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At least 379 records · Page 21Linked to original sources
PubMed1989

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↗
PubMed1982

Real time two dimensional echocardiography in constrictive pericarditis.

Real time two dimensional echocardiography was performed in five patients with constrictive pericarditis. The echocardiogram showed several typical features: (1) The heart was normal in size or decreased; the ventricles were small and the atria enlarged. (2) The pericardium was seen as a single or double dense rigid shell surrounding both ventricles and the apex; its immobility was striking. (3) The inferior vena cava and hepatic veins were greatly dilated in keeping with the severe clinical venous congestion. (4) Both interventricular and interatrial septa bulged into the left side of the heart on inspiration. (5) The atrioventricular valves were hypermobile. (6) A prominent ventricular diastolic filling half was seen. The two dimensional echocardiogram excluded other causes of severe cardiac failure such as congestive cardiomyopathy and valvular heart disease, while the dense immobile pericardial echo or echoes and the "normal" texture of the myocardial echoes made the diagnosis of restrictive cardiomyopathy unlikely.

Adolescent↗
PubMed1982

Immune reactions in tuberculous and chronic constrictive pericarditis. Clinical data and diagnostic significance of antimyocardial antibodies.

Humoral immune reactions were analyzed in 12 patients with exudative tuberculous pericarditis, 10 patients with constrictive pericarditis due to former tuberculosis, 10 patients with viral pericarditis, 20 patients with pulmonary tuberculosis, and 98 healthy donors. Pericarditis occurred in 12.5% of the patients with tuberculosis, whereas the incidence of tuberculosis in the 149 patients with pericarditis was 8%. Repeated pericardial puncture and pericardial effusions of greater than 500 ml with impending cardiac tamponade had to be performed in 4 patients. Clinical data indicated probable myocardial involvement in 4 of 12 patients. Antimyolemmal antibodies, which are a muscle-specific subtype of antisarcolemmal antibodies, were found in all patients with exudative tuberculous pericarditis and viral perimyocarditis, in only 1 of 12 patients with constrictive pericarditis, and in no patients with pulmonary tuberculosis. Antifibrillary antibodies--primarily of the antimyosin type--were missed in patients with viral heart disease but were demonstrated in 75% of patients with tuberculous pericarditis. Only sera with complement-fixing antimyolemmal antibodies of the IgG type in titers greater than 1:40 induced cytolysis of vital adult heterologous cardiocytes isolated and enriched by silica sol gradient centrifugation. These findings suggest not only that antimyolemmal antibodies are diagnostic indicators of perimyocardial involvement in tuberculous pericarditis, but also that they may play a significant role in its pathogenesis.

Antibody Specificity↗
PubMed1990

Echocardiographic demonstration of resolving intrapericardial mass in tuberculous pericardial effusion.

A patient with tuberculous pericardial effusion is described who presented with cardiac tamponade. Subsequent to pericardiocentesis, a large echodense intrapericardial mass was observed which disappeared completely with antituberculous chemotherapy. The resolution of the mass suggests that it was a conglomeration of fibrinous exudates deposited in the pericardial cavity. Presence of such exudates should not be considered an indication for surgical intervention.

Echocardiography↗
PubMed1990

Myocardial and endocardial involvement in tuberculous constrictive pericarditis: difficulty in biopsy distinction from endomyocardial fibrosis as a cause of restrictive heart disease.

Differentiation of constrictive pericarditis and endomyocardial fibrosis by the available diagnostic methods is difficult at present. With this in mind, we compared autopsy data in heart specimens from 8 patients of constrictive pericarditis of tuberculous origin and 6 patients with tropical endomyocardial fibrosis. Post-mortem endomyocardial biopsies were also performed from both the ventricles. Pericardial thickening and adhesions were present in all cases of constrictive pericarditis and in none of those with endomyocardial fibrosis. Interestingly, significant endocardial thickening was seen in four, and myonecrosis, lymphohistiocytic cellular infiltration and myofibrosis were observed in seven of the eight cases of constrictive pericarditis. This suggests that the tubercular insult to heart may result in involvement of all three layers with varying severity. The endomyocardial biopsy specimens from the affected areas revealed similar histopathological changes of endocardial thickening and focal myofibrosis with cellular infiltrates in patients with both constrictive pericarditis and endomyocardial fibrosis, making distinction of the two difficult. The hallmark of differentiation between these two clinical entities appears to be a diligent attempt at identification of the thickened pericardium.

