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Cardiovascular Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
A thickened, fibrotic and calcified pericardium progressively embarrasses cardiac function, resulting in systemic venous congestion and reduced cardiac output. In developing countries, tuberculous pericarditis can present as early constriction, especially after an effusion has been drained.
The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
Bacterial pericarditis usually complicates septicaemia or pyaemia, or arises due to direct spread from pneumonia, empyema, or an ulcerating carcinoma of the bronchus or oesophagus. S. aureus, Haemophilus spp. and streptococci are the most common organisms. Tuberculous pericarditis is due to either haematogenous spread from the lung or direct extension from the trachea, bronchi, or mediastinal lymph nodes. Granulomatous inflammation progresses to fibrous obliteration of the pericardial sac, calcification, and constrictive pericarditis.
Morphologic features and pathology of the elderly heart
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Atsuko Seki, Gregory A. Fishbein, Michael C. Fishbein
In contrast, in developing countries approximately 70% of large pericardial effusions and most cases of pericardial constriction are caused by tuberculosis. Mortality of tuberculous pericarditis is high, 17%–40% (165). Tuberculous pericarditis develops by retrograde lymphatic spread rather than contiguous spread from tuberculous lesions in the lungs or pleurae. The immune response to the M. tuberculosis bacilli penetrating the pericardium plays a fundamental role in the pathogenesis of tuberculous pericarditis. Four pathological stages of tuberculous pericarditis have been recognized: (1) fibrinous exudation with initial polymorphonuclear leukocytosis, abundant mycobacteria, and early granuloma formation; (2) serosanguineous effusion with a predominantly lymphocytic exudate with monocytes and foam cells; (3) absorption of effusion with granuloma formation, pericardial thickening, and subsequent fibrosis; and (4) constrictive scarring (165). Patients with HIV-associated tuberculous pericarditis often have associated with myocarditis.
Image focus: an uncommon cause of isolated right-sided heart failure
Published in Acta Cardiologica, 2020
Bert Zwaenepoel, Ann-Catherine Soenen, Els Viaene
Tuberculous pericarditis is an important complication of tuberculosis. The diagnosis is often delayed or missed, resulting in late complications. The most serious sequel is constrictive tuberculous pericarditis. As seen in Figure 1, cardiac constriction gives rise to a typical pattern on echocardiography. Constriction can be due to different causes (radiation therapy, previous cardiac surgery, repeated pericarditis, etc.). However, tuberculosis should always be kept in mind as the estimated number of new TB cases increases steadily over the past few years. Once the diagnosis is made, prompt anti-tuberculous therapy should be initiated, apart from diuretics to relieve the signs of right-sided heart failure. Pericardiectomy should be considered for selected patients who have failed to response to medical therapy.
Corticosteroids as an adjunct to tuberculosis therapy
Published in Expert Review of Respiratory Medicine, 2018
Charlotte Schutz, Angharad G Davis, Bianca Sossen, Rachel P-J Lai, Mpiko Ntsekhe, Yolande XR Harley, Robert J Wilkinson
Tuberculous pericarditis presents with a broad spectrum of clinicopathological phenotypes. At one extreme, the bacillary load within the pericardium is relatively high, pericardial fluid Mycobacterium tuberculosis cultures become rapidly positive, PCR-based diagnostic techniques are frequently positive and the pericardial involvement often occurs as part of disseminated disease with multi-organ involvement [24,25]. Such multibacillary pericardial tuberculosis has been ascribed to impaired host immunity such as that encountered in people with advanced HIV-1 coinfection with CD4 counts well below 200/mm3. The morbidity and mortality in the multibacillary form may be directly related to the bacillary replication, in conjunction with immune mediated injury [24]. At the other clinicopathological extreme is a paucibacillary condition, in which pericardial fluid cultures are frequently negative despite long incubation, PCR-based techniques are seldom positive, and the etiological diagnosis of tuberculous pericarditis is assumed, based on positive biomarkers and the absence of alternative diagnoses [26,27].
Advances in medical therapy for pericardial diseases
Published in Expert Review of Cardiovascular Therapy, 2018
Alessandro Galluzzo, Massimo Imazio
While viral/idiopathic form is the main etiology for pericarditis in the western world, an alternative cause is represented by bacterial pericarditis, and the most common pathogen in developing countries (and worldwide) is represented by TB. For bacterial pericarditis, prompt specific antibiotic treatment is indicated, together with pericardial drainage of a purulent PE, in order to prevent complications like constrictive pericarditis and fatal outcomes. However, despite an appropriate treatment, mortality at 6 months is around 26%, and approximately 40% among persons with the acquired immunodeficiency syndrome [8]. The attempt of optimizing medical therapy failed to show an improvement in survival in the last few years. The IMPI trial [34] randomized 1400 adults with definite or probable tuberculous pericarditis to either prednisolone or placebo for 6 weeks and to either M. indicus pranii or placebo, administered in five injections over 3 months. Two thirds of the participants had concomitant human immunodeficiency virus (HIV) infection. Nor MIP injections neither prednisolone had a significant effect on the composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. In addition, an increase in HIV-associated cancers was observed in patients who received injections of M. indicus pranii.