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[Purulent pericarditis in children: a 15 year-experience].

BACKGROUND: Purulent pericarditis is rare in developed countries, but its prognosis is regarded as serious. Early diagnosis and appropriate treatment should prevent complications. PATIENTS: Among the 119 pericarditis without congenital cardiopathy admitted in our pediatric cardiology unit between 1979 and 1994, 19 were purulent. The mean age of these 13 boys and six girls was 3 years (range: 3 months to 10 years). Symptoms always pointed to a chest disease whether pericarditis occurred first (n = 13) or it complicated evolution of a known infectious process (n = 6). Tamponnade was present in seven infants upon admission and required urgent pericardiocentesis or drainage. An extrapericardial infectious site was found in 11 cases: six pulmonary infections, three osteomyelitis, one cellulitis and one sinusitis. An organism was isolated in 17 cases, 14 times in the pericardial fluid, eight times on blood culture. The identified bacteria were: Staphylococcus aureus (n = 6), Haemophilus influenzae (n = 4), Streptococcus A (n = 3), Streptococcus pneumoniae (n = 3), Meningococcus (n = 1). Treatment consisted of intra-venous antibiotics associated 15 times to surgical drainage of the pericardium. One infant had no pericardiocentesis and no drainage because he presented late with constrictive pericarditis and needed pericardectomy. All infants healed but four developed contrictive pericarditis and required pericardectomy; none of these four patients had early drainage (two had no drainage at all). Pericardectomy, carried out between 2 and 6 months after the beginning of pericarditis with adiastolic signs and pericardial thickening, permitted healing in all cases and disappearance of all cardiac symptoms. CONCLUSIONS: Early diagnosis and treatment of purulent pericarditis, especially early pericardial drainage, are the best ways of avoiding constriction.

Child↗

Management of tuberculous constrictive pericarditis and tuberculous pericardial effusion in Transkei: results at 10 years follow-up.

BACKGROUND: Tuberculous pericarditis is common in Transkei (Eastern Cape). Two randomized trials showed benefits at two years for prednisolone in patients with constrictive pericarditis, and open drainage plus prednisolone in patients with pericardial effusion. AIM: To see whether the advantages of prednisolone and open drainage were maintained up to 10 years. DESIGN: Follow-up of randomized, double-blind, placebo-controlled trials. METHODS: All 383 patients (143 constriction, 240 effusion) received the same anti-tuberculosis chemotherapy. They were randomized to prednisolone or placebo for the first 11 weeks, and were followed-up over 10 years. Among the 240 with effusion, 122 were also randomized to immediate open surgical drainage of pericardial fluid versus pericardiocentesis as required. Adverse outcomes were: death from pericarditis, pericardiectomy, repeat pericardiocentesis, and subsequent open drainage. RESULTS: The 10-year follow-up rate was 96%. In constriction patients, adverse outcomes occurred in 19/70 (27%) prednisolone vs. 28/73 (38%) placebo (p = 0.15), deaths from pericarditis being 2 (3%) vs. 8 (11%), respectively (p = 0.098, Fisher's exact test). In effusion patients, adverse outcomes occurred in 14/27 (52%) with neither drainage nor prednisolone, vs. 4/29 (14%) drainage and prednisolone, 4/35 (11%) drainage and placebo, and 6/31 (19%) prednisolone and no drainage (p = 0.08 for interaction). Drainage eliminated the need for repeat pericardiocentesis. In the 176 with effusion and no drainage, adverse outcomes occurred in 17/88 (19%) prednisolone vs. 35/88 (40%) placebo patients (p = 0.003), with repeat pericardiocentesis 20 (23%) placebo vs. 9 (10%) prednisolone (p = 0.025). In a multivariate survival analysis (stratified by type of pericarditis), prednisolone reduced the overall death rate after adjusting for age and sex (p = 0.044), and substantially reduced the risk of death from pericarditis (p = 0.004). At 10 years, the great majority of surviving patients in all treatment groups were either fully active or out and about, even if activity was restricted. DISCUSSION: In the absence of a clear contraindication, a corticosteroid should be used in addition to antituberculosis chemotherapy in the management of patients with tuberculous pericarditis.

