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CHRONIC PERICARDITIS – REPORT CASES


Doina Butcovan¹, Catalina Arsenescu², Cleopatra Borza
Gr. Tinica², E. Sandica², V. Diaconescu², GIM Georgescu²
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We report 8 cases of chronic pericarditis diagnosed at Cardiology Center Iasi. The purpose of the study was to establish the disease and etiological diagnosis. The study was made on multiple cardiac investigations and on surgical biopsic specimens, obtained by making a pleuro-pericardial window and using routine morphological techniques. We evidentiated 2 cases of constrictive pericarditis and 6 cases of effusive-constrictive pericarditis. We specified their aetiology, as well. The microscopical examination revealed 5 cases of fibrinous pericarditis with tendency to organisation and 2 cases of calcified fibrotic pericardial thickening, all these morphological appearences being unspecific for an aetiological agent; in a case, we evidentiated a characteristic morphological aspect, corresponding to tuberculous pericarditis. The study revealed the importance of establishing the etiological disease diagnosis for indicating a target effective treatment. Key words: tuberculous pericarditis, constrictive pericarditis, effusive-constrictive pericarditis.
 

INTRODUCTION
     The chronic pericarditis is a pericardial inflammatory disease caused by different etiological agents. Silver (1) described two main forms: constrictive pericarditis and effusive-constrictive pericarditis. Constrictive pericarditis is a fibrous thickening of the pericardium with obliteration of the pericardial sac and the restriction of the diastolic filling (1). It has the same causes as acute pericarditis: idiopathic (42%), post-iradiation (31%), post-surgery (11%), post-infectious (6%), connective tissue diseases (4%), neoplasms (3%), dialysis (2%), sarcoidosis (1%), etc (2, 3). Clinical picture is often asymptomatic, but sometimes, the patient may present, increased pulmonary venous pressure (dispnea with ortopnea), increased systemic venous pressure (turgescent jugular veins, pleural effusion, hepatomegaly, ascite and lower leg oedema) (3, 4). The diagnosis is based on electrocardiography, X ray chest, echocardiography and morphology, as well (5, 6). Morphologically, on pericardial biopsy are evidentiated two subtypes of chronic pericarditis: adhesive pericarditis (pericardial fibrosis and adhesions) and constrictive pericarditis (fibrous thickening of the visceral pericardium associated with calcifications which are present in 50% of cases)(5). This form have to be differentiated by restrictive cardiomyopathy. Effusive-constrictive pericarditis is defined as a form of constrictive pericarditis characterised clinically and hemodinamicaly through signs of cardiac tamponade which is not resolved by pericardiocenthesis (1). Pericardial effusion has between 50 ml and over 1000 ml, being caused by the same etiological agents enumerated earlier (2, 3). Clinical picture is dominated by cardiac tamponade and clinical examination revealed a paradoxus pulsus (6). Morphologically, pericardial effusions may be serous, chilous and hemorrhagic (5, 6). The recommended treatment consists in resection of the epicardial fibrous tissue (7, 8). 
 

MATERIALS AND METHODS
     In 8 patients, 4 women and 4 men, with ages between 5 and 78 years, presenting with progressive dispnea and malaise, and having a previous diagnosis of pleuro-pericarditis of unknown aetiology, the repeated hospital admissions were indicated for draining the pleuro-pericardial fluid. 
     The surgical biopsic specimens, obtained through a pleuro-pericardial window, were fixed in buffered 10% formalin for 12 hours and quite totally sampled. Samples were processed using routine paraffin embedding, cutting (5 mm) and hematoxilin-eosin (HE) and Van Gieson (VG) staining. 

