heart. Abscess or hydatid cysts of the left lobe may push the organ up
and to the left. More rarely large hepatic tumors drag the diaphragm
down, and with it the heart. Very great splenic enlargement, as in
leukæmia, may push up the diaphragm and lift the heart.
Other abdominal growths, as large retro-peritoneal and ovarian tumors
or aneurism of the abdominal aorta, may occasionally produce the same
effect. Knowsley Thornton has given in Fothergill's work on the _Heart_
an excellent account of the upward displacement of the heart in ovarian
disease.
As a very rare circumstance, the heart is displaced by accidental
injury to the chest-walls. The case which Stokes relates of this kind
was probably, as he subsequently suggested, due rather to the effects
of the pleuritic effusion which followed the accident.
The dislocations of the heart when gradually induced rarely disturb to
any serious extent the functions of the organ.
Myocarditis.
Inflammation of the heart-muscle is rarely primary; usually it is
associated with endo- or pericarditis, strain,[7] embolic processes,
disease of the arteries, or the presence of certain
poisons--diphtheritic, rheumatic, etc.--in the blood.
[Footnote 7: Some French writers refer specially to the occurrence of
myocarditis from strain or prolonged muscular exercise--myocardite des
surmenes. Peter (_Maladies du Coeur_, Paris, 1883) gives two cases
(without autopsy), and quotes a case from Revilliod, whose work (_La
Fatigue_, Lausanne, 1880) I have not been able to consult.]
We may recognize three forms--acute suppurative, acute interstitial,
and chronic myocarditis. By many writers the parenchymatous
degeneration so frequent in fevers is regarded as an inflammation, but
it is the result of a process which we can scarcely term inflammatory.
Acute suppurative myocarditis is almost invariably associated with
pyæmia or with malignant endocarditis, and in most instances may be
regarded as embolic. In severe pyæmia from any cause foci of
suppuration are not infrequently met with in the walls of the
ventricles. There may be multiple abscesses or a single purulent
collection varying in size from a pea to a walnut. Numerous miliary
abscesses are not so often met with in ordinary pyæmia as in
endocarditis. If large, the abscess may burst into the heart or into
the pericardium and excite inflammation of this membrane; or, indeed,
without perforation, as I saw in one instance. The calcareous nodules
occasionally found in the muscle-substance have been regarded as healed
abscesses. Suppurative myocarditis is a frequent result of malignant
endocarditis, and we meet with it either in the form of miliary
abscesses, scattered in numbers through the substance, or as large
solitary abscesses at the bases of vegetative outgrowths or in
connection with excavating ulcers of the endocardium, valvular or
mural. The small embolic abscesses vary in size from {605} a pin's head
to a pea, and may occur in extraordinary numbers in the
muscle-substance of all the chambers. They present usually a central
grayish-white focus of suppuration surrounded by a zone of
deeply-congested and hemorrhagic tissue. Microscopically, there is a
central infiltration of leucocytes with destruction of the
muscle-fibres, and in every instance colonies of micrococci can be
readily discovered. These abscesses are identical in character with
those occurring in the kidneys, intestines, and brain. Sometimes at the
base of large endocardial outgrowths, particularly of the aortic
segments, abscesses are found extending deep into the muscle-substance,
and even perforating the wall. These occur most often in the left
ventricle, but occasionally in the right, as in a case of stenosis of
the pulmonary valves at the Montreal General Hospital, in which there
was an abscess cavity in the wall of the right ventricle the size of a
marble, situated at the base of some endocardial vegetations. The acute
ulcer of the heart is of the nature of a suppurative myocarditis,
having its starting-point, in the great majority of cases, in the
endocardium. It may perforate the wall of the ventricle, as in the
cases of Mackenzie[8] and Keating.[9] The blood-pressure in the
abscess-cavity may dilate the wall, and form what is known as acute
aneurism of the heart.
[Footnote 8: _Path. Soc. Trans. London_, xxxiii.]
[Footnote 9: _Trans. of the College of Physicians of Philadelphia_,
1879.]