Adolescent↗

Tuberculous pericarditis.

BACKGROUND: The incidence of tuberculous pericarditis is increasing in Africa as a result of the human immunodeficiency virus (HIV) epidemic. The primary objective of this article was to review and summarize the literature on the pathogenesis, diagnosis, and management of tuberculous pericarditis. METHODS AND RESULTS: We searched MEDLINE (January 1966 to May 2005) and the Cochrane Library (Issue 1, 2005) for information on relevant references. A "definite" diagnosis of tuberculous pericarditis is based on the demonstration of tubercle bacilli in pericardial fluid or on a histological section of the pericardium; "probable" tuberculous pericarditis is based on the proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated adenosine deaminase levels, and/or appropriate response to a trial of antituberculosis chemotherapy. Treatment consists of the standard 4-drug antituberculosis regimen for 6 months. It is uncertain whether adjunctive corticosteroids are effective in reducing mortality or progression to constriction. Surgical resection of the pericardium remains the appropriate treatment for constrictive pericarditis. The timing of surgical intervention is controversial, but many experts recommend a trial of medical therapy for noncalcific pericardial constriction, and pericardiectomy in nonresponders after 4 to 8 weeks of antituberculosis chemotherapy. CONCLUSIONS: Research is needed to improve the diagnosis, assess the effectiveness of adjunctive steroids, and determine the impact of HIV infection on the outcome of tuberculous pericarditis.

Africa↗

Rheumatoid pericarditis. Clinical significance and operative management.

The incidence of subclinical pericarditis associated with rheumatoid pericarditis may be as high as 50 percent, but significant impairment of cardiac performance owing to this type of pericarditis rarely occurs. In the past 7 years, we have encountered eight men with congestive heart failure owing to rheumatoid pericarditis. Cardiac catheterization and echocardiography were useful in establishing the diagnosis of pericardial constriction. Pericardiocentesis was unsuccessful in relieving symptoms in the three patients in whom the procedure was performed. Seven patients underwent pericardiectomy; six had constrictive pericarditis and one patient had an acute pericarditis with the sudden onset of cardiac tamponade. The other patient died of cardiac tamponade prior to operation. All patients improved after operation and have remained free of cardiac symptoms 3 months to 4 1/2 years later. The frequent occurrence of adhesive and obliterative pericarditis with loculated effusions suggests the need for pericardiectomy rather than pericardiocentesis in the patient with rheumatoid arthritis and symptomatic pericardial involvement. Immediate and lasting relief of this unusual nonarticular manifestation of rheumatoid arthritis can be expected after pericardiectomy.

Adult↗

[Biopsy of the pericardium. Diagnostic value in subacute and chronic pericarditis, apropos of 70 cases].

The aetiology of pericarditis is often difficult to assess. To try to clear up this problem, a pericardial biopsy through a left lateral thoracotomy was performed in 70 cases in which the cause could not be established by the usual means (including pericardial paracenthesis in 32 cases). They included either subacute pericarditis, dry or with effusion (biopsy being undertaken as an average 45 days after the clinical onset), or chronic pericarditis with effusion. Tuberculosis was thus demonstrated in 14 cases (8 of which were aged more than 60 years), inaugural pericardial tumours in 8 and suppuration in 3 cases. Microscopical examination gave support to pathogenic hypotheses concerning cholesterol pericarditis (5 cases) and multi-recurrent pericartitides (6 cases). By elimination with a high probability) of tuberculosis and tumours, it demonstrated definitely the diagnosis of post-radiotherapy pericarditis with effusion (4 cases) pericarditis with normal serous membrane (4 cases) and "idiopathic" forms (23 cases of common sclerogenous subacute inflammation). The inocuity of this method, its more accurate results than those obtained by cytological and bacteriological examination of the pericardial fluid obtained by paracenthesis, should induce to consider this procedure more often in the cases of pericarditis when the aetiology remains doubtful; not to mention the benefit derived from surgical drainage which results in a quicker and more complete cure than repeated paracentheses of chronic and subacute pericardial effusions.

