Doppler confirmed incidence of thrombosis of upper veins is relatively high and may vary from 21–65%.2,4 However, in most instances sufficient collateral circulation is well preserved and incidence of symptoms of clinically overt venous thrombosis, such as upper extremity edema, cervical venous engorgement or superior vena cava syndrome, seem not to be high.3,4 Displacement of pacemaker electrodes usually occurs in the first weeks after insertion. It occurs most frequently with atrial leads due to passive fixation in dilated right atria with reduced trabecula. The dislodged pacing wire usually remains, depending on the initial contact point either in the atria or the ventricle. Displacement becomes evident when subsequent exit and entrance block causes clinical symptoms or is diagnosed during routine pacemaker control or chest x-ray. Although early or late displacement of endocardial screw-in leads is known, only a few reports exist addressing the problem of self-freeing pacemaker leads migrating in atypical positions causing sometimes serious clinical symptoms.1,2,7–12 Our report describes one of the unique complications of late dislodgement and migration of an atrial screw-in pacemaker lead into the right internal jugular vein causing subsequent subclinical thrombus formation at the tip of the electrode. Although migration into the inferior vena cava7,10–12 and the pulmonary vascular system has been reported,7,9 only a few other comparable cases have been described earlier in the literature in which the migration of endocardial pacemaker leads caused thrombosis in central veins initially not containing the pacemaker lead.1,8,10 While Girard et al.8 reported a cerebral venous sinus thrombosis that occurred along with thrombosis of the jugular vein, subclavian vein and superior vena cava in association with an in-dwelling transvenous pacemaker, Toumbouras et al.10 described such a complication due to migration of a retained functionless pacemaker electrode with subsequent thrombosis of the inferior vena cava. Although the wire-associated thrombosis of the internal jugular vein did not lead to a symptomatic occlusion of cerebral venous sinus in our patient, the presented case nevertheless demonstrates a very rare, but potentially life-threatening, late complication of otherwise safe permanent pacemaker therapy. It is possible that the previously initiated anticoagulation for atrial fibrillation helped to prevent the internal jugular vein from complete thrombotic occlusion. Our case and those described in the literature suggest that anticoagulant prophylaxis should be considered in patients with displaced endocardial leads that migrate into central veins and cannot be removed, e.g., using novel extraction devices.
References
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