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Postpericardiotomy syndrome (PPS) may be associated with tamponade and pericardial constriction that may require procedural intervention. The aim of this study was to identify clinical features associated with adverse events requiring procedural intervention in patients with PPS. A total of 239 patients who developed PPS after cardiac surgery were monitored for 12 months. PPS was diagnosed if 2 of the 5 following findings were present: fever without infection, pleuritic pain, friction rub, pleural effusion, and pericardial effusion (

Contemporary series of postpericardiotomy syndrome (PPS) are lacking. The aim of this study was to evaluate the incidence, time course, features at presentation, risk factors, and prognosis of PPS. The study population consisted of 360 consecutive candidates to cardiac surgery enrolled in a prospective cohort study. PPS was diagnosed in 54 patients (15.0%; mean age 66 ± 12 years, 48.1% women): 79.6% in the first month, 13.0% in the second month, and 7.4% in the third month. Specific symptoms, signs, or features were pleuritic chest pain (55.6%), fever (53.7%), elevated markers of inflammation (74.1%), pericardial effusion (88.9%), and pleural effusion (92.6%). Cardiac tamponade was rare at presentation (1.9%). Female gender (hazard ratio 2.32, 95% confidence interval 1.22 to 4.39, p = 0.010), and pleura incision (hazard ratio 4.31, 95% confidence interval 2.22 to 8.33, p

Post-pericardiotomy syndrome (PPS) maybe associated with tamponade and pericardial constriction that may require procedural intervention. We sought to identify clinical features associated with adverse events requiring procedural intervention in patients with PPS. We monitored 239 patients who developed PPS after cardiac surgery for 12 months. PPS was diagnosed if 2 of the 5 following findings were present: fever without infection, pleuritic pain, friction rub, pleural effusion, and/or pericardial effusion (within 60 days post-surgery). Primary endpoint was the development of pericardial effusion or pericardial constriction requiring procedural intervention. Among 239 patients with PPS, 75 (31%) required procedural intervention. In a univariate analysis, the odds of a procedural intervention were decreased with older age (OR 0.98, 95% CI 0.96-0.99) and with colchicine used in combination with anti-inflammatory agents (OR 0.45, 95% CI 0.26-0.79). However, the odds were increased in patients withpreoperative heart failure (OR 1.84, 95% CI 1-3.39) and early postoperative constrictive physiology (OR 5.77, 95% CI 2.62-12.7). After multivariable adjustment, treatment with colchicine along with anti-inflammatory agents was associated with lower odds of requiring intervention (OR 0.43, 95% CI 0.95-0.99). Independent positive predictors of procedural intervention included age (OR 0.97, 95% CI 0.95-0.99), time to PPS (OR 0.97, 95% CI 0.95-0.99), and early postoperative constrictive physiology (OR6.23, 95% CI 2.04-19.07). In conclusion, younger age, early onset PPS, and postoperative constrictive physiology were associated with the need for procedural intervention in patients with PPS; whereas, colchicine was associated with reduced odds of adverse events and procedural intervention.

The natural history of postpericardiotomy syndrome (PPS), a relatively common complication of cardiac surgery, varies from mild self-limited episodes to cases with protracted courses, recurrences, and readmissions. Preventive strategies may be valuable to decrease morbidity and management costs. We thus aimed to conduct a comprehensive systematic review on available data for pharmacologic primary prevention of PPS. Controlled clinical studies were searched in several databases and were included provided they focused on pharmacologic primary prevention of PPS. Random-effect odds ratios (ORs) were computed for occurrence of PPS. From the initial sample of 343 citations, 4 controlled clinical trials for primary prevention of PPS were finally included (894 patients); 3 studies were double-blind randomized controlled trials (RCTs). Treatment comparisons were colchicine versus placebo (2 RCTs enrolling 471 patients), methylprednisolone versus placebo (1 RCT on 246 pediatric patients), and aspirin versus historical controls (1 nonrandomized study on 177 pediatric patients). Meta-analytic pooling showed that colchicine was associated with decreased risk of PPS (OR 0.38, 0.22 to 0.65). Data on methylprednisolone (OR 1.13, 0.57 to 2.25) or aspirin (OR 1.00, 0.16 to 6.11) were negative but inconclusive because these were based on 1 study and/or a nonrandomized design. In conclusion, clinical evidence for primary prevention of PPS is still limited to few studies of variable quality. Nevertheless, available data suggest a beneficial profile for colchicine and open a new therapeutic strategy for prevention of PPS.