Acute Disease↗

Constrictive pericarditis.

The diagnosis of constrictive pericarditis remains a challenge because its physical findings and hemodynamics mimic restrictive cardiomyopathy. Various diagnostic advances over the years enable us to differentiate between these two conditions. This review begins with a case report of constrictive pericarditis, followed by a brief history and discussions of etiologies. Clinical features, radiologic, electrocardiographic, angiographic findings, and hemodynamics of constrictive pericarditis are reviewed. The echocardiographic findings are detailed and the recent advances in Doppler flow velocity patterns of pulmonary, mitral, tricuspid valves and hepatic veins are reported. Nuclear ventriculograms depict rapid ventricular filling in constrictive pericarditis and differentiate it from restrictive cardiomyopathy. Endomyocardial biopsy helps further in recognizing the various types of restrictive cardiomyopathies. Computed tomography and magnetic resonance imaging delineate abnormal pericardial thickness in constrictive pericarditis. Association of characteristic hemodynamic changes and abnormal pericardial thickness > 3 mm usually confirms the diagnosis of constrictive pericarditis. Effusive and occult varieties of constrictive pericarditis are briefly described. This review concludes with emphasizing the importance of pericardial resection.

Adult↗

Effectiveness of colchicine in a case of recurrent compressive rheumatoid pericarditis.

Survival is impaired in rheumatoid pericarditis complicated by cardiac compression by either tamponade or constriction. Conventional therapy with non-steroidal anti-inflammatory agents and glucocorticoids is frequently ineffective in reversing severe cardiac impairment and/or in preventing recurrences. Colchicine, an effective and safe treatment of idiopathic and post-viral pericarditis, has not been studied in rheumatoid pericarditis. We describe the case of a 44-year-old woman with a 1-year history of rheumatoid arthritis who developed rheumatoid pericarditis complicated with tamponade. Pericardiocentesis relieved the symptoms, but pericarditis recurred at a high dose of prednisone of 70 mg/day. Colchicine at a dose of 1 mg/day prevented recurrences and had a significant sparing effect on steroids, which were reduced to 6 mg/day. This is the second case report describing the effectiveness of colchicine therapy in rheumatoid pericarditis complicated with tamponade. These cases suggest that colchicine should be considered in the treatment of rheumatoid pericarditis.

Adult↗

Pericarditis in acute myocardial infarction: characterization and clinical significance.

To determine the significance of pericarditis following acute myocardial infarction, the hospital course and 12-month follow-up were analyzed in 703 patients enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Pericarditis, defined by the detection of a pericardial rub, occurred in 20% of the patients (n = 141) and was more likely to follow Q wave than non-Q wave infarction (25% vs 9%, p less than 0.001). Patients with pericarditis experienced more serious myocardial damage compared to those without pericarditis, as evidenced by a larger infarct size (25 +/- 1 vs 17 +/- 1 MB-CK gm-Eq/m2, p less than 0.001), a lower admission left ventricular ejection fraction (42 +/- 1% vs 48 +/- 1%, p less than 0.001), and a higher incidence of congestive heart failure (47% vs 26%, p less than 0.001) and atrial tachyarrhythmias (16% vs 10%, p less than 0.05). When patients were classified by the presence of Q or non-Q wave infarction, these differences persisted although statistical significance was not always achieved due to smaller sample size. Mortality at 12-month follow-up for patients with pericarditis was 18% compared with 12% for patients without pericarditis (p = 0.055). This mortality difference could be accounted for in part by the lower ventricular ejection fraction in patients with pericarditis (p = 0.20 after adjustment).

Electrocardiography↗

Tuberculous pericarditis: long-term outcome in patients who received medical therapy alone.

