Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years.In individuals having been offered mitral valve surgery but refused, survival with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction. Cause
Almost all cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Uncommon causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease. However, there are primary causes of mitral stenosis that emanate from a cleft mitral valve. It is the most common valvular heart disease in pregnancy.Other causes include infective endocarditis where the vegetations may favor increase risk of stenosis. Other rare causes include mitral annular calcification, endomyocardial fibroelastosis, malignant carcinoid syndrome, systemic lupus erythematosus, whipple disease, fabry disease, and rheumatoid arthritis. hurler disease, hunters disease, amyloidosis. Pathophysiology
The normal area of the mitral valve orifice is about 4 to 6 cm2. In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. A normal mitral valve will not impede the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during ventricular diastole will be equal.
Eosinopenia is a form of agranulocytosis where the number of eosinophil granulocytes is lower than expected. Leukocytosis with eosinopenia can be a predictor of bacterial infection. It can be induced by stress reactions, Cushings syndrome, or the use of steroids. Pathological causes include burns and acute infections. See also
Eosinophilia
Hypereosinophilia

References
Further reading
Krause JR, Boggs DR (1987). "Search for eosinopenia in hospitalized patients with normal blood leukocyte concentration". Am. J. Hematol. 24 (1): 55–63. doi:10.1002/ajh.2830240108. PMID 3799595. S2CID 20021710. == External links ==