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Probable postcardiotomy syndrome following implantation of a transvenous pacemaker: Report of the first case
Probable postcardiotomy syndrome following implantation of a transvenous pacemaker: Report of the first case Donald Kaye, M.D.* William Frankl, M.D.* * Lucien I. Arditi, M.D.*** Philadelphia.
PG., and Neu* York, N. I’.
The postcardiotomy syndrome may follow cardiac surgery, myocardial infarction, and blunt and penetrating trauma to the chest.‘-’ To the knowledge of the authors, this syndrome has not been reported as a consequence of implantation of a transvenous pacemaker. As perforation of the right ventricle is a complication of placement of a pacemaker wire,” it is not unexpected that the “postcardiotomy syndrome” should occasionally follow placement of a transvenous pacemaker. The purpose of this report is to describe a patient who developed a probable “postcardiotomy syndrome” following placement of a transvenous pacemaker. Case
report
M. K., a 7%year-old, white male was admitted to the Hospital of the Medical College of Pennsylvania for a right inguinal herniorrhaphy. The past history was unremarkable except for the presence, on electrocardiogram, of a left bundle branch block starting six years prior to admission evolving into a right bundle branch block with left anterior hemiblock two years prior to admission. This electrocardiographic finding had been stable for the past two years during which time electrocardiograms were obtained at least every three months. Two years prior to admJ&on, digoxin therapy had been started and continued at a dose of 0.25 mg. each day because of presence of five to six atria1 and ventricular premature From the Department of Medicine, The Medical College of Pennsylvania, and The New York Hospital-Cornell Medical Center. Received for publication Nov. 19, 1973. Reprint requests to: Dr. Donald Kaye, Department of Medicine. The Medical College of Pennsylvania, 3300 Henry Ave.. Philadelphia, Pa. 19129. *Professor and Chairman, Department of Medicine, The Medical College of Pennsylvania, Philadelphia. **Professor of Medicine, The Medical College of Pennsylvania, Philadelphia. ***Clinical Associate Professor of Medicine, Cornell University, Medical College, New York.
November.
1975, Vol. 90, No. 5, pp. 627-630
contractions each minute. With digoxin, these had decreased to about one premature contraction per minute. There had never been any signs or symptoms of heart failure (i.e.. dyspnea, orthopnea, or edema) or episodes of chest pain. On May 3, 1973, a temporary transvenous demand pacemaker was inserted int.o the right ventricle without incident for prophylactic reasons because of the presence of bifascicular block, although we realize that this indication is questioned by some authors. On May 4, the hernia repair was performed and the pacemaker remained in place for 72 hours. On May 14.1973, a Cordis permanent-demand pacemaker was implanted subcutaneously in the left chest for prophylaxis against complete heart block. The patient was discharged from the hospital following an uneventful postoperative course. On about May 21, he resumed normal act.ivity which included walking long distances. Several days later he began to note bilateral ankle edema every evening which cleared hy morning. On dune 6, a chest x-ray on a routine visit demonstrated a 1.5 cm. increase in the transverse diameter of the heart which had been normal on May 15, 1973 (Figs. 1 and 2). There was also a small right pleural effusion. Electrocardiograms were unchanged and showed normal sinus rhythm. The pacemaker was suppressed because the inherent sinus rate exceeded that of the pacemaker. A magnet was then placed over the pacemaker causing it to fire in a fixed-rate mode. The pacemaker was thus found to be pacing well, and its failure to fire during sinus rhythm indicated that it was sensing well. On
American
Heart
-Jocrrnal
627
Kaye,
Frankl,
and
Arditi
Fig. 1. Chest x-ray taken on May 15, 1973 (the day following implantation of the permanent pacemaker). The transverse diameter of the heart is normal.
Fig. 2. Chest x-ray taken on June 6,1973, cm. increase in the transverse diameter small right pleural effusion.
demonstrating of the heart
a 1.5 and a
patient felt relatively well. Temperatures were recorded four times a day. To evaluate the possibility of a pericardial effusion, a carbon dioxide study was performed on July 23, and was consistent with a pericardial effusion (Fig. 4). The same day the patient had the onset of a nonproductive cough. Complete blood count and urinalysis were normal as were several determinations of: blood urea nitrogen, serum creatinine, serum electrolytes, CPK, SGOT, SGPT, and serum protein. The erythrocyte sedimentation rate was 20 (upper limit of normal, 10). Five blood cultures were negative. On July 25, the patient had mild left posterior pleuritic chest pain that lasted for only one day. On July 26, a pericardial friction rub was heard for the first time. The electrocardiogram was unchanged. The chest x-ray revealed clear lung
628
Fig. 3. Chest x-ray taken July 20, 1973, demonstrating cm. increase in the transverse diameter of the heart over ray of June 6.
