The initial injury is thought to release cardiac antigens and stimulate an immune response. The immune complexes that are generated then deposit onto the pericardium, pleura, and lungs, eliciting an inflammatory response [3] . The following observations are compatible with this hypothesis:
* The prolonged latent period from cardiac injury to the clinical onset of PPIS. Pleural effusion and/or pulmonary infiltrates in some cases. 
* Studies in patients undergoing cardiac surgery have found a statistically significant correlation between the postoperative to preoperative ratios of antiactin and antimyosin antibodies and the clinical occurrence of PPIS (see below) [8,9] . 
* The excellent response to steroid therapy, and the occasional relapses after steroid withdrawal [3] . 


Pathogenesis — The term postpericardiotomy syndrome was substituted for the previous postcardiotomy syndrome after it was discovered that the syndrome can occur after the pericardium is opened even if the heart is not invaded (eg, after surgery for bronchogenic carcinoma). Furthermore, the provoking cardiac injury may be surprisingly minor; examples include percutaneous intervention, insertion of a pacing lead, and radiofrequency ablation [15] .
A classic prospective study compared children who did and did not develop a postpericardiotomy syndrome after cardiac surgery; those who developed the syndrome had both an increase in viral titers and increased antimyocardial antibodies resulting from myocardial injury [16] . Based upon this observation, it was hypothesized that the infection may have been acquired from hospital personnel or the patients' visitors, or that infection may have been acquired intraoperatively when the pericardium was open.
Several subsequent studies have demonstrated the presence of antimyocardial antibodies in patients who develop the postpericardiotomy syndrome [8,9,17,18] . Antimyocardial antibodies have also been discovered in the pleural fluid of one such patient [19] .
However, there is controversy regarding the significance of these antibodies and their relation to the severity of myocardial injury.
* One study evaluated 19 patients undergoing cardiac surgery, seven of whom had the postpericardiotomy syndrome [9] . Myosin light chain and creatine kinase isoenzyme MB were elevated to the same level in all patients, but antimyosin antibodies were detected only in patients with the syndrome and the titer correlated with the size of the pericardial effusion [9] . 
Similar findings were noted in a series of 62 patients who underwent coronary artery bypass surgery [8] . Complete postpericardiotomy syndrome occurred in 13 percent and an incomplete syndrome in 26 percent. There was a significant correlation between the frequency and intensity of the syndrome and the ratio of postoperative to preoperative titers of antiactin and antimyosin antibodies.
* In contrast, a prospective study of 57 patients undergoing elective cardiac surgery found that anticardiolipin and antiheart antibody titers had low sensitivity and specificity for the diagnosis of postpericardiotomy syndrome [17] . 
Support for antiheart antibodies being an epiphenomenon comes from a prospective study of 20 surgical patients in whom serum was sampled for antiheart antibodies before and periodically after elective coronary artery bypass surgery [18] . Antiheart antibodies were absent in all patients on the day before surgery. Three patients developed postpericardiotomy syndrome. All were seronegative at the time of diagnosis, but became seropositive within the ensuing 14 days.





Treatment — The postmyocardial infarction and the postpericardiotomy syndromes are both treated with antiinflammatory agents. Aspirin may be tried first and, if that fails, a nonsteroidal antiinflammatory drug (NSAID) such as ibuprofen.
Anecdotal reports have suggested that colchicine may be beneficial in patients with PPIS [23] . This is consistent with the apparent benefit from colchicine in patients with recurrent acute pericarditis, which also appears to be mediated by immune mechanisms. (See "Recurrent pericarditis", section on Colchicine).
Colchicine also may prevent PPIS. This issue was addressed in a prospective randomized trial of colchicine compared to placebo beginning on the third postoperative day in 111 patients who underwent cardiac surgery [24] . There was a trend toward a lower incidence of PPIS with colchicine therapy (10.6 versus 21.9 percent, p<0.135). The Colchicine for the Prevention of Post-pericardiotomy Syndrome (COPPS) study is a multicenter, double blind trial that will randomize 360 cardiac surgery patients to colchicine or placebo, with the primary end point being postpericardiotomy syndrome [25] .
A short course of steroids is effective when the patient does not respond to the above drugs. Prednisone is begun at a dose of 60 mg/day [3] . Once the patient is asymptomatic and objective findings are beginning to improve, the dose is tapered, at first rapidly (eg, 5 mg every three days until a dose of 20 mg/day is achieved) and then more slowly. If pericarditis recurs, the dose is raised to the lowest that suppressed the syndrome, maintained there for some weeks, and then is tapered again.