Pathophysiology 

Large haemorrhages and fibrinous lesions vegetate along the inflaked edges of valves. The lesions develop on adjacent valve leaflets so that the edges adhere together. As the disease progress, the leaflets become so scarred that there is permanent leaflet fusion and limited valvular movement of the normally free- flapping edges. These changes occur over a period of time.

Clinical manifestations of stenosis or insufficiency do not usually show up until 10 to 40 years after onset of rheumatic fever. Mitral and aortic valves.are more susceptible. The tricuspid valves are less frequently affected and pulmonic valve is rarely affected by rheumatic fever.