a 1.5 the x-
fields and the heart size was unchanged from July 20. During the next five days (July 28 through Aug. l), the temperature reached only 101’ F., rectally, each day and the cough began to improve. From Aug. 2 through Aug. 14, the rectal temperature continued to reach 100.2” F. each day and the pericardial friction rub became louder. On Aug. 3, the heart had decreased by 1 cm. in transverse diameter on x-ray. The dependent edema in the evening diminished and disappeared. By Aug. 24, the patient had become completely afebrile, the cough had stopped, and heart size had decreased to normal (Fig. 5). The pericardial friction rub gradually became much softer; it was barely audible on Sept. 1, 1973, and disappeared by Sept. I, 1973. The pacemaker wire remained in proper position on chest x-rays taken at least weekly during the febrile illness and the pacemaker paced properly (when stimulated with a magnet) as judged by electrocardiograms taken at least weekly during the illness. At no time during the illness did the patient experience anterior chest pain, dyspnea, or orthopnea and the neck veins were flat on frequent examinations. In fact, except for the visits to the doctor, the patient worked eight hours a day during the entire illness. No therapy was given except for continuation of digoxin, 0.25 mg. each day. Cold agglutinins, latex agglutination, and serum antibody titers against Coxsackie viruses Bl through 6, and against Mycoplasma pneumoniae did not rise during the illness. The patient is well with a normal size heart on x-ray as of April, 1974.
Discussion
This 72-year-old man had fever documented for 26 days and he probably had fever for at least five days before documentation and for up to 10 days after. The only localizing findings on history and physical examination were cough, mild pleuritic
November,
1975, Vol. 90, No. 5
Postcarriiotorn~
oain of short duration, and a pericardial friction rub. It seems likely from the course, that the chest x-ray showing enlargement of the heart six weeks prior to documentation of fever represented a pericardial effusion. The illness most suggests either viral pericarditis or the “postcardiotomy syndrome.” However, the probable presence of a pericardial effusion for six weeks prior to onset of fever would be extremely unusual in viral pericarditis. Furthermore, viral pericarditis is unusual in elderly patients. Although there is no way of proving a diagnosis of “postcardiotomy syndrome,” the patient’s clinical course (appearance and resolution without therapy of febrile pericarditis) following insertion of a transvenous pacemaker most suggests this diagnosis. It is possible that the edema which appeared nine days after insertion of the permanent pacemaker and 20 days after insertion of the temporary pacemaker was related to pericardial effusion and resultant mild tamponade. At the time of appearance it was attributed to the period of inactivity following the hernia repair. Inadvertent perforation of the ventricle has been reported during insertion of transvenous pacemakers.” However, when it occurs, it is transient since the pacemaker wire is then pulled back until the position of the tip is correct. The physicians performing the procedures in our patient did not recall any difficulty with placement of either the temporary or permanent pacemakers. However, the possibility of ventricular wall perforation occurring without recognition certainly must be considered in any patient undergoing these procedures. The trauma caused by perforation of the ventricle with bleeding into the pericardial sac would be sufficient to account for the subsequent syndrome which is known to follow cardiotomy, myocardial infarction, and penetrating or blunt trauma to the chest. In our patient there was no evidence of a myocardial infarction nor was there blunt trauma to the chest. The “postcardiotomy syndrome” is presumed to occur from an autoimmune reaction6 and usually follows trauma to the heart or pericardium. It may appear from one week to three months after the event, but most often occurs within two to four weeks.’ Fever and pericarditis are the most common manifestations, but pneumonia and pleuritis are also reported. It is not, known why the “postcardiotomy
American
Heart
Journal
Fig. 4. X-ray of the heart following intravenoucarbon dioxide on July 23, 1973. demonstrating effusion.