This study documents a decrease in the incidence of postoperative pericardial effusions following open heart surgery in children from 53% to 85% in published reports to 13.6% in this study. The incidence of postpericardiotomy syndrome has also decreased from a reported 25% to 30% to 2.3% in this study. These findings may reflect improvement in surgical and myocardial protection techniques.

The clinical course of 41 consecutive pediatric patients (mean age 7.6 +/- 5.8 years, weight 27 +/- 22 kg) who underwent percutaneous pericardial drain placement during a 3-year period were reviewed. The most common diagnoses were malignancy (20%), postpericardiotomy syndrome (17%), aseptic pericarditis (12%), and patients recovering from a Fontan type of operation (12%). Indications for drainage included increasing effusion size determined by 2-dimensional echocardiogram (48%), clinical deterioration (33%) and echocardiographic evidence of hemodynamic compromise (12%). Only 3 (7%) patients had clinical evidence of cardiac tamponade. Drainage catheter placement was accomplished percutaneously from the subxiphoid approach. Insertion was successful in all but 1 patient (98%) and successful evacuation of the pericardial space was achieved in 93% of patients. There was 1 death in a critically ill 2-week-old infant and 4 complications, 3 of which occurred in patients aged less than 2 years. Drainage catheters remained in position from 1 to 18 days (mean 3 +/- 3 days) with no late complications. There were 3 instances (7%) of drainage catheter occlusion. These data support the notion that placement of a percutaneous pericardial catheter is safe and effective in providing definitive drainage of the pericardial space in the pediatric age group. Children younger than age 2 years may be at increased risk for complications.

Although postoperative constrictive pericarditis is rare, the diagnosis should be considered when unexplained right-sided heart failure develops after cardiac surgery. Within a 6 week interval, evidence of constrictive pericarditis developed in three patients who had recently undergone myocardial revascularization. One patient presented with biventricular failure, pericardial effusion and suspected tamponade. Severe constrictive pericarditis was demonstrated at subsequent operation. An apparent postpericardiotomy syndrome preceded evidence of right heart failure in the other two patients. Etiologic considerations include the possibility that pericardial irrigation with povidone-iodine (Betadine) solution may have contributed to subsequent fibrosis.

Complications after heart valve replacement remain a substantial source of morbidity and mortality despite continuing advances in surgical care and prosthetic design. Infectious endocarditis occurs in about 4 percent of patients and may appear early (within 60 days) or late after operation. Endocarditis of early onset is commonly due to staphylococcal, fungal or gram-negative organisms and is fatal in 70 percent or more of cases. Infection of late onset is more often of streptococcal origin and the mortality rate is lower, about 35 percent. With either type, prompt recognition, vigorous and appropriate antimicrobial therapy and early consideration of surgical intervention are crucial. The postperfusion and postpericardiotomy syndromes are relatively common and relatively benign syndromes associated with postoperative fever. Their recognition is important to prevent confusion with endocarditis or sepsis and thus to reassure the patient and physician. Treatment is primarily symptomatic. Intravascular hemolysis occurs with most prosthetic heart valves but is more common with certain prostheses and with paraprosthetic valve regurgitation, with significant hemolytic anemia in 5 to 15 percent. Oral iron replacement therapy is effective in the majority of patients, but occasionally blood transfusion or reoperation for leak around the prosthesis is necessary. Prosthesis dysfunction due to thrombus may be recognized clinically by recurrence of heart failure, syncope, cardiomegaly and altered prosthetic valve sounds or new murmurs. Hemodynamic studies verify the diagnosis, and prompt reoperation is indicated for this potentially lethal problem. Systemic embolization has decreased markedly with the introduction of cloth-covered prostheses and is frequently related to erratic or ineffective anticoagulant therapy. We continue to recommend anticoagulant therapy for all patients with prosthetic heart valves unless there is a major contraindication.