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¹ Department of Pathology - UMF – Iasi,
² Cardiology Center Iasi
 

RESULTS AND DISCUSSIONS 
     The study represents 8 report cases of chronic pericarditis, of unknown cause, presenting for repeated hospital admission for paracenthesis. 
Physical examination, revealed the most common found physical findings, as fever and tachycardy, cardiomegaly (50%), followed by hepatomegaly. The pericardial friction rub was soft and distant heart sounds were common. Pleural effusions and peripheral oedema were evident, as well, while patients with constrictive pericarditis had inspiratory swelling of the neck veins known as Kussmaul’s sign. Similar findings were reported by Muir (9) in a study of 27 patients. Hepatomegaly was found in 95%, jugular venous distention in 88%, ascites in 73%, oedema in 25%, and a pericardial friction rub in 18%. 
     The laboratory tests were not relevant for a specific agent. In circulating blood, we found only a mild anaemia and an average total white blood cell count of 7.000, similar resulting were reported by Hageman (10) in his study.
     The chest X-ray, evidentiated an enlarged cardiac silhouette in 50% of cases, comparative with 40 of 48 of patients described by Hageman (10), and 100 of 103 patients described by Strang (8). Cardiomegaly was usually due to pericardial effusion or effusive-constrictive pericarditis. We revealed in 5 cases an associate pleural fluid reaction, predominant to the bases, while Muir (9) found radiological evidence of pleural effusion in 2 of 35 patients in his series. In our series of 8 patients, only 1 (12,5%) had an evidence of a right micronodular apical sequel, while in the series of the Strang (8), 32% of 19 cases had radiological evidence of active pulmonary tuberculosis.
     Generally, the echocardiografic findings were not specific. If, in the early fibrinous phase the echocardiogram was normal, later, we found evidences of pericardial effusion with some adhesions or pericardial thickening (6 cases), while Brisson (11) in his series, of 13 from 17 patients, noted moderate or large effusions, 4 patients having evidence of tamponade. In our series, the two remaining cases, had constrictive pericarditis, as Symmers (2) who found similar pericardial thickening to his cases. Computed tomographic scanning also gave us informations concerning the cause of a pericardial effusion and thickening, in a case. 
     In our series of 8 patients, pericardial fluid was examined in 3 cases. Acid-fast bacilli were not found on stained smear. The fluid was usually an exudate, with a high protein content. There was a fluid increased leukocyte count, with lymphocytes and monocytes predominating, with slight elevation of polymorphonuclear leukocytes. The fluid was serosanguineous in a case, and even grossly hemorrhagic in another case. We didn’t find tubercle bacilli on stained smear; in this case pericardial biopsy remained an important diagnostic tool. But, in a case, we evidentiated characteristic tuberculous lesions on histologic examination of the pericardium. Brisson (11) recommended a method based on DNA amplification, that may be used on sputum, or lymph node biopsy material, to provide a more rapid diagnosis. Virmani (5) appreciated, the diagnosis is probable when there is evidence of pericarditis in a patient with tuberculosis demonstrated elsewhere in the body. We had 2 cases with history of pulmonary tuberculosis, with negative stained smears and cultures of sputum for tubercle bacilli, while positive sputum cultures were found in 11% of 184 patients in the study by Strang (8). Strang considers tuberculin skin tests, chest roentgenograms, electrocardiograms, and differential cell count in the pericardial fluid may be useful screening tests in patients suspected of having tuberculous pericarditis. So, he evidentiated, in adults, especially those more than 60 to 65 years old, as many as 30% of patients with idiopathic pericarditis a positive skin test. In our study, a patient, without tuberculous history and with negative skin test, responded very well to tuberculostatics, demonstrating tuberculous etiology. Two cases had a sepsis history and another one had evidences of chronic uraemia. We couldn’t demonstrate a specific etiological agent, in a case, noted as idiopathic case.
     The surgically intervention evidentiated a tickened fibrous pericardium and moderate effusion requiring a pleuro-pericardial drainage and a pleuro-pericardial window. The histological examination of the surgical biopsic specimen revealed different lesions, illustrated by few photogrames: 5 cases of fibrinous pericarditis with tendency to organisation (fig 1) ; at these cases the persistence of the inflammation was demonstrated morphologically by a hyperplastic mesothelial reaction (fig.2) ; 2 cases of constrictive pericarditis, demonstrated by fibrous calcified pericardial thickening; in a case, we revealed a thick pericardium through an extensive fibrosis enclosing multiple specific tuberculous granulomas (fig. 3, 4) 
     Medical treatment was the first pattern of choice. Corresponding with Waller recommendations (4), for the definite or probable cases of tuberculous pericarditis, the patients were hospitalized and observed for evidence of cardiac tamponade. In tuberculous pericarditis, a triple drug therapy is generally recommended for a minimum of 9 months, with at least 6 months of therapy following culture conversion. Hageman (10), also added a 40 to 60 mg dose of prednisone daily in divided doses to antituberculous therapy when there is persistent or recurrent pericardial effusion, despite therapy with antituberculous drugs. Using adrenal corticosteroids he was able to avoid pericardial resection . 
Surgical treatment was the second pattern of choice. Symmers (2) recommended the placement of a pericardial window for both diagnostic and therapeutic purposes in patients with chronic pericarditis. If pericardial thickening is present, pericardiectomy was recommended by Waller (4). Surgical resection of the pericardium was indicated early for recurrent or life-threatening tamponade, or later when there was a continuing elevation of systemic venous pressure after 4 to 6 weeks of drug therapy. Waller reported that one third of patients presenting with hepatomegaly and oedema responded to medical treatment; the others required surgical treatment. In the latter case, continued venous pressure elevation may be the result of cardiac tamponade, constrictive pericarditis, or effusive-constrictive pericarditis. Since, the surgical mortality rate appears higher in the late calcific stage of constrictive pericarditis, Muir (9) recommended pericardial resection to be performed early. Pericardiectomy for all patients with tuberculous pericarditis has been recommended by some authors (6, 7), as well.

