**5. Pathological anatomy (by the example of aortic stenosis)**

The basis of pathological changes in aortic disease, in this case, aortic stenosis is rheumatic inflammation – valve valvulitis. Rheumatic valvulitis gradually leads to thickening and compaction of the aortic cusps. This is facilitated by the organization of fibrous overlays on the ventricular surface of the valve, as well as the growth of valve tissue due to mechanical irritation by blood flow. These factors underlie the soldering of the free edges of the leaflets, as a result of which the valve opening gradually decreases. In the area of commissures, fibrin plates form bridges that connect the valves between themselves and the aortic wall. Subsequently, the plates are organized into fibrous tissue. The narrowed valve opening has a triangular or slit-like shape and is usually located eccentrically. When the valves are wrinkled, one or another degree of aortic insufficiency is formed. In the altered valve, degenerative processes develop, followed by calcification. Calcification can move to structures adjacent to the aortic valve: the interventricular septum, the anterior leaflet of the mitral valve, the wall of the left ventricle. Bicuspid AV is often associated with a subvalvular membrane, sometimes with abnormal origin and course of the coronary arteries, the presence of three or even four coronary orifices, and in adulthood is complicated by calcification and/or endocarditis of the AV. Under the valvular membrane (Williams' disease) in the left ventricular outflow tract (LVOT) may or may not fuse with the AV leaflets, be circular or semilunar in shape in a limited area. Such patients have a characteristic "elf face" and lag behind in mental development. LVOT obstruction in hypertrophic cardiomyopathy (HCM) is often associated with anterior leaflet prolapse of the mitral valve (AMVP). Aortic stenosis causes significant morphological changes in the

myocardium of the left ventricle (LV). Prolonged illness leads to progressive hypertrophy and the development of relative coronary insufficiency. Dystrophic changes develop in the heart muscle: protein and fatty degeneration of muscle fibers, and later diffuse and focal sclerosis [14].