THE postpericardiotomy syndrome as described by Ito et al.1,2 is a febrile illness with pericardial and sometimes pleuropulmonary reaction that follows extensive pericardiotomy. This clinical entit...

The postpericardiotomy syndrome in a patient with aortic stenosis occurred as a direct consequence of percutaneous left ventricular puncture during left heart catheterization. The dangers of anticoagulation therapy following this procedure are discussed.

Pleural and pericardial effusions are a common complication after modified Fontan procedures. 1,2 Most of these effusions resolve within the first postoperative month, but in some cases may last longer than a year after this operation. 3 The causes of these effusions include infection, thoracic duct injury, elevated right atrial pressure, hypoproteinemia, renal failure and postpericardiotomy syndrome. Frequently, a cause cannot be identified and the treatment consists mainly of repeated thoracenteses, chest tube placement, diuretics, fluid restriction and, occasionally, pericardiectomy or pleural membrane sclerosing therapy. We describe 2 patients who had pleural and pericardial effusions more than 6 months after modified Fontan procedures. After identifiable causes for the effusions, including postpericardiotomy syndrome, were ruled out and conventional methods of therapy were unsuccessful, each was treated with anti-inflammatory agents. Both patients showed prompt resolution of the pleural effusions with the anti-inflammatory agents, recurrence of effusions after rapid drug tapering, and permanent resolution after slower tapering of the drugs.

Three patients with unusual complications after insertion of an epicardial pacemaker are described. In one patient pericarditis and severe cardiac tamponade developed that required emergency pericardiocentesis 8 weeks after pacemaker insertion. No evidence of myocardial perforation was observed at operation. In another patient two unusual complications developed: (1) migration of the pulse generator from the epigastric site of implantation into the pelvis, and (2) recurrent pericarditis with occult signs of constriction. In another patient recurrent pericarditis and clinical evidence of constriction developed. All three patients required pericardiectomy. Recurrent pericarditis after insertion of an epicardial pacemaker requires careful medical follow-up because either life-threatening tamponade or chronic constrictive pericarditis may develop.

The physiopathologic results of mitral commissurotomy were studied at intervals of several months, one year, two years, and three years after the operation. Pericarditis occurred after the operation in 90 per cent of the cases; and postpericardiotomy syndrome (the so-called postcommissurotomy syndrome) in 12.5 per cent, with no correlation between this and the results of biopsy of the auricular appendage. The results of mitral commissurotomy were evaluated by preoperative and postoperative cardiac catheterization, phonocardiogram, electrocardiogram, vectorcardiogram, electrokymogram, ballistocardiogram, roentgenogram, pulmonary angiocardiogram, and pulmonary function tests. The physiopathologic data did not always correspond to the clinical results. Sometimes the clinical improvement was greatly superior to the results furnished by these tests. In this series of 200 patients, excellent or good clinical results were obtained in 67 to 70 per cent of the cases. There was a mortality of 6 per cent. Finally, some factors are present which condition the physiopathologic results of mitral commissurotomy: postoperative mitral insufficiency, valvular calcification, postoperative emboli, insufficiency of the myocardium, sub-valvular stenosis, insufficient commissurotomy, and recurrent rheumatic reactivation, which may cause rcstenosis.

Two cases of postpericardiotomy syndrome following percutaneous left ventricular puncture have been reported. Both had symptoms identical with the other “cardiotomy” syndromes and responded promptly to adrenal steroid therapy. The fact that one of the patients had a second episode of pericarditis four weeks following open heart surgery may mean that the development of this syndrome following left ventricular puncture may be associated with the development of the postpericardiotomy syndrome following cardiac surgery.