Biopsy↗
PubMed1979

Computerized tomographic diagnosis of aneurysms of the thoracic aorta.

Accurate diagnosis of aneurysms of the thoracic aorta and its major branches can easily be performed by CT scanning of the mediastinum. The use of contrast enhancement aids in the diagnosis and allows distinction between flowing and clotted blood within the aneurysm. CT scanning of these lesions seen on chest radiographs may obviate the need for arteriography for diagnosis.

Aged↗
PubMed1988

Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment.

Thirteen patients with tuberculous pericarditis (12 men and 1 woman aged 13 to 70 years [mean 41]) were identified in a group of 294 patients consecutively admitted for primary acute pericardial disease. The diagnosis was made by the following studies: sputum culture (n = 4), culture of pericardial fluid obtained by pericardiocentesis (n = 3), histologic study and culture of pericardial biopsy (n = 3), lymph node biopsy (n = 2) and pleural biopsy (n = 1). Clinical presentation was remarkably variable: four patients had an acute, apparently self-limited course, one had relapsing tamponade, four had tamponade effectively treated with pericardiocentesis and four had toxic symptoms with persistent fever. The interval from hospital admission to diagnosis ranged from 1 to 14 weeks (mean 5.2). Constrictive pericarditis developed in six patients and effusive-constrictive pericarditis in one; all seven required pericardiectomy 2 to 3.5 months after admission. No patient died. It is concluded that 1) tuberculous pericarditis has a variable clinical presentation and therefore it should be considered in the evaluation of all instances of pericarditis without a rapidly self-limited course; 2) the diagnosis should be based only on objective data obtained with a systematic study protocol; 3) early definitive diagnosis is still difficult to achieve; and 4) development of subacute constrictive pericarditis requiring pericardiectomy is common.

Acute Disease↗
PubMed1996

Surgical treatment of infected thoracic and abdominal aortic aneurysms.

Twelve patients with infected aneurysms of the thoracic and abdominal aorta were evaluated. Aneurysmal location, aetiology, bacteriology and treatment modality were analysed to determine the relationship between these factors and outcome. Patients were divided into two groups based on the preoperative states of their infections. Group 1 patients (n = 7) underwent resection after resolution of their active infection. The causative organisms included Staphylococcus epidermidis (two cases). Salmonella spp. (one). Acinetobacter (one), Mycobacterium tuberculosis (one) and unknown organisms (two). Group 2 patients (n = 5) required urgent surgery because of uncontrolled sepsis despite intensive treatment with antibiotics. The causative organisms included Staphylococcus aureus (two cases). Pseudomonas aeruginosa (two) and Salmonella spp. (one). In group 1, three patients underwent closed en bloc excision of the aneurysm with in-situ graft replacement, and four underwent partial resection with in-situ graft replacement. In group 2, three patients underwent resection of the aneurysm with ligation of aorta and extra-anatomic bypass, and two underwent in-situ graft replacement after débridement of infected tissue. Overall, patients in group 1 had a mortality rate of 14% compared with 80% in group 2. These results suggest that the operative approach and method chosen to restore arterial continuity have less of an impact on outcome. The primary determinants of outcome are virulence of the infecting organism and the preoperative state of the infection.

Acinetobacter Infections↗
PubMed2006

Tuberculous pericardial effusion after coronary artery bypass graft.

We describe a case of a recurrent pericardial effusion after coronary artery bypass grafting. This was initially considered to be due to post-pericardiotomy syndrome, but was later treated empirically as tuberculosis. After definitive surgery for this condition, pericardial histology and immunohistochemistry confirmed the diagnosis of tubercular pericarditis. At 4-months follow-up, while continuing anti-tuberculous therapy and corticosteroids, the patient showed consistent improvement without further recurrence of his pericardial effusion. Local reactivation of tuberculosis after pericardiotomy has not been previously reported and merits careful consideration in population groups in which tuberculosis is highly endemic.

Antitubercular Agents↗