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Histopathological Evaluation Of Chronic Rheumatic Mitral Valve Stenosis:the Association With Clinical Presentation, Pathogenesis And Management At A National Cardiac Institute.
Reuben Kato Mutagaywa1, Amos Mwakigonja1, Pilly Chillo1, Advera Ngaiza1, Moses Byomuganyizi1, Lulu Fundikira1, Gideon Kwesigabo1, Appolinary Kamuhabwa1, Maarten Cramer2, Steven Chamuleau3.
1Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania, United Republic of, 2University Medical Centre Utrecht, Utrecht, Netherlands, 3Univeristy Medical Centre Amsterdam, Amsterdam, Netherlands.

OBJECTIVE: The histopathology of mitral valve (MV) tissues have been reported in necropsy and retrospective studies. We prospectively studied the histopathological changes in rheumatic mitral stenosis using advanced histologic techniques and corroborated these with clinical presentation, pathogenesis, and management.
METHODS: Surgically excised rheumatic stenotic MV from 54 Tanzanian patients were studied. These were examined using hematoxylin-eosin, von Kossa staining, and immunohistochemistry.
RESULTS: The median (range) age of the patients was 39 (14 - 57) years with a female 34 (63%) predominance. There was a low rate 7 (13%) of patients on secondary prophylaxis and 2 (3.7%) had rheumatic fever (RF). With hematoxylin-eosin, 37 (68.5%) specimens showed fibrinoid degeneration (FD), 44 (81.5%) polymorphonuclear leucocytes (PMNL), 6 (11.1%) Aschoff nodules, 30 (55.6%) calcification, and 39 (72.2%) fibrosis. Thirty-five (64.8%) specimens were positive to von Kossa. The proportion of specimens positive for CD3, CD20, CD68, and CD8 were 46 (85.2%), 35 (64.8%), 39 (72.2%), and 8 (14.8%) respectively. Valvular calcium was high among: older patients, males and with higher trans-MV gradient. A statistically significant association existed between the degree of inflammatory cellular infiltration and valvular calcification and between the presence of FD and RF, PMNL and disease < 10 years, and fibrosis and the absence of atrial fibrillation. C-reactive protein and anti-streptolysin titres were statistically significantly high in CD20 and CD8 staining cells.
CONCLUSIONS: This study confirms that high MV calcium are found in patients who are old, male, and with severe mitral stenosis and that valvular calcification is associated with cellular infiltration. Our findings compare with those from other countries suggesting similar pathogenesis and thus intervention modalities. We recommend: i) pre-operative workup to rule out active inflammation, ii) uptake of secondary prophylaxis, and iii) the role of anti-inflammatory and antibiotic prophylaxis post-surgery.


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