Angina is a most important symptom; attacks may recur for years, and death may take place in a paroxysm. Asthmatic attacks are very common: a feeling of impending suffocation, and gasping for breath amounting in some instances to urgent dyspnoea. Oedema of the lungs may occur in these attacks. Fainting and pseudo-apoplectic attacks are frequent symptoms. The physical signs are not very definite or constant. The apex-beat may be displaced and weak, perhaps unrecognizable. With an increase in the area of dulness this is a sign of dilatation. A systolic murmur at the apex is not infrequent. There may be the bruit de galop; gradual heart failure, with general dropsy, is the mode of termination in a considerable number of cases.
The DIAGNOSIS can rarely be made with certainty. The combination of weakened heart, atheromatous arteries, and angina attacks occurring in a person above fifty years of age is certainly suggestive of the existence of this condition; but, as will be seen, this group of symptoms occurs also in fatty degeneration, although the anginoid attacks are probably not so frequent.
In spite of the admirable clinical memoirs above referred to, we are still in need of careful studies of an extensive series of cases, whereby we can get information which will enable us to distinguish more clearly than we can at present the diseases of the myocardium from one another. In this respect our pathological knowledge is in advance of our clinical.
The TREATMENT is largely that of cardiac dilatation and angina, which will be elsewhere considered. The condition is a chronic one, and often associated with hypertrophy, and many of the symptoms are dependent upon failing compensation. Under such circumstances digitalis is indicated, but when there are attacks of angina caution must be exercised in its use.
The Degenerations of the Heart-Muscle.
Under this division we shall consider the following conditions, all of which are characterized by an alteration in the quality and an impairment of function in the affected tissue: 1. Anæmic necrosis; 2. Parenchymatous degeneration; 3. Fatty changes, infiltration and degeneration; 4. Brown atrophy; 5. Amyloid degeneration; 6. Hyaline degeneration; and 7. Calcareous degeneration.
1. Anæmic necrosis is a condition which results in the heart-muscle when a branch of the coronary artery is blocked either by a thrombus or an embolus, or is obliterated by a progressive sclerosis. The region supplied by the affected vessel is deprived of blood and undergoes a process of infarction. In some instances the tissue is not infiltrated with blood, as in an ordinary infarct, but has a pale yellowish color and is very soft. When there is extravasation the color is more reddish-brown. Histologically, the muscle-cells are found in a state of granular degeneration, and on staining the nuclei do not take the tint, and the whole tissue ultimately assumes the homogeneous granular aspect of coagulation necrosis. There may be fatty degeneration in the contiguous muscle-fibres, and finally, as with infarcts in other organs, fibroid induration takes place. This process, as before mentioned, plays an important part in the production of the fibroid patches scattered through the myocardium. When fresh, the softening of the affected region may be marked, and the name myomalacia cordis which Ziegler22 has suggested is so far suitable, but it seems more appropriately applied to that condition of general softening of the organ met with in severe fevers. This process most frequently affects the left ventricle, and if extensive may lead to rupture.
22 Loc. cit.
The clinical aspects of this condition, as induced by sclerosis of the coronary arteries, have been recently studied with great care by Leyden.23 In acute cases death occurs in a few hours with symptoms of intense angina pectoris and heart failure. The subacute cases are characterized by recurring anginoid attacks lasting from a few minutes to half an hour. There may be attacks of asthma with heart weakness, and signs of oedema of the lungs. The clinical picture is that of angina pectoris, and the patient may have had similar attacks on previous occasions.
23 Zeitschrift f. klin. Med., Bd. vii., 1884.