Most cases of arteriosclerosis sooner or later present symptoms referable to the heart. When the organ is hypertrophied and is already working against an enormous peripheral resistance, a slight excess of work put upon it may cause a dilatation of the chambers with the resulting broken compensation. There is dyspnea on slight exertion, possibly some precordial distress, slight edema of the ankles and lower legs and possibly scanty urine. With proper care, a patient with such symptoms may recover, but the danger of another break in compensation is enhanced. The next attack is more severe. The edema is greater, there may be signs of edema of the lungs, effusions into the serous cavities may occur. The heart shows marked dilatation. There is gallop or canter rhythm and there are loud murmurs at the apex. When a patient is first seen in this stage, it may be quite impossible to state whether or not there is true valvular disease of the heart. The muscle is usually diseased in that there is fibroid degeneration of more or less extensive character. This factor causes the heart to lose much of its elasticity and increases the tendency to permanent dilatation. Such cases must be watched before one can say that true valvular insufficiency is not present. The fatal termination of such a case is quite like that of true valvular disease. There is increasing dyspnea, increasing anasarca, and the patient usually succumbs to edema of the lungs, drowned in his own secretions. [Illustration: Fig. 59.--Aneurysm of the heart wall. (Milwaukee County Hospital.)]