Transvenous cardiac pacemaker, mural thrombosis,

and pulmonary embolism

James Reynolds, M.D.* David Anslinger, M.D.** Richard Yore, M.D.*** Robert Paine, M.D.*“*”

5-t. Louis, MO.

T reatment of heart block by trans- venous catheter pacing is an effective

therapy which does not require a major surgical procedure. However, complications have been encountered including pace- maker failure because of displacement of the electrode from the right ventricle, power unit failure, wire breakage or loss of contact with a responsive endocardium, wound infection, and perforation of the heart.

Thromboembolic complications have been rare during transvenous pacing and no dif- ference in voltage requirement or thrombo- embolism has followed anticoagulant pro- phylaxis. l-3 Deposition of “a black mate- rial” about an electrode has been reported by Gordon,4 and venous inflammation and thrombosis have been noted.4p” Fatal pul- monary embolism followed the develop- ment of a right ventricular thrombus in a case described by Goldberger.6

We are reporting a case of pacemaker

failure with unusual and illuminating fea- tures.

Case report, A 76-year-old man developed complete heart

block in 1966. A left ventricular transthoracic pace- maker was implanted and he did well until June 1, 1968, when he had an acute episode of weakness and dizziness due to battery failure. On June 6, 1968, a permanent trunswenous pacemaker was inserted into the right ventricle. He was readmitted on Sept. 21, 1968, because of intermittent episodes of weakness and dizziness during the preceding two weeks. Three days prior to admission, he had noted episodes of paroxysmal nocturnal dyspnea.

Upon admission, response to pacemaker impulses was irregular and ventricular rate varied from 40 to 60 beats per minute. Increasing the amplitude and the rate of stimulation failed to remedy the situa- tion. However, positioning the patient on his left side increased the number of impulses that were effective.

On Sept. 24, 1968, a temporary demand pace- maker was inserted under fluoroscopy. During the insertion of the new pacemaker catheter into the right ventricle, it passed alongside the old pace- maker wires (Fig. 1). At this time, the patient

From the Department of Medicine, St. Luke’s Hospital. St. Louis. MO. Received for publication Dec. 3. 1968. *Fellow io Cardiology. Reprint requests to: Dr. Reynolds. St. Luke’s Hospital, 5505 Delmar Blvd., St. Louis. MO.

63112. **Assistant Resident in Medicine. ***surgeon. ****Chief of Medicine, St. Luke’s Haspital. and Associate Professor of Clinical Medicine. Washington University

Medical School, St. Louis. MO.

688 American Heart Journal November, 1969 Vol. 78, No. 5, pp. 688-691

Volume 78 Number 5 Transuen.ous pacemaker, thrombosis, and pulmonary entbolism 689

Fig. 1. The position of the second electrode alongside the malfunctioning transvenous catheter is seen. inactive old transthoracic pacemaker remains implanted in the left ventricle.

The

suddenly complained of acute left anterior chest pain. The new demand pacemaker was placed “on standby.” However, after the onset of chest pain the patient followed the original pacemaker regu- larly, regardless of position.

The chest pain was pleuritic in character and within 30 minutes a pleural friction rub could be heard over the left lower chest. Chest rwntgenogram 1% hours after the onset of his pain showed blunting of the left costophrenic angle. On Sept. 2.5, 1968, a lung scan was compatible with a left lower lobe pulmonary embolus (Fig. 2). Creatine phosphokinase activitv (CPK1 was 36 U. (normal): serum lactic dehyd;og&aae iLDH) was 25‘5 U (n&ma1 0 to 200); bilirubin was 0.6 mg. per cent. Heparin was ad- ministered and the old pacemaker continued to function well. The new temporary demand pace- maker remained on standby.

Over the next 48 hours, chest pain subsided and the pleural friction rub disappeared. On Sept. 28, 1968, a large painful hematoma appeared in the right buttocks at the site of an injection given prior to anticoagulation. Due to this, heparin therapy was interrupted on Oct. 1, 1968. During the evening of Oct. 2, 1968, several episodes of nonconducted pace- maker impulses occurred. The irregular cardiac re- sponse to the pacemaker continued despite ample

impulse voltage. Heparin therapy was restarted on Oct. 4, 1968, and by the evening of Oct. 5, 1968, pacemaker response returned to normal. On Oct. 8, 1968, the temporary pacemaker wires were removed. A bit of material attached to the electrode tip proved to be an organizing thrombus upon histologic exami- nation. Coumadin was administered and when prothrombin times were within therapeutic range, heparin was discontinued. The pacemaker has func- tioned normally since then.

Difbcussion

Pacemaker failure occurred in this pa- tient despite the fact that the electrode position in the right ventricle was con- firmed radiologically. The pacemaker im- pulse “blip” was large and rhythm was regular. These observations are consistent with an increased impedance between the electrode and the endocardium which could be modified by changes in the pa- tient’s position.

Abrupt recovery of effective stimulation when a second nonenergized catheter was

690 Reynolds et al. Am. Heart 3. November, 1969

Fig. 2. P-A lung scan showing decreased perfusion in area of pleural friction rub.

passed into the right ventricle alongside the malfunctioning electrode might have resulted from the dislodgement of clot around the catheter tip or from a shift of electrode position. The virtually simul- taneous occurrence of pleuritic pain fol- lowed by a pleural friction rub and enzy- matic and isotopic evidence of pulmonary embolism and infarction are persuasive evidence that the second catheter sheared away a clot and restored electrical contact between the pacing electrode and the endo- cardium. We are aware of no previous in- stance of this form of pulmonary embolism.

The remarkable sequence of events in- cluded the development of a loud pleural friction rub within 1 to 2 hours after em- bolism occurred.

The subsequent failure of electrode pac- ing during cessation of heparin therapy with recovery of function upon reinstitu- tion clearly suggests recurrent perielectrode thrombosis. The histologic identification of organizing clot about the extracted catheter lends credence to this possibility.

The effectiveness of Coumadin anti- coagulation in this instance is suggested by the continued functioning of the pacemaker after heparin was supplanted by warfarin therapy.

Summary

In a case of pacemaker failure, insertion of a second transvenous electrode into the right ventricle resulted in apparent im- mediate pulmonary embolism and simul- taneous restoration of effective stimulation by the original malfunctioning electrode.

The case provided an exceptional oppor- tunity to recognize an offending perielec- trode thrombus and to time precisely the sequence of events after pulmonary em- bolism. The effectiveness of anticoagulant therapy in preventing electrode inter- ference by thrombosis was suggested.

REFERENCES

1. Schwedel, J. B., and Escher, D. J. W.: Trans- venous electrical stimulation of the heart, Ann. New York Acad. SC. 1112972, 1964.

2. Yucecglu, Y. Z., Lunger, M., and Dresdale, D.:

Volwne 78 Nrmber 5 Transvenous pacemaker, thrombosis, and pulmonary embolism 691

Transvenous electrical pacing of the heart, Axr. HEART J. 715, 1966.

3. Harris, A. M.: Endocardial pacing, AM. HEART J. 7S13.5, 1966.

4. Gordon, A. J.: Catheter pacing in complete heart block, J. A. M. A. 193:1091, 1965.

5. Zucker, K., Parsonett, F., Gilbert, L., and Asa, M.: Dipolar electrode in heart block, J. A. M. il. 184549, 1963.

6. Goldberg, E.: Complications of pacemaker therapy for heart block, Am. J. Cardiol. 17:439, 1966.