It has sometimes seemed that high blood pressure has caused the left ventricle to act with such force as to irritate this mitral valve, and later develop from such irritation a sclerosis or narrowing, and stenosis occurs. It has been suggested that, though lime may be of advantage in heart weakness, as will be stated later, if the blood is overfull of calcium ions the valvular irritations may more readily have deposits of calcium, in other words, become calcareous, and therefore cause more obstruction. It is quite likely, however, that this sort of deposit is only a piece of the general calcification of tissue in arteriosclerosis and old age, and could not be caused by the administration of calcium to a younger patient, and might then occur in older patients even if substances containing much calcium were kept out of the dict. Calcium metabolisim in arteriosclerosis and in softening of the bones is not well understood. Patients with this lesion are seriously handicapped when any congestion of the lungs occurs, such as pneumonia, pleurisy, or even bronchitis. Asthma is especially serious in these cases, and these patients rarely live to old age. The pulse is generally slow, unless broken compensation occurs; dyspnea on exertion is a prominent symptom; the increased secretion of mucus in the bronchial tubes and throat is often troublesome, and there is liable to be considerable cough. If these patients have an acute heart attack, a feeling of suffocation is their worst symptom and the dyspnea may be great, although there may be no tachycardia, these hearts often acting slowly even when there is serious discomfort. When compensation fails, there is an occurrence of all the usual symptoms, as previously described. The distinctive diagnostic physical sign of this lesion is the diastolic and perhaps presystolic murmur heard over the left ventricle, accentuated at the apex and transmitted some distance to the left of the heart. There is also an accentuated pulmonary closure. To palpation this lesion often gives a characteristic presystolic thrill at and around the apex. The first symptoms of weakening of the compensation are irregularity in the beat and venous congestion of the head and face, causing bluing of the lips, often nosebleed, and sometimes hemoptysis and insomnia. Later the usual series of disturbances from dilatation of the right ventricle occurs. As previously stated, with the absence of good coronary circulation and the consequent impaired nutrition, the left ventricle may also dilate and the mitral valve may become insufficient. Sudden death from heart failure may occur with this lesion more frequently than with mitral insufficiency but less frequently than with aortic insufficiency.