Rheumatic mitral stenosis

An overview of rheumatic valvular heart disease is acute rheumatic fever violations of the heart left after chronic heart change, Currently in China is still quite styles. Rheumatic heart disease with mitral valve is most common, followed by the aortic valve, the tricuspid valve is rare, pulmonary valve is even more rare. Chronic rheumatic heart disease can affect a number of valves. Clinical is the most common single mitral valve disease, accounting for about 70%. followed for mitral with aortic valve disease accounts for about 25%, isolated aortic valve disease accounts for about 2 ~ 3%. tricuspid and pulmonary valve disease were more or mitral and aortic valve disease associated with the existence. Cause pathogenesis most rheumatic fever incidence in adolescence is a allergic diseases. Against the connective tissue diseases of collagen fibers, produce mucus changes to cellulose-like change and gradual emergence fibroblast proliferation, lymphocytes and monocyte infiltration formed rheumatoid body. With the course of development, rheumatoid body into scar tissue fibrosis. Rheumatic course development relatively slow and usually lasted 4 ~ 6 months, but often repeated attack, causing injury gradually worsened. Rheumatic fever often violations of the heart caused wholeheartedly in charge involved pericardium, myocardium and endocardium. Rheumatic fever recurrent damage caused by the most serious is the endocardium, in particular the mitral heart tissue. Long-term repeated rheumatoid inflammation and blood turbulence of mechanical injury and platelet accumulation of the main mitral valve disease Membrane fusion junction, valve thickening fibrosis, tendons and / or shorten the papillary muscle fibrosis, integration and valve calcification. These lesions usually lasted 10 ~ 30, but the junction of integration and valve fibrosis sometimes just 2 ~ 3 years. Mitral valve junction of the first integration of the former occurred within the diplomatic community, and after the junction, and then gradually to the central portion of the valve extension. Mild mitral stenosis in diameter 1.3 cm, moderately narrow 0.8-0.8cm, severe stenosis in the following 0.8 cm. Fusion scope of the junction over a long valve stenosis is more than serious. Mild cases of stenosis, in spite of valve and the junction of fusion but a small valve activity is fairly good, the valve diaphragm was like. Severe mitral valve stenosis patients diameter only a few millimeters before and after the valve is the valve thickening fibrosis, shortened or calcium deposition. After the valve lesions more often than before the valve is more serious. After the valve activity loss, before the valve still retain a certain degree of activities. Tendons, the papillary muscle is thickened, adhesion, shortened lesions, the valve shall be pulling into the left ventricle, activities restricted, Mitral funnel-shaped. Inter alia valve stenosis accompanied regurgitation. Cases of mitral stenosis of left atrial hypertrophy often expand, blood stranded in the left atrium, the appendage formed thrombus. The cases of atrial fibrillation is more common in thrombosis. As the pulmonary circulation of blood to return blocked, a long-term lung tissue blood Yu, interstitial edema and fibrosis. There were many may have swallowed hemosiderin macrophages (heart failure cells). Adults mitral valve opened at about 4 ~ 6cm2, valve length of about 3.5cm, which can mean two-three. When the junction of integration, the valve reduced to 50% or more valve area of less than 2.5 ~ 3.0cm2. left atrial blood by mitral valve left ventricular inflow began to encounter obstacles. Valve less than 2 ~ 2.5cm2. Left atrial pressure began to increase to two-kPa (15 ~ 20mmHg). pulmonary circulation increased blood volume that is beginning to show tired after short breath. Valve further narrow to 1.5 cm2 below Left atrial pressure can be increased to ~ 3.3 kPa (25 ~ 30 mmHg). pulmonary capillary leakage of fluid began to enter the alveoli, the bottom there will be wet rales. With increased pressure on the left atrium, left atrial hypertrophy gradually, often showing atrial fibrillation. As a result of exertion or emotional excitement to speed up the heart rate, the patient may suddenly has short breath and respiratory center so acute pulmonary edema. Moreover, due to reduced cardiac output and systemic blood pressure reduced accordingly, patients feel dizziness, weakness, easy tired. Associated with atrial fibrillation in patients with mitral stenosis due to blood stranded in the left atrium can be formed in atrial appendage thrombi Thrombosis can cause shedding systemic embolism. Long left atrium and pulmonary circulation increased pressure, pulmonary artery spasm in the state initially, and then the wall thickening, lumen narrow lead obstructive pulmonary vascular disease, pulmonary alveolar capillary membrane and membrane thickening interface, alveolar fluid leakage into the cause of pulmonary edema but rare. Chronic severe mitral stenosis cases pulmonary artery pressure increased gradually up to 12 seriously-16kPa (90-120mmHg). Chronic pulmonary hypertension prompted right ventricular hypertrophy, finally appeared right heart failure, has rolled jugular, hepatomegaly and signs of lower extremity edema. Right atrioventricular ring can be expanded caused functional tricuspid regurgitation.