Acute interstitial myocarditis occurs in connection with the infectious
fevers, and also with pericarditis, more rarely endocarditis. It is
characterized by the presence of numerous round cells in the
interfibrillar tissue, multiplication of the corpuscles, and
degeneration, granular or fatty, of the muscle-fibres. The coarse
appearances are--a relaxed state of the cardiac walls, pale or turbid
condition of substance, in extreme instances a sodden, soft friable
state, so that the muscle readily tears on pressure. In acute
pericarditis the superficial myocardium, for a line or two beneath the
membrane, frequently presents this condition in a typical manner; it
looks pale and turbid, contrasting strongly with the deeper parts, and
on examination presents infiltration of leucocytes, swelling of the
interstitial tissue, sometimes effusion of blood-corpuscles, and a
swollen, granular, or fatty state of the muscle-fibres. Although the
process may be intense, suppuration rarely occurs, whereas in
myocarditis supervening upon inflammation of the endocardium it is, as
we have seen, not uncommon. A similar diffuse interstitial process is
met with in many of the fevers. In rheumatism, typhus, scarlet fever,
small-pox, and diphtheria the myocardium may be found relaxed and soft,
the chambers dilated, the substance pale, easily torn, in some
instances extremely soft; and this condition has been variously
described as inflammatory or degenerative. While not denying that such
a state of the muscle-fibre may be brought about by the action of the
fever or the influence of some specific poison without any signs of
inflammatory action, yet in other instances changes have been found
which are evidently of the nature of a myocarditis. In these cases the
intermuscular connective tissue is swollen, infiltrated with round
cells and nuclei, the vessels are dilated, and often there are minute
extravasations and the muscle-fibres are granular and fatty, with
indistinct striæ and nuclei. As Leyden[10] has pointed out, this
condition probably affords an explanation of some of the cases of
sudden death in diphtheria. It may occur without the coarse or
microscopic appearance of degeneration of the muscle-fibres, and when
of any duration may produce areas of atrophy. Though usually diffuse,
it may be patchy and limited in distribution. Martin[11] has described
in cases of sudden death in diphtheria and typhoid fever an acute
endarteritis of the small branches of the coronary arteries, which
probably has a close relationship with this acute interstitial
myocarditis.
[Footnote 10: _Zeitschrift für klinische Medicin_, Bd. iv.]
[Footnote 11: _Revue de Médecine_, 1881.]
{606} The SYMPTOMS of acute myocarditis are those of cardiac weakness
and irritability, and it is the conditions under which these occur
which make us suspect involvement of the myocardium rather than any
special features pertaining to the disease. We may reasonably suspect
its presence in a case of rheumatism, puerperal fever, or other
specific fever when the patient complains of cardiac distress or actual
pain, with shortness of breath, and on examination we find a weakened
impulse, feeble, indistinct first sound, and a small, irregular pulse.
The area of heart-dulness is increased, and there may be a murmur due
to muscular incompetence. There is usually fever, but this is generally
due to the primary affection. The symptoms are those of a weak and
dilated heart, and are peculiar only in the mode of onset and the
circumstances under which they arise. A point of note observed by
Stokes is the weakening or disappearance of organic murmurs during an
attack of acute myocarditis. In acute pericarditis grave implication of
the myocardium may be suspected when the pulse gets small and rapid,
dyspnoea urgent, and the cardiac pain is increased. Such symptoms, in
the absence of copious effusion, would appear to indicate extension of
the inflammation to the heart-muscle. Even the occurrence of
suppuration has no distinctive symptoms, as it almost invariably occurs
as part of a pyæmic process, and the cardiac weakness which supervenes
may be regarded as an outcome of the septic or febrile condition. The
bursting of an abscess into the pericardium will excite violent
pericarditis. In the case of Kortüm, referred to by Friedrich,[12] an
abscess in the septum burst into the ventricle; the symptoms, which
developed suddenly during a lecture, were a sense of constriction in
the chest, dyspnoea, and lividity, and death occurred in six hours.
[Footnote 12: _Virchow's Handbuch_, Bd. v.: "Herzkrankheiten," S. 275.]
The DIAGNOSIS can rarely be made with certainty; at the best we can
suspect its presence under the conditions above mentioned.
The course of suppurative myocarditis is always unfavorable, but the
fatal termination of the case is usually dependent on concomitant
causes. The possibility of recovery in some instances of abscess of the
heart is suggested by the occurrence of caseous and cretaceous masses,
probably the remnants of collections of pus.
The chief danger in interstitial myocarditis is heart paralysis and
sudden death, as occur in diphtheria and occasionally in rheumatism.
From mild grades of the disease recovery may take place, and even when
general and severe it has often been some indiscretion which has
induced the collapse, as sudden sitting up in bed or getting out to
attend to the calls of nature. Possibly the slight intramuscular scars
and spots of atrophy furnish evidence of past acute myocarditis.
When suspected, the TREATMENT should consist of absolute rest, muscular
and mental, with careful feeding and stimulation. If a rheumatic case
upon the alkaline or salicylate treatment, the remedies should be
stopped. I saw sudden death from heart failure in a case of acute
rheumatism in which during four days the full alkaline treatment of
Fuller was followed, and in which, by mistake, a much larger quantity
of the bicarbonate of soda was given each day than had been intended.