CONCLUSIONS
The study revealed the importance of establishing the etiological disease diagnosis for indicating a target effective treatment. 
 

REFFERENCES
1. Silver MD. Pericarditis. In Silver MD. Gotlieb AI. Eds. Cardiovascular Pathology. Churchill Livingstone 2001, 385-389. 
2. Symmers WSC.  The pericardium. In: Symmers WSC. Cardiovascular System. Springer-Verlag, New York, 1980, 672-675.
3. Colin MB.  Pericarditis. In: Colin MB Ed. Heart Pathology.  Churchill Livingstone  1980, 265-272.
4. Waller BF. Pericardial Disease. In: Waller BF. Pathology of the Heart and great vessels, The Mosby Company, 1998, 1173-1178.
5. Virmani R. Tuberculous Pericarditis. In: Allen Burke and Renu Virmani. Atlas of Cardiovascular Pathology. Ed. AFIP. Washington DC 1966: 104-106.
6. Blomm J. Pericarditis. In: Sternberg SS. Diagnostic Surgical Pathology. Ed. Raven Press, 1944: 1216-1217.
7. Gilbert E. Pericarditis. In: Silverberg SG. Principles and Practice of Surgical Pathology and Cytopathology. Ed. Churchill Livingstone 1997, 1318-1321.
8. Strang JIG, Kakaza HS, Gibson DG, et al. Controlled clinical trial of complete open surgical drainage and of prednisolone in treatment of tuberculous pericardial effusion. Lancet. 1988; 2: 759-764
9. Muir P, Nicholson F et al: Chronic relapsing pericarditis. Lancet I: 804-7, 1989.
10. Hageman JH, D’Esopo ND, Glenn WL. Tuberculosis of the pericardium on a long term analysis of forty-four proved cases. N Engl J Med. 1964; 270: 327-332
11. Brisson NA, Gicquel B, Le Cossier D. Rapid diagnosis of tuberculosis by amplification of mycobacterial DNA in clinical samples. Lancet 1989; 2: 1069-1071
 

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