Fig.
return
svndrorne
iltjection of a pericardial
5. Chest
x-ray taken on August 24, 1973. tirmonstrating of the transverse diameter of thr heart .I) norma!.
syndrome” has not been described before in patients receiving transvenous pacemakers. Several explanations may be offered. The syndrome may be rare because of relatively little myocardial trauma (from perforation) as compared with the extent during cardiac surgery or rnyocardial infarction. Furthermore, the syndrome may not be detected in its milder forms. Our patient had few symptoms, was not even aware of fever, and
629
Kaye,
Frankl,
and
Arditi
continued to work during the entire illness. Another factor to be considered is that other diagnoses are more likely to be made in patients following pacemaker implantation because the “postcardiotomy syndrome” has not, to date, been reported to follow this procedure. It is hoped that this case report will cause physicians to be alerted to the possibility of this syndrome developing following implantation of pacemakers and thus evoke other reports. Summary
The syndrome of fever and pericarditis is reported following implantation of a transvenous pacemaker in a 72-year-old man. The pacemaker was placed for prophylactic reasons (i.e., presence of bifascicular block). The syndrome resolved spontaneously after over four weeks of fever and a pericardial friction rub. Perforation of the right ventricle, although not recognized in this patient, is a complication which occurs with passage of a transvenous pacemaker.
630
There were no other antecedent events to explain the syndrome such as myocardial infarction or trauma to the chest. REFERENCES
1. Dresdale,
2. 3.
4.
5. 6. 7.
D. T., Ripstein, C. B., Guzman, S. V., and Greene, M. A.: Postcardiotomy syndrome in patients with rheumatic heart disease. Cortisone as a prophylactic and therapeutic agent, Am. J. Med. 21:57, 1956. Dressier, W.: The postmyocardial infarction syndrome: a report on forty-four cases, Arch. Intern. Med. 103:28, 1959. Goodkind, M. J., Bloomer, W. E., and Goodyer, A. V. N.: Recurrent pericardial effusion after nonpenetrating chest trauma: report of two cases treated with adrenocortical steroids. N. Enel. J. Med. 263:874. 1960. Segal, F., and ’ Tabatznik, B.: Postpericardiotomy syndrome following penetrating stab wounds of the chest: comparison with the postcommissurotomy syndrome, AM.HEART J. 59:175,1960. Kosowsky, B. D., and Barr, I.: Complications and malfunctions of electrical cardiac pacemakers, Progr. Cardiovasc. Dis. 14:501, 1972. Davies, A. M., and Gery, I.: The role of autoantibodies in heart disease, AM.HEART J. 60:669,1960. Friedberg, C. K.: Diseases of the heart, Ed. 3, Philadelphia, 1966, W. B. Saunders Co., p. 958.
November,
1975, Vol. 90, No. 5
PG., and Neu* York, N. I’.
The postcardiotomy syndrome may follow cardiac surgery, myocardial infarction, and blunt and penetrating trauma to the chest.‘-’ To the knowledge of the authors, this syndrome has not been reported as a consequence of implantation of a transvenous pacemaker. As perforation of the right ventricle is a complication of placement of a pacemaker wire,” it is not unexpected that the “postcardiotomy syndrome” should occasionally follow placement of a transvenous pacemaker. The purpose of this report is to describe a patient who developed a probable “postcardiotomy syndrome” following placement of a transvenous pacemaker. Case
report
M. K., a 7%year-old, white male was admitted to the Hospital of the Medical College of Pennsylvania for a right inguinal herniorrhaphy. The past history was unremarkable except for the presence, on electrocardiogram, of a left bundle branch block starting six years prior to admission evolving into a right bundle branch block with left anterior hemiblock two years prior to admission. This electrocardiographic finding had been stable for the past two years during which time electrocardiograms were obtained at least every three months. Two years prior to admJ&on, digoxin therapy had been started and continued at a dose of 0.25 mg. each day because of presence of five to six atria1 and ventricular premature From the Department of Medicine, The Medical College of Pennsylvania, and The New York Hospital-Cornell Medical Center. Received for publication Nov. 19, 1973. Reprint requests to: Dr. Donald Kaye, Department of Medicine. The Medical College of Pennsylvania, 3300 Henry Ave.. Philadelphia, Pa. 19129. *Professor and Chairman, Department of Medicine, The Medical College of Pennsylvania, Philadelphia. **Professor of Medicine, The Medical College of Pennsylvania, Philadelphia. ***Clinical Associate Professor of Medicine, Cornell University, Medical College, New York.
November.