A conservative approach to operative intervention in the treatment of active tuberculous pericarditis was adopted and only 4 of 16 consecutive patients underwent pericardiectomy, all within 2 months of diagnosis. One patient died of constrictive pericarditis despite pericardiectomy, and one died of acute bronchopneumonia after 8 months of otherwise successful medical management. All 14 long-term survivors were reevaluated to exclude chronic constrictive pericarditis and other potential sequelae of tuberculous pericarditis. Reevaluation included physical examination, chest radiograph, electrocardiogram, M-mode and two-dimensional echocardiogram, computed tomography (CT) scan, and in patients less than or equal to 75 years of age, incremental cycle exercise to maximum oxygen consumption. None were found to have chronic constrictive pericarditis or convincing evidence of other recognized complications of tuberculous pericarditis. Our results suggest that when pericardiectomy is not required for the relief of cardiac compression during the acute phase of tuberculous pericarditis and patients are treated with medical therapy alone, an excellent long-term outcome may be anticipated.

Adrenal Cortex Hormones↗

Doppler evaluation of patients with constrictive pericarditis: use of tricuspid regurgitation velocity curves to determine enhanced ventricular interaction.

OBJECTIVES: This study sought to examine the value of analyzing Doppler echocardiographically derived tricuspid regurgitation signals during respiration in relation to the diagnosis of constrictive pericarditis. BACKGROUND: A physiologic hallmark of constrictive pericarditis is enhanced ventricular interdependence, which produces reciprocal changes in right and left ventricular filling and ejection dynamics during the respiratory cycle. It was hypothesized that these changes could be detected noninvasively by analyzing Doppler echocardiographically derived tricuspid regurgitation signals and that this information could assist in noninvasively diagnosing constrictive pericarditis. METHODS: Simultaneous Doppler echocardiography and catheterization studies of the right and left sides of the heart with high fidelity pressure manometers were performed in 5 patients with surgically confirmed constrictive pericarditis and 12 patients (control subjects) with heart failure due to other causes. RESULTS: Changes observed in tricuspid regurgitation Doppler echocardiographic variables from onset to peak inspiration in patients with constrictive pericarditis were significantly different from those in control subjects. Mean (+/- SD) percent change in maximal tricuspid regurgitation velocity was 13% +/- 6% and -8% +/- 7% in the constrictive pericarditis and control groups, respectively (p < 0.0001); mean percent change in tricuspid regurgitation signal duration was 18% +/- 2% and -2% +/- 7%, respectively (p < 0.0001); mean percent change in tricuspid regurgitation time velocity integral was 27% +/- 15% and -10% +/- 12%, respectively (p < 0.0001). CONCLUSIONS: Respiratory changes in Doppler echocardiographically derived tricuspid regurgitation peak velocity and velocity duration are increased in patients with constrictive pericarditis and may be helpful in diagnosing this condition noninvasively.

Aged↗

Autonomic functions in restrictive cardiomyopathy and constrictive pericarditis: a comparison.

BACKGROUND: This study was undertaken to analyze autonomic functions in restrictive cardiomyopathies. Restrictive cardiomyopathies have clinical and hemodynamic similarity with chronic constrictive pericarditis. Autonomic dysfunction has been described in the latter. METHODS AND RESULTS: Autonomic function analysis has not been reported in restrictive cardiomyopathy. Six consecutive patients with restrictive cardiomyopathy were included in this study (5 men, 1 woman, mean age 35+/-5.4 years). The tests performed were designed to test the sympathetic efferent pathway, that is, by cold hand immersion and loud noise tests, parasympathetic efferent pathway by Valsalva ratio and expiration/inspiration ratio and the baroreceptor function by testing their sensitivity slope. The results were compared with 20 patients with chronic constrictive pericarditis and with 10 healthy age- and sex-matched control subjects previously studied. The rise of systolic blood pressure after cold hand immersion and sudden loud noise was not significantly different compared with control subjects. The expiration/inspiration ratio was 1.1+/-0.01 compared with 1.57+/-0.1 in the control group (p < 0.01). The Valsalva ratio was significantly lower (1.1+/-0.04) compared with control subjects (1.83+/-0.1, p < 0.01). The baroreceptor sensitivity was not reduced compared with that in control subjects. In comparison to constrictive pericarditis, sympathetic efferent pathway is preserved in restrictive cardiomyopathy (p < 0.0001). The parasympathetic efferent pathway is borderline abnormal in restrictive cardiomyopathy but not significantly as compared with constrictive pericarditis (p=not significant). The baroreceptor sensitivity slope is normal in patients with restrictive cardiomyopathy as compared with significant depression seen in constrictive pericarditis (p < 0.05). Autonomic functions are better preserved in patients with restrictive cardiomyopathies compared with chronic constrictive pericarditis. CONCLUSIONS: Autonomic dysfunction is localized to parasympathetic efferent pathway. This is in comparison to constrictive pericarditis, in which severe autonomic dysfunction is a universal feature and includes all segments of autonomic nervous system.