Strychnia and small doses of quinine may be given. Shall digitalis be
employed in acute myocarditis? Upon this point authorities differ. If
we regard it as simply increasing the force of the muscular
contractions, we can understand the fear of straining a weakened heart;
but digitalis has important trophic influences, and, while it
stimulates the vigor of the contraction, improves the nutrition of the
heart-muscle and renders it better able to contract. After all, the
question amounts to the giving of digitalis in dilatation, and with a
weak first sound and feeble action the careful administration, in
conjunction with stimulants, will be found beneficial. Peter[13] speaks
highly of the application of a blister in the region of the heart.
[Footnote 13: _Loc. cit._]
{607} Chronic Myocarditis (Fibroid Heart).
A condition characterized by the substitution in areas of variable
extent of a fibrous connective tissue for the muscular substance. It is
an interstitial growth, comparable to the cirrhosis of other organs,
and the muscle-elements in the affected regions are wasted or entirely
destroyed. The process may occur in a mild grade throughout the organ,
but it is more common to find it distributed in certain parts which
seem specially prone to this form of degeneration.
The conditions under which it is most likely to occur are those which
we find in connection with arterio-sclerosis. It is an affection of
adult and advanced life, and is met with most frequently associated
with disease of the coronary arteries. In chronic valvular affections
it is very common, and may be part of the so-called cyanotic induration
or an extension from the thickened endocardium. Sometimes it seems a
part of a general arterio-capillary fibrosis. In a few cases there is
direct extension from the pericardium. Rheumatism is in this way
indirectly responsible; possibly some of the cases are directly
traceable to acute interstitial myocarditis occurring in this disease.
Chronic alcoholism, syphilis, and gout are prominent factors in the
etiology. Some of the most marked cases give no clue in the history or
habits of any conditions which we could reasonably connect with the
disease. Males are more often affected than females. The tendency to
arterio-sclerosis seems to run in some families. Mental anxiety is not
without influence, and when the disease is established seems very
liable to bring on the anginoid attacks. The situation and extent of
the fibrosis are very variable. The papillary muscles and the columnæ
carneæ of the left ventricle are most frequently affected, less often
the corresponding structures on the right side. The middle portion of
the muscular bundles and the apices of the papillæ are first involved.
In the latter the process may extend almost to their bases, but on
section it will be found that it is more advanced in the superficial
than the deep parts. This change is very common in cases of valvular
disease with hypertrophy, especially mitral stenosis, but it often
occurs in elderly persons who have had no special heart symptoms.
Beneath patches of pearly-white thickened endocardium local fibrosis
may occur, often seen at the upper part of the septum in left
ventricle, and in the dilated and thickened left auricle of mitral
stenosis, and occasionally in other parts. This is usually regarded as
an extension from a chronic endocarditis. More rarely the fibrosis
extends from a thickened pericardium, but cases are on record of the
conversion of the outer layers of the muscular fibres into a firm, hard
tissue. We frequently meet with scattered areas of fibrosis in septum
and ventricular walls without any implication of peri- or endocardium.
During foetal life an endo-myocarditis may occur in the conus of the
right ventricle, less frequently in the left, and produce very great
narrowing by the gradual contraction of the newly-formed tissue. But
the condition to which the term fibroid heart can be most properly
given is an extensive affection of the left ventricle, involving most
commonly the anterior wall near and at the apex and the lower part of
the septum. In these cases there may be marked bulging at the apex, and
on section the wall cuts with great resistance, and a dense fibrous
tissue of a grayish-white appearance occupies the position of the
myocardium. In extreme cases a large part of the septum and anterior
wall is in this state, and may present only traces of muscular tissue.