1975, Vol. 90, No. 5, pp. 627-630
contractions each minute. With digoxin, these had decreased to about one premature contraction per minute. There had never been any signs or symptoms of heart failure (i.e.. dyspnea, orthopnea, or edema) or episodes of chest pain. On May 3, 1973, a temporary transvenous demand pacemaker was inserted int.o the right ventricle without incident for prophylactic reasons because of the presence of bifascicular block, although we realize that this indication is questioned by some authors. On May 4, the hernia repair was performed and the pacemaker remained in place for 72 hours. On May 14.1973, a Cordis permanent-demand pacemaker was implanted subcutaneously in the left chest for prophylaxis against complete heart block. The patient was discharged from the hospital following an uneventful postoperative course. On about May 21, he resumed normal act.ivity which included walking long distances. Several days later he began to note bilateral ankle edema every evening which cleared hy morning. On dune 6, a chest x-ray on a routine visit demonstrated a 1.5 cm. increase in the transverse diameter of the heart which had been normal on May 15, 1973 (Figs. 1 and 2). There was also a small right pleural effusion. Electrocardiograms were unchanged and showed normal sinus rhythm. The pacemaker was suppressed because the inherent sinus rate exceeded that of the pacemaker. A magnet was then placed over the pacemaker causing it to fire in a fixed-rate mode. The pacemaker was thus found to be pacing well, and its failure to fire during sinus rhythm indicated that it was sensing well. On
American
Heart
-Jocrrnal
627
Kaye,
Frankl,
and
Arditi
Fig. 1. Chest x-ray taken on May 15, 1973 (the day following implantation of the permanent pacemaker). The transverse diameter of the heart is normal.
Fig. 2. Chest x-ray taken on June 6,1973, cm. increase in the transverse diameter small right pleural effusion.
demonstrating of the heart
a 1.5 and a
patient felt relatively well. Temperatures were recorded four times a day. To evaluate the possibility of a pericardial effusion, a carbon dioxide study was performed on July 23, and was consistent with a pericardial effusion (Fig. 4). The same day the patient had the onset of a nonproductive cough. Complete blood count and urinalysis were normal as were several determinations of: blood urea nitrogen, serum creatinine, serum electrolytes, CPK, SGOT, SGPT, and serum protein. The erythrocyte sedimentation rate was 20 (upper limit of normal, 10). Five blood cultures were negative. On July 25, the patient had mild left posterior pleuritic chest pain that lasted for only one day. On July 26, a pericardial friction rub was heard for the first time. The electrocardiogram was unchanged. The chest x-ray revealed clear lung
628
Fig. 3. Chest x-ray taken July 20, 1973, demonstrating cm. increase in the transverse diameter of the heart over ray of June 6.
a 1.5 the x-
fields and the heart size was unchanged from July 20. During the next five days (July 28 through Aug. l), the temperature reached only 101’ F., rectally, each day and the cough began to improve. From Aug. 2 through Aug. 14, the rectal temperature continued to reach 100.2” F. each day and the pericardial friction rub became louder. On Aug. 3, the heart had decreased by 1 cm. in transverse diameter on x-ray. The dependent edema in the evening diminished and disappeared. By Aug. 24, the patient had become completely afebrile, the cough had stopped, and heart size had decreased to normal (Fig. 5). The pericardial friction rub gradually became much softer; it was barely audible on Sept. 1, 1973, and disappeared by Sept. I, 1973. The pacemaker wire remained in proper position on chest x-rays taken at least weekly during the febrile illness and the pacemaker paced properly (when stimulated with a magnet) as judged by electrocardiograms taken at least weekly during the illness. At no time during the illness did the patient experience anterior chest pain, dyspnea, or orthopnea and the neck veins were flat on frequent examinations. In fact, except for the visits to the doctor, the patient worked eight hours a day during the entire illness. No therapy was given except for continuation of digoxin, 0.25 mg. each day. Cold agglutinins, latex agglutination, and serum antibody titers against Coxsackie viruses Bl through 6, and against Mycoplasma pneumoniae did not rise during the illness. The patient is well with a normal size heart on x-ray as of April, 1974.
