Abstract
One day after implantation of a permanent pacemaker in an 82-year-old man, transthoracic echocardiography showed a mass in the right ventricle and a small pericardial effusion. Transesophageal echocardiography revealed a mass attached to the pacemaker lead. Subcutaneous administration of enoxaparin was begun, and the patient remained free of symptoms for the duration of his hospital stay. Follow-up echocardiography performed before discharge failed to show the right ventricular mass, but a lung perfusion scan revealed multiple bilateral perfusion defects consistent with pulmonary emboli. The patient was discharged on a regimen of enoxaparin for another 30 days. Two years later, he remained asymptomatic. (Tex Heart Inst J 2001;28:318–9)
Key words: Aged; aged, 80 and over; electrodes; male; pacemaker, artificial/adverse effects; pulmonary embolism; thrombosis/etiology
In July of 1997, an 82-year-old man with a history of exertional dyspnea was admitted to the emergency room after an episode of syncope. The electrocardiogram showed complete heart block with a ventricular rate of 25 beats/min. A temporary transvenous pacemaker was implanted through the right femoral vein. On the next day, an unsuccessful attempt was made to implant a permanent pacemaker through the left subclavian vein; 48 hours later, the attempt was successful.
A transthoracic echocardiogram performed on the 5th day of hospitalization (1 day after successful pacemaker implantation) showed a small pericardial effusion and a 2-cm-diameter mass in the right ventricle, with no obvious site of attachment. Transesophageal echocardiographic investigation revealed a 1.4-cm-diameter round, mobile mass attached to the pacemaker lead (Fig. 1). Subcutaneous administration of enoxaparin (40 mg daily) was begun, and the patient remained free of symptoms for the duration of his hospital stay. Follow-up transesophageal echocardiography performed 24 hours after initiation of enoxaparin treatment, and again 6 days after, failed to show the right ventricular mass, although the latter study disclosed a moderate pericardial effusion (1.7 cm). A lung perfusion scan revealed multiple bilateral perfusion defects consistent with pulmonary emboli (Fig. 2). The patient was discharged on a regimen of 40 mg enoxaparin daily, which was continued for another 30 days. At his last follow-up appointment, in August of 1999, he remained asymptomatic.

Fig. 1 Transesophageal echocardiogram shows a mobile mass (large arrows) attached to the pacemaker lead (small arrows).
LA = left atrium; LV = left ventricle; RV = right ventricle

Fig. 2 Lung perfusion scan reveals multiple bilateral perfusion defects compatible with pulmonary emboli.
Discussion
Permanent cardiac pacing is a safe and widely used therapeutic intervention for bradyarrhythmias. In a 1969 autopsy series involving 7 patients who died 5 days to 18 months after insertion of a pacemaker, Robboy and colleagues found no pulmonary emboli. 1 However, the incidence of asymptomatic pulmonary embolism associated with pacemaker implantation has been reported to be as high as 15%, 2 and at least 1 such case of multiple pulmonary embolism has resulted in death. 3 Possible precipitating factors for thrombosis in association with pacemaker implantation are as diverse as damage to the subclavian vein, paroxysmal atrial fibrillation, and stasis secondary to immobilization. 4 Thrombolysis with infusion of rTPA (tissue plasminogen activator) for 2 hours has been recommended for patients with pacemaker-associated right atrial thrombus. 5 Although prophylactic administration of low doses of heparin after implantation has been recommended, 2 hematoma formation at the pulse-generator site is a cause of major concern. It has been suggested that patients with venous thrombosis around the pacemaker leads, or with pulmonary embolism, receive lifelong anticoagulation. 6,7
Our patient had a pericardial effusion after pacemaker implantation. We felt that full-dose anticoagulation would be dangerous if the pericardial effusion was due to right ventricular perforation by the lead of the temporary transvenous pacemaker. Therefore, an antithrombotic dose of low-molecular-weight heparin was begun and was continued for 30 days after discharge. However, the sudden disappearance of the mass and the result of the pulmonary lung scan strongly suggest that pulmonary embolism occurred within 24 hours after initiation of treatment.
Footnotes
Address for reprints: Manuel Martínez-Sellés, MD, Servicio de Cardiología, Hospital Universitario Gregorio Marañón, Doctor Esquerdo 46, 28007 Madrid, Spain
References
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