Endocarditis may be acute, subacute, or chronic. In acute inflammation we find a thickening and a roughened appearance of the endocardium throughout the cavities of the heart. This condition may be followed by a coagulation of fibrin upon the inflamed surface, which adheres to it, and by attrition soon becomes worked up into shreddy-like granular elevations. This may lead to a formation of fibrinous clots in the heart and sudden death early in the disease the second or third day. Subacute endocarditis, which is the most common form, may not become appreciable for several days after its commencement. It is characterized by being confined to one or more anatomical divisions of the heart, and all the successive morbid changes follow each other in a comparatively slow process. Often we would not be led to suspect heart affection were it not for the distress in breathing, which it generally occasions when the animal is exercised, especially if the valves are much involved. When coagula or vegetations form upon the inflamed membrane, either in minute shreds or patches, or when formation of fibrinous clots occurs in the cavity affected, some of these materials may be carried from the cavity of the heart by the blood current into remote organs, constituting emboli that are liable to suddenly plug vessels and thereby interrupt important functions. In the great majority of either acute or subacute grades of endocarditis, whatever the exciting cause, the most alarming symptoms disappear in a week or 10 days, often leaving, however, such changes in the interior lining or valvular structures as to cause impairment in the circulation for a much longer period of time. These changes usually consist of thickening or induration of the inflamed structures. But while the effects of the inflammation in the membrane lining the walls of the ventricles may subside to such a degree as to cause little or no inconvenience, or even wholly disappear, yet after the valvular structures have been involved, causing them to be thicker, less flexible than normal, they usually remain, obstructing the free passage of the blood through the openings of the heart, thereby inducing secondary changes, which take place slowly at first, but ultimately seriously impair the animal's usefulness. What was but a slight obstruction to the circulation during the first few weeks after the subsidence of the cardiac inflammatory attack becomes in process of time so much increased as to induce increased growth in the muscular structure of the heart, constituting hypertrophy of the walls of the ventricles, more particularly of the left, with corresponding fullness of the left auricle and pulmonary veins, thereby producing fullness of the capillaries in the lungs, pressure upon the air cells, difficult or asthmatic breathing--greatly increased in attempts to work--until in a few months many of these cases become entirely disabled for work.