Discussion
This 72-year-old man had fever documented for 26 days and he probably had fever for at least five days before documentation and for up to 10 days after. The only localizing findings on history and physical examination were cough, mild pleuritic
November,
1975, Vol. 90, No. 5
Postcarriiotorn~
oain of short duration, and a pericardial friction rub. It seems likely from the course, that the chest x-ray showing enlargement of the heart six weeks prior to documentation of fever represented a pericardial effusion. The illness most suggests either viral pericarditis or the “postcardiotomy syndrome.” However, the probable presence of a pericardial effusion for six weeks prior to onset of fever would be extremely unusual in viral pericarditis. Furthermore, viral pericarditis is unusual in elderly patients. Although there is no way of proving a diagnosis of “postcardiotomy syndrome,” the patient’s clinical course (appearance and resolution without therapy of febrile pericarditis) following insertion of a transvenous pacemaker most suggests this diagnosis. It is possible that the edema which appeared nine days after insertion of the permanent pacemaker and 20 days after insertion of the temporary pacemaker was related to pericardial effusion and resultant mild tamponade. At the time of appearance it was attributed to the period of inactivity following the hernia repair. Inadvertent perforation of the ventricle has been reported during insertion of transvenous pacemakers.” However, when it occurs, it is transient since the pacemaker wire is then pulled back until the position of the tip is correct. The physicians performing the procedures in our patient did not recall any difficulty with placement of either the temporary or permanent pacemakers. However, the possibility of ventricular wall perforation occurring without recognition certainly must be considered in any patient undergoing these procedures. The trauma caused by perforation of the ventricle with bleeding into the pericardial sac would be sufficient to account for the subsequent syndrome which is known to follow cardiotomy, myocardial infarction, and penetrating or blunt trauma to the chest. In our patient there was no evidence of a myocardial infarction nor was there blunt trauma to the chest. The “postcardiotomy syndrome” is presumed to occur from an autoimmune reaction6 and usually follows trauma to the heart or pericardium. It may appear from one week to three months after the event, but most often occurs within two to four weeks.’ Fever and pericarditis are the most common manifestations, but pneumonia and pleuritis are also reported. It is not, known why the “postcardiotomy
American
Heart
Journal
Fig. 4. X-ray of the heart following intravenoucarbon dioxide on July 23, 1973. demonstrating effusion.
Fig.
return
svndrorne
iltjection of a pericardial
5. Chest
x-ray taken on August 24, 1973. tirmonstrating of the transverse diameter of thr heart .I) norma!.
syndrome” has not been described before in patients receiving transvenous pacemakers. Several explanations may be offered. The syndrome may be rare because of relatively little myocardial trauma (from perforation) as compared with the extent during cardiac surgery or rnyocardial infarction. Furthermore, the syndrome may not be detected in its milder forms. Our patient had few symptoms, was not even aware of fever, and
629
Kaye,
Frankl,
and
Arditi
continued to work during the entire illness. Another factor to be considered is that other diagnoses are more likely to be made in patients following pacemaker implantation because the “postcardiotomy syndrome” has not, to date, been reported to follow this procedure. It is hoped that this case report will cause physicians to be alerted to the possibility of this syndrome developing following implantation of pacemakers and thus evoke other reports. Summary
The syndrome of fever and pericarditis is reported following implantation of a transvenous pacemaker in a 72-year-old man. The pacemaker was placed for prophylactic reasons (i.e., presence of bifascicular block). The syndrome resolved spontaneously after over four weeks of fever and a pericardial friction rub. Perforation of the right ventricle, although not recognized in this patient, is a complication which occurs with passage of a transvenous pacemaker.
630
There were no other antecedent events to explain the syndrome such as myocardial infarction or trauma to the chest. REFERENCES
1. Dresdale,
2. 3.
4.
5. 6. 7.
D. T., Ripstein, C. B., Guzman, S. V., and Greene, M. A.: Postcardiotomy syndrome in patients with rheumatic heart disease. Cortisone as a prophylactic and therapeutic agent, Am. J. Med. 21:57, 1956. Dressier, W.: The postmyocardial infarction syndrome: a report on forty-four cases, Arch. Intern. Med. 103:28, 1959. Goodkind, M. J., Bloomer, W. E., and Goodyer, A. V. N.: Recurrent pericardial effusion after nonpenetrating chest trauma: report of two cases treated with adrenocortical steroids. N. Enel. J. Med. 263:874. 1960. Segal, F., and ’ Tabatznik, B.: Postpericardiotomy syndrome following penetrating stab wounds of the chest: comparison with the postcommissurotomy syndrome, AM.HEART J. 59:175,1960. Kosowsky, B. D., and Barr, I.: Complications and malfunctions of electrical cardiac pacemakers, Progr. Cardiovasc. Dis. 14:501, 1972. Davies, A. M., and Gery, I.: The role of autoantibodies in heart disease, AM.HEART J. 60:669,1960. Friedberg, C. K.: Diseases of the heart, Ed. 3, Philadelphia, 1966, W. B. Saunders Co., p. 958.
November,
1975, Vol. 90, No. 5