Case in which death occurred amid the symptoms of fatty heart followed by angina pectoris. The post-mortem findings showed the immediate cause of death to have been fatty degeneration of the heart. This did not appear to be dependent on atheronm or occlusion of the coronaries, which seemed every where sound and competent, though im bedded in an abnormal amount of fat. In places, as in the wall of the left ventricle below the auriculo-ventricular furrow at the apex, the muscular tissue was entirely replaced by adipose. Pri mary fatty degeneration of the heart found apart from valvular lesions or marked atheromatous change in the ar teries in a young or middle-aged person with no known hereditary predisposition or diathesis is strongly suggestive of chronic alcoholism. In fact, it is re garded by some authorities as almost peculiar to this form of poisoning. E. P. Hurd (Boston Med. and Slug. Jour..
ii, '93).
The history, particularly if this points to the existence of arteriosclerosis, the age of the patient, and the symptoms of cardiac insufficiency coupled with re tardation of the pulse (though the latter may be increased in frequency), apoplec tic attacks, the Cheyne-Stokes respira tion, in the absence of antecedent hyper trophy, may be regarded as significant features. Again, with a clear history of the presence of the more character istic symptoms, including the signs of dilatation following hypertrophy, fatty degeneration may be inferred with some degree of assurance, and yet even this state of affairs should not lead to a posi tive statement of opinion.
In persons having reached middle life, in whom a weak and irregular action of the heart is manifested, it becomes an important question to decide whether this be due to functional disturbances or organic disease. Broadbent states that usually this is accomplished by making the patient walk briskly. A few steps will often be sufficient. Tf the heart is sound it rises to the occasion. The pulse and beat sounds are all more distinct, and strong and regular, whereas the fatty heart "goes to pieces," and the pulse be comes irregular and shorter than ever or may even disappear.
Fatty degeneration may follow fatty in filtration of the heart, and while in con sequence of this fact the two conditions are sometimes found in association, they are to be looked upon as separate and dis tinct morbid processes. In attempting to discriminate one from the other a recognition of the differences in causa tion is all-important. Fatty overgrowth is due to, and associated with, polysarcia, while the leading causal factor of fatty degeneration of the heart is arterio sclerosis affecting the coronaries, or atheromatous changes in the valves or walls of the aorta, causing obstruction at the mouths of the coronaries: conditions that would lead to weakness of the car diac walls due to degenerative change. Among favoring causes of fatty degener ation are to be reckoned all the various factors that tend to bring about arterio sclerosis, as syphilis, diabetes, and alco holic excess, though the latter may also act primarily upon the myocardium or the blood itself. Cases of fatty heart
occur independently of coronary disease (ride supra). Thus, the disease co-exists with pernicious anwmia, chronic alco holism, and not infrequently follows acute forms of disease, as acute aortitis and typhoid fever. In typical arsenical and phosphorus poisoning the fatty heart is constantly encountered.
The symptomatology of these two car diac affections present differences of con siderable significance. Both may exist, however, without the production of symptoms, and both have symptoms in common, such, for example, as dyspncea upon exertion, and arhythmia, including reduplication. In fatty degeneration the volume of the pulse is diminished to a greater extent, and the disturbance of the rhythm of the pulse is also greater than in fatty infiltration. The breath lessness of fatty infiltration after exer tion is associated with obesity; not so in fatty degeneration, as a rule.
The occurrence of "syncopal, apoplec tiform, and epileptiform attacks" in con nection with the factors of etiological importance mentioned above, point strongly to fat-degeneration, and these symptoms are attributable to insufficient pressure in the arterial tree. Mild syn copal attacks may arise in fatty over growth, but when they become more severe, more frequent and prolonged, and particularly with associated coldness and clamminess of the extremities and body-surface, then fatty degeneration should be suspected. Much the same remarks apply to the symptom angina. The symptoms of bronchitis and asth ma, either separately or combined, are oftener met in fatty overgrowth. In the latter condition the heart-sounds are weak and distant or muffled, owing to abnormal fat-deposits; in fatty degener ation, the sounds are short, flapping in character, due to associated dilatation, but they are clear, and an apical systolic murmur is not uncommonly audible. The so-called therapeutic test is an aid in the discrimination. Thus, as the re sult of appropriate treatment for the obesity the abnormal deposits of fat in and around the heart can be made to gradually disappear, with marked or even complete relief from the inconven iences occasioned thereby. On the other hand, slight temporary improvement, if any, is all that can be hoped for in ad vanced fatty degeneration, or at a time when the diagnosis is reasonably assured. Finally, it may be said that the recogni tion of fatty infiltration is an easy matter, while that of fatty degeneration is scarce feasible until a late stage is reached. That form of fatty degeneration which follows compensatory hypertrophy is tinguished from fatty overgrowth by the special history, absence of obesity, and obviously dissimilar physical signs. It is to be recollected that dilatation ing hypertrophy is not invariably due to fatty change.