At the height of the attack or later on when a larger artery is oc cluded, especially the one running in the anterior longitudinal sulcus, death may occur either suddenly, or gradually by exhaustion of the heart, with symptoms of paralysis of the organ. This serious affec tion and such termination are not so frequent in arteriosclerosis complicating obesity as under other circumstances. Equally rare is rupture of the heart from softening of the muscle, or after thrombosis of a larger vessel.
In most cases the attacks pass over after a shorter or longer time ; the injury suffered by the heart muscle is repaired, a collateral cir culation is established, and the muscular substance destroyed by the myomalacic process is replaced by a deposit of connective tissue. Should a larger portion of the cardiac muscle have perished and been replaced by connective tissue, the heart wall at that point be comes thinned more and more and finally an aneurism develops. This termination likewise is more rarely observed in cases of obesity and fatty heart.
After the stenocardic attack has passed the patient feels for a con siderable time weak and wretched, but recovers gradually and the sub jective condition is nearly as good as before. The attack may remain isolated or return after a longer interval, or slighter more frequently repeated attacks may increase in severity and one of them be fatal, or death may result from the sequelm.
In the majority of cases, after recovery from the attack, the in sufficiency of the heart increases, the arteriosclerosis has caused ex tensive muscular degeneration and chronic myocarditis, the dilata tion becomes greater and is no longer compensated by hypertrophy. Fatigue of the heart occurs after a few contractions, and the muscle labors to propel the blood accumulated in the right heart and the lungs by incomplete, irregular, partly accelerated contractions, and to maintain the circulation approximately for the performance of the most important vital functions.
In the further course of the disease the congestions multiply, the excretion of urine becomes still more incomplete, the attacks of poly- . aria are rarer or absent, and on determining the differences between ingestion of fluids and excretion of urine large deficits are found which can no longer be compensated for by restricting the quantity of liquids consumed. No more surplus of urine is obtained, but a diminution
of the fluids ingested is followed by a small excretion. The water con sumed in the food and drink can no longer be completely expelled even by the greatest activity of the vicariously acting organs. The cutane ous arteries supply the sweat glands with less and less blood and while the patient perspires easily the secretion is not great enough to take the place of the lessened urinary secretion. The hydrmmia increases, the water accumulates in the tissues, the return flow in the lymph vessels becomes more and more defective by reason of the reduced tension of the tissues resulting from the immense serous transudation and imbibition. The water accumulates first in accordance with the weight of the stagnant column of blood and the most restricted return flow, i.e., in the lower extremities, in the cellular tissue of the foot around the ankle, and forms cedemas which may disappear for some time after the circulation is relieved by spontaneous or artificial diuresis, but they soon return or increase rapidly from the start.
Wherever (edema develops the secretion of sweat diminishes more and more and finally ceases so that perspiration no longer appears even under the influence of great heat, in hot dry-air or in Russian and Turkish baths. Hence the greater the surface over which the cedema extends the more the excretion of water by the skin dimin ishes, and this in its turn adds to the hydiwinia. The cedema spreads slowly over the lower extremities, above the thighs, and on the surface of the abdomen. The scrotum, penis, and prepuce, in women the labia majora and minora, swell and assume enormous and unshapely dimensions owing to the great transudation of serous fluid into the loose meshes of their cellular tissue, and this materially increases the troubles of the patients. The high pressure of the accumulated water and the saturation of the tissues as far as the epidermis may cause excessive stretching and tension of the skin, fissures, and detachment of the epidermis. The thin watery serum exudes from the wound, the epidermis is macerated, ulcers form, and erysipelas may appear and spread far over the legs and thighs, the scrotum, or the labia.