Adolescent↗

Recurrent acute pericarditis: follow-up study of 31 patients.

Thirty-one patients with recurrent pericarditis were observed for periods of 2 to 19 years. Twenty-four had idiopathic pericarditis; four had postoperative or posttraumatic pericarditis, two had postinfarction pericarditis and one had recurrent pericarditis after anticoagulant-induced intrapericardial bleeding. In 24 patients (Group I), recurrences were documented by electrocardiographic changes, echocardiographic evidence of pericardial fluid or a pericardial rub as well as chest pain. In seven patients (Group II), recurrences were documented only by increased white blood cell count, increased erythrocyte sedimentation rate or fever in addition to pain. In 19 patients, the duration of the active or recurrent process was 5 years or more; in 7, it was 8 years or more. Three patients had cardiac tamponade in the initial attack; none had tamponade during recurrences. No patient developed congestive heart failure, constrictive pericarditis or cardiac arrhythmias with recurrences. Immunoelectrophoresis showed normal findings or minor deviations in 11 patients studied; B cell and T cell lymphocyte counts were normal in 10 patients and showed minor deviations in 3. Antinuclear antibody studies were normal in 19 of 22 patients and positive in low titer in 2. Most patients required adrenal steroid therapy for pain relief; steroid withdrawal was often difficult. Pericardiectomy was done in nine patients; in only two was this followed by clear-cut relief. In this group of 31 patients, 22 of whom were observed for 5 years or more, recurrent attacks of chest pain were the only major disabling feature of their pericarditis.

Acute Disease↗

Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis.

OBJECTIVE: This study was conducted to determine whether Doppler recording of superior vena cava flow velocities can differentiate chronic obstructive pulmonary disease from constrictive pericarditis in patients with a respiratory variation of > or = 25% in mitral inflow E velocity. BACKGROUND: Although respiratory variation (> or = 25%) in mitral E velocity is the main diagnostic criterion for constrictive pericarditis by Doppler echocardiography, it can also be present in chronic obstructive pulmonary disease. Because the respiratory variation is due to increased change in intrathoracic pressure with respiration in chronic obstructive pulmonary disease, and to dissociation of intrathoracic-intracardiac pressure changes in constriction, it was hypothesized that the Doppler flow velocity pattern in the superior vena cava (affected by intrathoracic pressure) would be different in these two conditions. METHODS: Pulsed-wave Doppler recording of mitral and superior vena cava flow velocities in 20 patients with chronic obstructive pulmonary disease who had > or = 25% respiratory variation in mitral E-wave velocity were compared with those of 20 patients who had surgically proved constrictive pericarditis. RESULTS: Constrictive pericarditis and chronic obstructive pulmonary disease had similar respiratory variation in mitral E velocity (41% versus 46%). In the latter, the E/A ratio was lower (inspiration, 0.8+/-0.3 versus 1.5+/-0.7 [p < 0.0001]; expiration, 1.0+/-0.3 vs. 1.9+/-0.7 [p < 0.0001]) and deceleration time longer (inspiration, 198+/-53 ms versus 137+/-32 ms; expiration, 225+/-43 ms vs. 161+/-33 ms [p < 0.0001]). Inspiratory superior vena cava systolic forward flow velocity was significantly higher in chronic obstructive pulmonary disease (72.9+/-22.6 cm/s versus 36.2+/-9.3 cm/s, p < 0.0001), while expiratory systolic forward flow velocity was similar. Hence, there was a significantly greater respiratory variation in superior vena cava systolic forward flow velocity in chronic obstructive pulmonary disease without an overlap with constrictive pericarditis (39.5+/-18.8 cm/s vs. 4.2+/-3.4 cm/s, p < 0.0001). CONCLUSIONS: Despite a similar respiratory variation in mitral E wave velocities, mitral inflow variables in chronic obstructive pulmonary disease are less restrictive compared with those in constrictive pericarditis. More importantly, patients with chronic obstructive pulmonary disease show a marked increase in inspiratory superior vena cava systolic forward flow velocity, which is not seen in patients with constrictive pericarditis.