A patient is described in whom the postpericardiotomy syndrome developed secondary to a gunshot wound to the chest with the retained missile in close proximity to the pericardium. Steroid therapy produced a prompt and sustained clinical remission. The literature is reviewed, and it is suggested that retained foreign bodies in or near the pericardium are still another precipitating cause of the postpericardiotomy syndrome. Possible etiologic mechanisms, the role of corticosteroids in therapy, and indications for surgery are discussed.

Clinical and experimental evidence for the role of viruses in the production of heart disease in man is reviewed. The data indicate that viral myocarditis, viral endocarditis, viral pericarditis and viral pancarditis are true entities that must be considered by clinicians in diagnosis and treatment of patients. It is suggested that viruses may be involved in the production of chronic heart disease and that “conditioning” factors possibly including streptococcal infections are important, both in the original infection and in activation of latent or dormant viruses. Viral infections may be responsible for much heart muscle disease, that is, cardiomyopathy, as well as for “rheumatic heart disease” of undetermined origin. The role of viruses, particularly rubella and Coxsackie, in the production of congenital heart disease is emphasized. Conceivably, viral infection acquired in utero might produce heart disease later in life. Many viruses are known to cause clinical pericarditis, some followed by chronic constriction. A possible role of viruses in the production of the postpericardiotomy syndrome or cardiac causalgia is suggested. Measures for the prevention of viral heart disease and methods of treatment, with particular emphasis on prolonged bed rest, are discussed. The need for laboratory facilities for routine viral studies is stressed.

The term “postcommissurotomy” syndrome should be discarded and permanently replaced with the more accurate description, “postpericardiotomy” syndrome. The clinical expression of this entity appears to be identical with the various forms of traumatic pericarditis reported in the past. The postpericardiotomy syndrome is described in 10 to 40 per cent of patients following commissurotomy for acquired valvular stenosis, and in 30 per cent of 100 consecutive survivors following open heart surgery for repair of atrial and ventricular septal defects and the relief of pulmonic and aortic stenosis. The clinical picture is one of recurrent fever and retrosternal pain described as dull or, more commonly, knifelike or stabbing, and in most patients a pericardial friction rub. The electrocardiogram often suggests pericardial changes that may disappear during periods of remission. They may also persist for weeks following resolution of the syndrome. The cardiac silhouette on x-ray examination is generally enlarged. The postpericardiotomy syndrome is a benign illness with an excellent prognosis. Therapy, for the most part, is supportive although in certain instances corticosteroids are used.

I MPROVEMENTS in the emergency management of acute traumatic cardiac tamponade, both by pericardial aspiration [-1° and by operative therapy,"-IS have considerably lowered the mortality rate of patients suffering from traumatic heart disease . As a result, attention has been directed toward the more remote sequelae of traumatic hemopericardium, of which the late development of constrictive pericarditis19-27 is important but fortunately rare . 1,10,14,29 A complication that is substantially more frequent and that adds greatly to the morbidity of traumatic heart disease is the development of recurrent pericardial and often pleural effusion, accompanied by chest pain, pyrexia and occasionally cardiac tamponade occurring weeks or months after the original injury . This complication has been known to surgeons for many ycars4,r,9,20,36-37 but it has only recently commanded wider clinical interest because of its striking similarityd 8-4 o to such conditions as the postmyocardial infarction syndrome," recurrent idiopathic pericarditis42,43 and the postpericardiotomy syndrome that follows intracardiac surgery for rheumatic44,46 and congenital4s ,47 heart disease . Some degree of controversy concerning the etiology of the postcommissurotomy syndrome still exists, 48-51 and views as to its pathogenesis and that of the postmyocardial infarction syndrome and recurrent pericarditis are purely speculative ."-54 The presence of blood in the pericardial sac is a feature common to traumatic hemopericardium and the surgical postpericardiotomy syndrome, and a hemorrhagic pericardial reaction is seen in a significant number of cases of postmyocardial infarction syndrome" 5 5 and idiopathic pericarditis . 56 Furthermore, the intrapericardial injection of autogenous blood and lipid fractions