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Ann Thorac Surg 1995;59:1272-1273
© 1995 The Society of Thoracic Surgeons


Correspondence

Postpericardiotomy Syndrome After Pacemaker Implantation

Yasushi Terada, MD, Toshio Mitsui, MD, Yuichiro Kaminishi, MD, Yukihiro Yoshimura, MD

Institute of Clinical MedicineUniversity of Tsukuba Hospital University of Tsukuba Tsukuba Ibaraki-ken 305 Japan

To the Editor:

Postpericardiotomy syndrome may occur after nearly any form of cardiac operation in which the pericardium is opened. Here we report a case of postpericardiotomy syndrome after pacemaker implantation, with difficulty in differentiating this condition from pacemaker infection. We also show an important finding that thickening of the pericardium vanished as the syndrome improved.

A 64-year-old woman was admitted to the hospital to undergo a pacemaker reimplantation because of depletion of the implanted pulse generator due to an insulation disruption of the transvenous lead. Because the patient had thrombosis of the brachiocephalic vein, a permanent pacemaker (model 2040T; Siemens-Elema, Stockholm-Solna, Sweden) was installed using epicardial leads through a subxyphoid pericardiotomy, and the generator was placed subcutaneously in the left upper abdominal quadrant on October 13, 1994. The patient received prophylactic antibiotics and had an uneventful postoperative course.

Beginning on the tenth postoperative day, the patient had a spiking fever up to 38° to 38.5°C every afternoon associated with shaking chills and precordial chest pain, which was intensified by deep inspiration and lying supine. No friction rub was audible. The wound was not infected and the skin overlying the pulse generator was not erosive. The white cell count was 8,300/µL with a normal differential count. The C-reactive protein value was 5.6 mg/dL (normal range, less than 0.2 mg/dL). Cultures of blood were sterile. A chest x-ray film showed enlargement of the cardiac silhouette and pleural effusion. An echocardiogram showed minimal pericardial effusion. A chest computed tomographic scan demonstrated that the pericardium was thickened markedly all around (Fig 1Go).



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Fig 1. . Chest computed tomographic scan showing the thickened pericardium (between arrows).

 
To exclude infection around the pulse generator and leads, the pericardial cavity was reentered through the same incision. There was no infection around the pacemaker system. The pericardial cavity contained only a small amount of bloody fluid, smears and cultures of which were sterile. The pericardium adhered loosely with thickening. Skin patch tests were negative for titanium, polyurethane, and silicone. Viral tests were negative. We diagnosed this case as postpericardiotomy syndrome, and administration of loxoprofen sodium, 180 mg a day by mouth, was started. The chest pain and fever were relieved for the subsequent 3 weeks. A chest computed tomographic scan performed 6 weeks after the operation showed that the thickening of the pericardium had disappeared (Fig 2Go).



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Fig 2. . Chest computed tomographic scan performed after the syndrome improved showed that thickening of the pericardium vanished.

 
The postpericardiotomy syndrome first was described as the postcommissurotomy syndrome by Soloff and associates in 1953 [1], and it became clear that this syndrome could occur after any operation that involved opening the pericardium [2]. Although viral tests were negative in the case presented herein, we suggest that the syndrome was due to an immunologic response and a viral infection [3, 4]. Heart-reactive antibodies in the serum and titers to one or more viral agents are particularly higher in one-fourth of patients in whom this syndrome develops [3, 4]. Clinically, symptoms consist primarily of fever and chest pain [5], which appear a few weeks to a few months after cardiac operation with a median postoperative time of onset of 4 weeks [6]. The syndrome is self-limiting, and recurrences are common [6].

We speculate that the thickened pericardium demonstrated on the chest computed tomographic scan may represent an overreactive healing precess of the damaged pericardial tissue. Blood and its products superimposed on injured pericardial surfaces occasionally may lead to pericardial adhesions with thickening [7]. The fact that thickening of the pericardium vanished as the syndrome improved supports our speculation.

We believe that postpericardiotomy syndrome after pacemaker implantation is a rare condition; however, a chest computed tomographic scan is helpful to make a diagnosis and differentiate this condition from pacemaker infection.

References

  1. Soloff LA, Zatuchui J, Janton OH, O'Neill TJE, Glover RP. Reactivation of rheumatic fever following mitral commissurotomy. Circulation 1953;8:481–93.
  2. Ito T, Engle MA, Goldberg HP. Postpericardiotomy syndrome following surgery for non-rheumatic heart disease. Circulation 1958;17:549–56.
  3. Engle MA, McCabe JC, Ebert PA, Zabriskie JB. The postpericardiotomy syndrome and antiheart antibodies. Circulation 1974;49:401–6.
  4. Engle MA, Zabriskie JB, Senterfit LB, Gay WA Jr, O'Loughlin JE, Ehlers KH. Viral illness and the postpericardiotomy syndrome: a prospective study in children. Circulation 1980;62:1151–8.
  5. Kirsh MM, McIntosh K, Kahn DR, Sloan H. Postpericardiotomy syndromes. Ann Thorac Surg 1970;9:158–79.
  6. Nishimura RA, Fuster V, Burgert SL, Puga FJ. Clinical features and long-term natural history of the postpericardiotomy syndrome. Int J Cardiol 1983;4:443–54.
  7. Cliff WJ, Grobety J, Ryan GB. Postoperative pericardial adhesions. The role of mild serosal injury and spilled blood. J Thorac Cardiovasc Surg 1973;65:744–50.



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This Article
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