Aged↗

Pericarditis following renal transplantation.

We analyzed data on renal allograft recipients over a 27-year period in order to investigate the frequency, etiology, and outcome of pericarditis developing during the first two months following renal transplantation. Of the 1497 patients receiving renal transplants between 1963 and 1990, 34 patients developed 36 episodes of pericarditis and/or pericardial effusions, for an overall incidence of 2.4%. Pericarditis was attributed to uremia in 14 episodes, cytomegalovirus infection in three, both uremia and CMV infection in four, nonspecific bacterial infection in three, and tuberculosis and minoxidil therapy in one episode each. No etiologic diagnosis could be established in 10 episodes. No statistically significant differences were found between pericarditis and case-matched control patients considering demographic features, the number of immediately functioning grafts, the duration of posttransplant acute renal failure, the number of supportive dialysis days, pre- and postoperative CMV status of the patients, and pretransplant BUN and serum creatinine levels. There were more uremic-related complications (pulmonary edema, gastrointestinal bleeding, central nervous system symptoms) in the pericarditis group. Five allografts in the pericarditis group never functioned, versus only one in the control group. Three patients with pericarditis developed pericardial tamponade. Early diagnosis, close follow-up, and in the case of cardiac tamponade early invasive treatment, should improve the prognosis of this potentially life-threatening complication.

Adolescent↗

Pericarditis in the patient with uremia: clinical and echocardiographic evaluation.

Over a 4-year period, 94 of 248 patients with end-stage renal disease were evaluated echocardiographically because of clinically suspected pericarditis. The clinical diagnosis was established in 39 patients based on the development of a friction rub at some time during their course. 15 of the 55 patients, in whom the diagnosis of pericarditis could not be established, had a small pericardial effusion. The rest had no pericardial fluid. 15 patients developed pericarditis prior to the initiation of dialysis and all responded to dialysis alone. 4 had no effusions, 3 had small effusions and 8 had moderate or large effusions. In 9 of 24 dialysis patients with pericarditis, a presumptive etiology other than uremia was identified. In these 24 patients, 9 had no effusions, 2 had small effusion and 13 had moderate or large effusions. Only 9 patients, all with moderate or large effusions, required operation. The data suggest that: t1) pericarditis present at the initiation of dialysis regularly resolves with dialysis; (2) specific etiologies are common; (3) small pericardial effusions are common in dialysis patients without pericarditis; (4) pericardial effusions are frequently not present in uremic patients with pericarditis and, (5) the size of the pericardial effusion is of some value in predicting which patients may subsequently require operative intervention.

Adult↗

Case-control study of factors associated with fibrinous pericarditis among horses in central Kentucky during spring 2001.

