As soon as a valve has become injured the heart muscle hypertrophies to force the blood through a narrowed orifice or to evacuate the blood coming into a compartment of the heart from two directions instead of one, as occurs in regurgitation or insufficiency of a valve. The heart muscle becomes hypertrophied, like any other muscle which is compelled to do extra work. Which part or parts of the heart will become most enlarged depends on the particular valvular lesion. In some instances this enlargement is enormous, increasing a heart which normally weighs from 10 to 12 ounces to a weight of 20 or even 25 ounces, and extreme weights of from 40 to 50 ounces and even more are recorded. As long as the heart remains in this hypertrophied condition, which may be called normal hypertrophy since it is needed for the work which has to be done in overcoming the defect in the valve, there are no symptoms, the pulmonary and systemic circulation is sufficient, and the patient does not know that he is incapacitated. Sooner or later, however, the nutrition of the heart, especially in atheromatous conditions, becomes impaired, and the lack of a proper blood supply to the heart muscle causes myocardial disturbance, either a chronic myocarditis or fatty degeneration. If there is no atheromatous condition of the coronary arteries, and arterial disease is not a cause of the valvular lesion, compensation may be broken by some sudden extra strain put on the heart, either muscular or by some acute sickness or a necessary anesthetic and operation. From any of these causes the muscle again becomes impaired, and the heart, especially the part which is the weakest and has the most work to do relatively to its strength, becomes dilated, compensation is broken, and all of the various circulatory disturbances resulting from an insufficient heart strength develop. PRECAUTIONS TO BE OBSERVED