There is usually thinning, sometimes thickening, of the affected
portions, and the septum bulges toward the right ventricle. The
endocardium is opaque, often much thickened, and directly continuous
with the fibrous tissue. The columnæ carneæ may be narrow and
flattened, and the lacunæ {608} between them very small. The chamber is
usually dilated. The upper third of the septum and the base and
posterior wall of the ventricle in such cases present a marked contrast
to the affected parts, and may look natural, but more commonly are
hypertrophied. The other chambers may not show any special change or
there may be scattered areas of fibrosis. The thinning and dilatation
at the apex and septum are the conditions which precede and lead to the
formation of cardiac aneurism. The valves may be normal, but in many
cases there is sclerotic endocarditis and retraction. The histological
appearance varies much with the stage of the process. When early or
where advancing, the muscle-bundles are seen separated by round and
elongated cells. The process is usually more marked about groups of
fibres, which gradually become isolated by the increase of the growth,
and in this way one often sees streaks or patches of muscle-tissue
surrounded by the fibrous elements. The destruction of the muscle-cells
is apparently by pressure; they gradually waste and present the
condition of brown atrophy, the pigment of which remains and indicates
the position of the fibres. The intimate pathology of the process is of
great interest. Doubtless in some instances we may attribute the
fibrosis to an extension of an indurative process from the endo- or
pericardium, but the researches of Tautain,[14] Martin,[15] Huber
(Karl),[16] and others have thrown a new light on the subject, and it
seems probable that in most instances the fibroid degeneration is
associated with changes in the coronary arteries. The former describes
an endarteritis and a periarteritis of the small vessels, leading to
disturbance of nutrition and increase of the connective tissue
(sclérose dystrophique). Huber in a considerable number of cases has
traced the connection between the arterio-sclerosis, chiefly of the
smaller twigs, and the indurative process. The region supplied by the
obliterated arteriole is in the condition of an infarct and undergoes
an anæmic necrosis, and subsequently by a proliferating myocarditis is
transformed into a fibroid area. The condition is well described and
figured by Ziegler.[17] Why this obliterating endarteritis should be so
limited in the majority of cases to the vessels of the left ventricle
is not very clear. The parts most distant from the aorta seem most
liable to the process, as the apex and the tips of the papillæ; and it
is interesting in this connection to note that the left coronary artery
is more frequently diseased than the right.
[Footnote 14: _Thèse de Paris_, 1878.]
[Footnote 15: _Revue de Medicine_, 1883.]
[Footnote 16: _Virchow's Archiv_, Bd. lxxxix.]
[Footnote 17: _Pathologische Anatomie_, Lief. ii., 1884.]
In the milder grades of fibrous myocarditis, when only the apices of
the papillæ and thin layers beneath the endocardium are involved, the
heart does not appear to be seriously affected; but when of any extent
the vigor and force of the contractions are impaired, and the ventricle
is unable to do the work of a healthy muscle. Compensatory hypertrophy
is not readily established, possibly on account of the arterial
sclerosis on which many of the cases seem to depend, although in rare
instances, as in a specimen referred to by Quain,[18] there may be very
great muscular hypertrophy. Dilatation of the left ventricle is much
more apt to follow, as the fibroid walls have not the resisting power
of muscular tissue, and the patients finally present a clinical picture
of heart failure. The gradual yielding of the fibroid region may result
in aneurism.
[Footnote 18: "Lumleian Lectures," _Lancet_, 1872, i.]
There are no characteristic symptoms to indicate the condition. The
fibroid heart is a weak heart, and it is scarcely possible to
distinguish it from fatty degeneration. A feeble, irregular, sometimes
slow, pulse, dyspnoea on exertion, and painful anginoid
attacks--symptoms which may have persisted for many years--are special
clinical features in many cases. In a patient I examined some years ago
for Palmer Howard of Montreal--a typical instance of the condition
under consideration--the first symptoms began eight years before death
with angina, and there were repeated attacks of cardiac asthma. {609} A
careful study of the case was made by Howard[19] extending over several
years, and weak heart, dyspnoea on exertion, and anginoid attacks were
the prominent symptoms.
[Footnote 19: "Fibroid Disease of the Heart," _Canada Med. and Surgical
Journal_, vol. viii., 1880.]
Several very careful studies of the disease have been made within the
past few years.[20] Among the symptoms the following may be specially
considered. The first place seems accorded by all to the cardiac
weakness, and in consequence the pulse is feeble. By some (Rühle)
irregularity is regarded as a special feature (delirium cordis), but
Ebstein refers to three cases in which the pulse was always regular.
Juhel-Renoy also speaks of it as frequent and regular. In many cases
the number of beats appears about normal; in others there is a great
increase; while in a third set the pulse may be very slow, sinking to
40 or 50 per minute. It is evident that in regard to regularity and
frequency of the pulse there are very great differences. In this
connection it is interesting to refer to the case of thrombosis of the
coronary artery reported by Hammer,[21] in which the pulse sank to 8
per minute.
[Footnote 20: Rühle, "Zur Diagnose der Myocarditis," _Deutsches Archiv
f. klin. Med._, Bd. xxii.; Ebstein, _Zeitschrift für klinische
Medicin_, Bd. vi.; Leyden, _Ibid._, Bd. viii.--a most important and
exhaustive article; Welch, in a paper read before the Medical Section
of the American Medical Association, Washington Meeting, 1884;
Juhel-Renoy, _Archives gén. de Médecine_, Juillet, 1883.]
[Footnote 21: _Wiener Med. Wochenschrift_, 1878, No. 5.]
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.