degeneration has developed. In the weak fatty heart of chlorosis and
anæmia, with a return to a normal blood-condition, the nutrition of the
heart is improved and its action strengthened. Doubtless many cases of
failing compensation are due to it, and a subsidence of the symptoms
under {616} rest, digitalis, and careful feeding may simply mean
improved nutrition of heart-muscle and disappearance of the fat which
clogs its action. Where due to atheromatous changes, no permanent
improvement can be expected; and in these cases, particularly if
combined with fatty infiltration, rupture or fatal syncope may occur.
In not a few of such cases the persons have not complained either to
their physicians or friends of cardiac distress. The case of the
celebrated Scotch divine, Chalmers, described by Begbie,[29] is an
illustration of advanced fatty heart with sudden death in a man of
extraordinary vigor of mind and body.
[Footnote 29: _Contrib. to Pract. Med._, 1862.]
The TREATMENT should be directed to the removal of the cause when
possible, as the anæmia, febrile condition, etc. In all cases rest,
quiet, and avoidance of excitement are to be rigidly enforced. Sudden
exertions may prove instantly fatal. In the cases where there is
hypertrophy with or without valvular disease, and the failing
compensation is due to this cause, digitalis acts well, and should be
combined with stimulants. In the senile and atheromatous cases great
care must be exercised: the bowels should be kept loose, and the
patient cautioned not to strain at stool or make any sudden exertion.
He should lead a very quiet, regular life, and exercise great
moderation in food, drink, and venery. Warm and Turkish baths are most
dangerous. Iron, arsenic, and nux vomica are remedies from which
benefit may be expected. Digitalis is, as a rule, contraindicated. We
must remember that, as Sir William Jenner has remarked, fatty
degeneration is sometimes a preservative lesion, and induces a due
proportion between the cardiac strength and the arterial resistance,
reducing the former when there is great atheroma and brittleness of the
vessels. The application of blisters is often of use in allaying the
pain, and nitrite of amyl should be given in the anginoid attacks.
4. Brown atrophy is a very common degenerative change in the
heart-muscle, particularly in the hypertrophied organ of valve
affections. In old people and in persons dead of wasting diseases it
seems invariably present. When advanced, the color of the muscle is
quite distinctive--a dark red-brown and the consistence may be greater
than normal. Microscopically, the fibres present a central accumulation
of brown pigment, generally arranged about the nuclei and extending up
and down the cells. The cement-substance between the cells is often
unusually distinct in these cases, and seems more fragile than in
healthy muscle. The composition of the pigment has not, so far as I
know, been determined, but it is doubtless, like that of the brown
induration of the lung and red atrophy of the liver, derived from the
hæmoglobin, and possibly, as in these latter conditions, is connected
with feeble venous circulation.
5. Amyloid degeneration of the heart is occasionally met with, but
rarely in so advanced a grade as to be recognizable macroscopically. It
occurs in the intermuscular connective tissue and in the blood-vessels,
not in the fibres, and occasionally may be extensive, as in a case
mentioned by Ziegler.[30]
[Footnote 30: _Pathologische anatomie_, 3te Aufl., Lief. i., §59.]
6. The hyaline degeneration of Zenker is sometimes seen in the
heart-muscle in cases of prolonged fever. The affected fibres are
swollen, homogeneous, translucent, and the striæ very faint or entirely
absent.
7. Calcareous degeneration may occur in the myocardium, involving the
fibres and forming a definite calcareous infiltration of the
protoplasm, as well figured and described by Coats.[31] It is a rare
condition, whereas extensive calcified plates in endo- and pericardium
are by no means uncommon.
[Footnote 31: _Pathology_, 1883.]
{617} Spontaneous Rupture of the Heart.
Laceration of the wall of the heart is usually associated with fatty
infiltration or degeneration, most frequently the latter. It is
doubtful if in any instance the healthy muscle has broken. Rare causes
are--acute softening, in consequence of embolism of a branch of a
coronary artery; abscess from pyæmia; or an acute ulcer of the
endocardium. Cysts simple or hydatid are mentioned, but the extreme
rarity of causes other than fatty changes may be inferred from the
statistics of Quain,[32] who states that of 100 cases of rupture
collected by him, fatty degeneration was noted (microscopically) in 77,
and in the others there was softening in all but 2, or no mention was
made of the condition of the wall.
[Footnote 32: _Loc. cit._]
Males are more frequently the subject of this accident than females,
and the great majority of cases occur in persons over sixty years of
age--two-thirds of the eases tabulated by Quain.[33]
[Footnote 33: _Loc. cit._]
The rent may occur in any of the chambers, but the most frequent site
is the left ventricle on the anterior wall, not far from the septum.
Statistics give, for 55 cases,[34] 43 in left ventricle, 7 in right
ventricle, and 3 in right auricle and 2 in the left auricle.
[Footnote 34: Elleaumé, _Essai sur les Ruptures du Coeur_, Paris,
1857.]
The break is generally a ragged, irregular rent in the course of the
fibres, and the trajét may be oblique and crossed by strands of muscle.
The internal orifice may be larger than the external; the opposite is
rarely the case. Two or more rents have been found. Usually the fissure
is not very long--from a quarter of an inch to an inch--but there are
cases of long rents extending from base to apex. Clots usually block
the orifices, and the pericardium also contains large coagula. Evidence
is sometimes found to indicate that the tear has occurred slowly, as
attempts at repair may be present.
The wall in the vicinity of the break has usually been found in a state
of degeneration, and we can readily understand how sudden and violent
contractions might strain a weak part and tear the substance. Perhaps
irregularity in the contractions may be an important factor, such as we
may suppose occurs when a wave of contraction reaches a patch of
advanced fatty change or softening from embolism.
The accident usually takes place during exertion or excitement. Many
cases are reported during straining at stool, others while lifting
weights, running, or during coitus. Cases are mentioned as occurring
during sleep or while at rest.
There may be no preliminary symptoms, and without warning the patient
falls, and with a few gasps or a cry is dead. This occurred in 71 of
the 100 cases collected by Quain. In other instances there is great
pain in the præcordial region, a sense of suffocation and anguish, with
vomiting, and life may be prolonged several hours. In one instance the
patient lived eleven days.[35] Probably in such cases there is a small
rent at first which gets blocked with clots, and only a small amount of
blood oozes into the pericardium with each systole. The symptoms may be
those of simple heart failure, as in a case I examined for Burland of
Montreal, in which the patient lived thirteen hours after the onset of
the symptoms, and was able, though with difficulty, to continue his
walk up a rather steep hill.[36] Death appears to occur from shock or
syncope, sometimes from compression of the heart by the extravasated
blood. In the case just mentioned the amount of blood in the
pericardium was {618} very much less than I have seen in cases of
rupture of an aneurism into this sac.
[Footnote 35: Barth, _Archiv. générales_, 1871.]
[Footnote 36: This was a case which illustrated well the latency of
many cases of fatty heart. The patient was an active merchant, aged
sixty, who had never complained of cardiac trouble, and had only a
short time before his death effected a reinsurance upon his life for a
large amount.]
In protracted cases the nausea and vomiting may for a short time lead
to the supposition that the case is one of severe indigestion, but, as
mentioned above, in the great majority of cases death occurs at once,
and in the others there can rarely be any question of diagnosis, and
still less of treatment.
Atrophy of the Heart.
DEFINITION.--A diminution in size and weight of the organ, due to
degeneration and atrophy of the muscular fibres.
The old writers applied the term phthisis of the heart to this
condition. The decrease is always in weight, and usually in size; it is
doubtful if there is an atrophic and dilated heart in which, with the
wasting, the size is maintained by the dilatation. In many of the
degenerations, particularly fatty and fibroid, there is local atrophy
of the muscle-fibres and yet the weight and size of the organ are not
changed.
The varieties which have been recognized correspond to those of
hypertrophy--viz. the simple, eccentric, and concentric forms, but the
two latter are probably only conditions of contraction or dilatation in
a wasted heart. The post-mortem contraction in the small left ventricle
of persons dead of chronic disease may be excessive; and here, as in
concentric hypertrophy, the examination must be made with care.
ETIOLOGY.--The atrophy is either congenital or acquired. The congenital
atrophy which is most frequently seen in women is in association with
defective development of the arterial system and the generative organs.
This is occasionally very marked in chlorosis, and is described and
figured by Virchow in his monograph on this subject.[37] But apart from
this general hypoplasia of the heart and vessels in women, we sometimes
in the post-mortem room find in a man, dead perhaps of an acute disease
and without any cardiac symptoms, a heart small out of all proportion
to the size and general nourishment of the body. Many of the older
writers mention this. Gowers refers to a case which Allan Burns
narrates, in which the heart of an adult was not larger than that of a
child of six or seven. Morgagni has a similar observation.
[Footnote 37: _Ueber die Chlorose_, Berlin, 1872.]
The great majority of the cases are secondary or acquired, and are met
with in the wasting diseases, as cancer, phthisis, prolonged
suppuration, and diabetes. The cardiac wasting is part of the general
marasmus which affects the whole body. In about half the cases of
phthisis the heart is small.[38] In cancer of the pylorus the most
extreme wasting has been found. Disease of the coronary arteries is an
occasional cause, but it most frequently produces local atrophy or
degeneration. Compression by pericardial effusion, fatty infiltration,
and pericardial adhesions are mentioned as rare causes.
[Footnote 38: Quain, _loc. cit._]
A rough guess at the proportional size of the heart may be made by
comparing it with the closed right fist of the person. Weighing gives
the most accurate test, and in each instance regard must be had to the
size of the body. In some instances the organ has weighed only two or
three ounces. The heart figured by Bramwell,[39] one of the smallest on
record, weighed only 2 ounces and 2 drachms. Quain[40] refers to one,
from a girl aged fourteen, which weighed only 1 ounce 14 drachms.
[Footnote 39: _Diseases of the Heart_, 1884.]
[Footnote 40: _Loc. cit._]
Usually, in secondary atrophy, the visceral pericardium is wrinkled and
the coronary arteries prominent and tortuous--two features of great
importance in determining atrophy and in distinguishing between the
acquired and {619} congenital forms. The pericardial fat is variable in
amount. Microscopically, brown atrophy is the most constant change;
fatty degeneration much less common. Senile atrophy may present very
similar appearances. The heart may be tough and firm from an increase
in the fibrous elements. The pericardial fluid I have often noticed to
be much increased.
There are no characteristic SYMPTOMS. The heart-muscle may be able to
fulfil the requirements of the wasted frame. A feeble impulse and
diminished area of dulness may be present, but in the marasmus of
middle-aged or elderly people emphysema of the anterior margin of the
lung may seriously interfere with a proper examination. The increased
pericardial effusion occurs toward the end. The heart sounds are feeble
and the pulse weak. Palpitation is frequent, and there may be the usual
signs of anæmia, dizziness, etc.
The condition may be suspected, but is rarely diagnosed during life.
The PROGNOSIS depends upon the disease to which the atrophy is
secondary, to the amelioration of which also the treatment must be
directed.
Hypertrophy of the Heart.
DEFINITION.--An increase in the size of the heart due to an increased
thickness, total or partial, of the muscular walls.
VARIETIES.--Two forms may be recognized--simple hypertrophy, in which
the cavity or cavities remain of the normal size; and eccentric
hypertrophy, in which with increased thickness of the walls there is
enlargement of the cavities. Dilated hypertrophy and hypertrophy with
dilatation are terms by which the latter form is most frequently
described.
By many writers a third variety, concentric hypertrophy, is recognized,
in which there is diminution in the size of the cavity with thickening
of the walls; but in these cases we have to deal with a post-mortem
change--rigor mortis; and if the organ is kept for twenty-four hours or
soaked in water, the so-called concentric hypertrophy will usually
disappear.
The increased size may affect the entire organ, general hypertrophy; or
only one side or one cavity, partial hypertrophy. The latter is the
most common. Of the single chambers the left ventricle is most
frequently involved, then the right. The auricles are rarely affected
alone, but the left is more often than the right.
ETIOLOGY.--Disturbed innervation and increased work are the two
principal causes of cardiac hypertrophy. We see hypertrophy from
deranged innervation (1) in Basedow's disease (exophthalmic goitre);
(2) in long-continued nervous palpitation from any cause, particularly
sexual excesses; (3) certain poisons and articles of diet appear to act
in this way, as tea, coffee, alcohol, and tobacco.
In all these cases there is simple over-action or increased functional
activity, which, if prolonged, certainly produces some degree of
hypertrophy. How this condition is brought about is not very clear. We
may suppose the increased frequency of contraction to result from
stimulation of the accelerator nerves, as seems probably the case in
exophthalmic goitre; from irritability of the cardiac ganglia
themselves, owing to the influence of such toxic agents as tea,
tobacco, etc.; or from defective vagus control. Long-continued neurotic
palpitation in reality causes hypertrophy by increasing the work of the
heart, for under perverted stimuli the ventricular contractions are
doubled in frequency--sometimes in force as well--while maintaining the
circulation in normal vessels offering no increased resistance to the
blood-flow.
There can be no doubt of the occurrence of actual hypertrophy as a
sequence of the irritable heart induced by sexual excesses and tobacco.
I had under observation on and off for several years a very emotional
and {620} hypochondriacal young man addicted to venery, whose left
ventricle became strongly developed and beat outside the nipple-line.
His entire thoughts became centred in his heart trouble, and he
travelled from one authority to another in this country and Europe
seeking advice.[41] The smoker's heart rarely leads to much
hypertrophy, but in young lads it may do so, and even induce more
serious disease, as indicated by the presence of murmurs and signs of
cardiac failure. The abuse of spirits as a cause of hypertrophy is not
very clearly established. Alcoholism appears to be a factor in the
production of atheroma. I have been struck by the fact that in four
typical instances of so-called idiopathic hypertrophy occurring in
powerfully-built workers there was a history of intemperance; and it is
quite possible that this may have combined with the muscular efforts in
inducing the heart disease; at any rate, it would prove an important
element in hastening the final breakdown when from any cause
hypertrophy had arisen.
[Footnote 41: After three or four years of most unnecessary worry in
the expectation of death from heart disease, this patient has quieted
into the belief that there is not anything seriously wrong with his
heart, and has now rarely any indications of trouble.]
The majority of cases of hypertrophy of the heart are due to mechanical
causes leading to increased resistance and increased work on the part
of the organ. Under these circumstances, as in other hollow viscera,
the muscle develops, gets thicker and firmer, and capable of
accomplishing the extra labor thrown upon it. Defects in the valvular
mechanism, obstruction, or incompetency, and increased resistance to
the blood-flow in the arteries, are the most important causes of
hypertrophy. The ultimate factor in all is heightened pressure within
the cardiac cavities due to one of two things--increased volume of
blood to be moved or difficulty in propelling the normal volume, caused
by obstruction to the flow either central or peripheral.
Pericardial adhesions may impede the action of the heart, and either
directly cause hypertrophy or induce dilatation and a consequent
hypertrophy.
The details regarding the etiology are best considered in a study of
hypertrophy as it affects the individual chambers.
Left Ventricle.--This chamber is much more frequently affected than any
other, and may be involved alone or as part of a general enlargement of
the organ. The more important causes are as follows:
(1) Aortic Stenosis.--To send the normal charge of blood through a
narrowed orifice the muscle must contract with increased force, and to
accomplish the work the walls increase in thickness. There may be
simple hypertrophy without dilatation of the chamber, but in the later
stages this inevitably supervenes.
(2) Aortic Regurgitation.--Curling and foreshortening of the aortic
cusps permits of a backward flow into the ventricle during its
diastole, with the production of dilatation and increased pressure, to
overcome which the walls thicken--eccentric hypertrophy. This is one of
the most common causes, and leads to enormous enlargement of the heart.
(3) