Are we missing something? What really is the post cardiotomy syndrome?

Wessman and Stafford (1) in this issue of the SMJ review the conundrum of the post-cardiac injury syndrome (PCIS). Many physicians have said that since we treat the myocardial infarction (MI) patients so aggressively, we minimize muscle damage, hence the syndrome is rarely seen. We did an informal and unscientific survey of cardiologists at a recent meeting and this was the consensus. However, one Chief of Cardiology stated that 10 to 25% of postoperative cardiac surgery patients develop variations of the syndrome, due to the pericardium being opened. A retired cardiac surgeon reported seeing 5 to 10% of cases postoperatively. Mott et al (2) reported that of 246 children who had cardiac surgery, 39% had PCIS. In 1953, Soloff (3) felt that mitral commissurotomy caused rheumatic fever to be reactivated. The classical picture as described in 1958 by Dressler (4) included chest pain, fever, fatigue, myalgia, arthralgia pericardial friction rub with effusion and pleuritis. The electrocardiogram (EKG) was nondiagnostic, but there was an elevated sedimentation rate (ESR) and C-reactive protein (CRP) level. It usually began from a few days postinfarct to several weeks or months and generally responded well to steroids. It had a variable course length (weeks to months) with minimal sequelae. He reported one death due to cardiac tamponade.

We have all had patients who did not seem to "snap back" well following a cardiac surgical procedure or revascularization despite an apparently satisfactory initial course. They remained fatigued, and vaguely unsatisfactory with limited reserve. Most of them eventually improved, but not as much as we had expected. Also, there is the patient on anti-coagulation who may develop pericarditis. The picture of PCIS has been reported following angioplasty with stenting, (5) simple angioplasty, (6) radio-frequency ablation, (7,8) implantation of pacemaker leads, (9) by-pass surgery, (10) and minimally invasive bypass surgery. (11)

The inflammatory picture was suspected to be a reactivation of Rheumatic fever (RF), but it also occurred after surgery for congenital heart disease with no suspicion of RF. Viral infection was suspected but never proved. (12) Tissue studies have shown hyperemia and myxomatous changes in the pericardium (10) and diffuse obliteration of vein grafts, with inflammatory cells, but no intimal hyperplasia. (10) Pleural fluid analysis showed serosanguineous exudative changes, lowered complement levels and anti-myocardial antibodies (AMA) on immunofluorescence staining. (13) In 1964, van der Geld showed in sera or myocardial tissue in 309 patients that anti-heart antibodies were present in 13 of 15 cases of PCIS, in 8 of 14 cases with post-myocardial infarction syndrome and also in many patients after cardiac surgery who had no sign of PCIS. (14) McCabe et al (15) examined myocardial tissue samples prospectively in 60 postoperative patients and concluded that 3 patterns could be identified: 22% showed no antibody titers, 50% had low levels and 28% had high levels of antimyocardial antibodies and they persisted for long periods. PCIS occurred in those with the high titers with one case in the low titer group. No antibodies were found to the pericardium.

The myocardium is well known to be hyper-reactive as illustrated by the cardiac manifestations of Rheumatoid Arthritis and Lupus Erythematosus (LE). Congenital heart block is seen in infants born of women with LE and with antibodies to SSA/RO and SSB/lr. (16) This appears to be a reaction to apoptotic myocytes with macrophages.

A similar mechanism may occur in some patients with anti-cardio lipid syndrome (ACL) with IgG antibodies in association with anti-beta 2 glycoprotein antibodies. These patients have increased incidence of cardiac events (MI, etc) in the absence of an autoimmune state. (17) Ansari et al (18) showed that macrophages infiltrating cardiac tissues and endothelial cells that are apoptotic develop cardiac tissue-specific as well as nonspecific peptides leading to sensitization and activation of T-cells. This is particularly relevant in cases of cardiomyopathy or transplanted hearts, but may relate to PCIS.

Westerberg et al (19) reported that 29 patients undergoing coronary artery surgery who did not receive an auto transfusion of shed blood had less inflammatory activation, myocardial injury and bleeding postoperatively than those who did. Levels of cytokines, tumor necrosis factor alpha, interleukin 6 and complement factor C3 were lower than controls. CRP, ESR and Troponin T levels were the same in both groups.

The message to take home from Wessman and Stafford is that patients undergoing any cardiac invasive procedure may develop PCIS. The pattern does not always resemble the classical picture described by Kessler, but may take many forms and should be sought. One wonders how often the early graft closure, the early "restenosis" and the patient who does not seem to "bounce back" as we expect may be a case of PCIS. The treatment is easy and successful. I suspect we do not follow our patients closely enough, as noted by Spodick. (20) We should examine the patient with clothes off, take the time to let the patient tell us how he or she really feels, take the opportunity to reinforce the good health practices we all advise and do a few simple tests. After all, our job is not to just do a procedure, but to really care for the patient.

References

1. Wessman DE, Stafford CM. The postcardiac injury syndrome: case report and review of the literature. South Med J 2006;99:309-314.

2. Mott AR, Fraser CD, Kusnoor AV, et al. The effect of short-term prophylactic methylprednisone on the incidence and severity of postpericardiotomy syndrome in children undergoing cardiac surgery with cardiopulmonary bypass. J Am Coll Cardiol 2001;37:1700-1706.

3. Soloff LA, Zatuchni J, Janton OH, et al. Reactivation of rheumatic fever following mitral commissurotomy. Circulation 1953;8:481-497.

4. Dressler W. The post myocardial syndrome. Arch Intern Med 1959;103:28-42.

5. Hearne C, Forjuoh SN. Postcardiac injury syndrome after coronary angioplasty and stenting. J Am Board Fam Pract 2003;16:73-74.

6. Velander M, Grip L, Mogensen L. The postcardiac injury syndrome following percutaneous transluminal coronary angioplasty. Clin Cardiol 1993;16:353-354.

7. Rovang KS, Hee TT, Pagano TV, Mohiuddin S. Dressler's syndrome complicating radiofrequency ablation of an accessory atrioventricular pathway. Pacing Clin Electrophysiol 1993;16:251-253.

8. Turitto G, Abordo Jr, MG Mandawat MD, et al. Radiofrequency ablation for cardiac arrhythmias causing postcardiac injury syndrome. Am J Cardiol 1998;8:369-370.

9. Snow ME, Agatston AS, Kramer HC, Samet P. Postcardiotomy syndrome following transvenous pacemaker insertion. Pacing Clin Electrophysiol 1987;10:934-936.

10. Urschel Jr, HC Razzuk MA, Gardner M. Coronary artery bypass occlusion secondary to postcardiotomy syndrome. Ann Thorac Surg 1976;22:528-531.

11. Burgwardt K, Smally AJ. Postcardiotomy syndrome following minimally invasive coronary artery bypass. J Emerg Med 1998;16:737-739.

12. Burch GE, Colcolough HL. Postcardiotomy and postinfarction syndrome: a theory. Am Heart J 1970;80:290-291.

13. Kim S, Sahn SA. Postcardiac injury syndrome: an immunologic pleural fluid analysis. Chest 1996;109:570-572.

14. Van der Geldt H. Anti-heart antibodies in the post cardiotomy and post myocardial infarction syndromes. Lancet 1964;18:617-621.

15. McCabe JC, Ebert PA, Engle MA, Zabriskie JB. Circulating heart-reactive antibodies in the postpericardiotomy syndrome. J Surg Res 1973;14:158-164.

16. Barron WM, Lindheimer MD, Davison JM. Medical Disorders During Pregnancy Mosby, 2000, pp 365-366.

17. Bili A, Moss AJ, Francis CW, et al. Anticardiolipin antibodies and recurreent coronary events: a prospective study of 1150 patients: Thrombogenic Factors and Recurrent Coronary Events Investigators. Circulation 2000;102:1258-1263.

18. Ansari AA, Neckelmann N. Wang C, et al. Immunologic dialogue between cardiac myocytes, endothelial cells and mononuclear cells. Clin Immunol Immunopathol 1993;68:208-214.

19. Westerberg M, Bengtsson A, Jeppsspon A. Cardiac surgery without cardiotomy suction and autotransfusion reduces the postoperative systemic inflammatory response. Ann Thorac Surg 2004;78:54-59.

20. Spodick DH. Decreased recognition of the post-myocardial infarction (Dressler) syndrome in the post infarct setting: does it masquerade as 'idiopathic pericarditis' following silent infarcts? Chest 2004;126:1410-1411.</p> <pre> I not only use all the brains that I have, but all that I can borrow. --Woodrow Wilson </pre> <p>George Ritter, MD, FACP, FACC 

From Providence Hospital, Southfield, MI.

Reprint requests to George Ritter, MD, FACP, FACC, 16001 West Nine Mile Road, Providence Hospital, Southfield, MI 48075. Email: [e-mail]

Accepted December 21, 2005.