OBJECTIVE: To identify factors significantly associated with an epidemic of fibrinous pericarditis during spring 2001 among horses in central Kentucky. DESIGN: Case-control study. ANIMALS: 38 horses with fibrinous pericarditis and 30 control horses examined for other reasons. PROCEDURE: A questionnaire was developed to solicit information regarding a wide range of management practices and environmental exposures from farm owners or managers. RESULTS: The following factors were found in bivariate analyses to be significantly associated with an increased risk of pericarditis: being from a farm with mares and foals affected by mare reproductive loss syndrome, exposure to Eastern tent caterpillars in or around horse pastures, younger age, shorter duration of residence in Kentucky and at the farm of current residence, being fed hay grown outside Kentucky, a lack of access to pond water, access to orchard grass for grazing, and a lack of direct contact with cattle. In multivariate logistic regression analyses, only variables related to caterpillar exposure and age were significantly associated with fibrinous pericarditis. CONCLUSIONS AND CLINICAL RELVANCE: Results suggest that fibrinous pericarditis in horses may be associated with mare reproductive loss syndrome. Exposure to Eastern tent caterpillars was the greatest risk factor for development of fibrinous pericarditis. The distribution of times of diagnosis of fibrinous pericarditis was consistent with a point-source epidemic.

Abortion, Veterinary↗

[Diagnosis of pericarditis].

Acute pericarditis can be divided into primary pericarditis--of unknown etiology and secondary pericarditis--caused by earlier diagnosed disease. The diagnosis of acute pericarditis is based on clinical manifestations and accessory investigations, among which the most important is echocardiography. However, the etiologic diagnosis of pericarditis seems to be much more difficult, being ascertained in no more than 30%. It makes the causative treatment impossible in many cases. The good knowledge of epidemiology and symptoms of different pericardial diseases is important to make the proper choice of investigative procedures. At the beginning, usually less invasive investigations are planned to confirm etiologic diagnosis. Subsequently, more invasive procedures like pericardiocentesis, pericardiotomy and pericardial biopsy are reserved to explain the cause of pericarditis. The exceptions are cardiac tamponade and suspected purulent pericarditis, when pericardiocentesis and surgical drainage are made promptly in the therapeutic and diagnostic aim.

Biopsy↗

[Toxoplasma pericarditis without immunosuppressant disorder detected by polymerase chain reaction of pericardial fluid: a case report].

There have been several case reports, a total of 22 up to the present, of toxoplasma pericarditis. Out of them, in only a few cases the diagnosis was properly made with a proof of the microscopic presence of Toxoplasma gondii. This is the first report of toxoplasma pericarditis in which the presence of Toxoplasma gondii was detected by polymerase chain reaction of pericardial effusion. In addition, the previous reports will be reviewed, and compared to this present case. A 29-year-old woman, without immunosuppressant disorder, suffering from fever and orthopnea was admitted to our hospital. Blood chemistry findings indicated mild liver dysfunction and inflammation. Chest radiography showed cardiac enlargement. Electrocardiography showed sinus tachycardia and ST elevation. Echocardiography revealed a massive pericardial effusion. Pericardiocentesis demonstrated 638 ml of bloody fluid. Cytologic study of the fluid was class II for malignancy, and polymerase chain reaction to tuberculosis was negative. However, a high titer of the anti-toxoplasma antibody of 1: 20,480 (passive hemagglutination) indicated pericarditis caused by Toxoplasma gondii. Subsequently, Toxoplasma gondii was identified in the pericardial effusion by polymerase chain reaction. Clinical symptoms improved after pericardiocentesis, but 2 months later pericarditis recurred. Treatment was started with 800 mg acetylspiramycin daily but failed to improve the symptoms. Because of the development of pleuritis, treatment was changed to sulfadoxine 1,000 mg/pyrimethamine 50 mg. After the treatment with them, her symptoms improved. Only 22 cases of toxoplasma pericarditis have been reported worldwide and 15 of those cases were without immunosuppressant disorder. The usual symptoms at the onset of pericarditis without immunosuppressant disorder are fever, dyspnea and chest pain. Seven patients developed cardiac tamponade. Pericardiocentesis was performed in 8 cases and the pericardial fluid was hemorrhagic in 6. Pericardial thickening was detected in 5 cases. The diagnosis of toxoplasma infection is very difficult, because asymptomatic infection of Toxoplasma gondii is very common. Pericarditis is a disease difficult to confirm the etiology. Detection of Toxoplasma gondii in pericardial effusion by the polymerase chain reaction is very useful for its diagnosis.

Adult↗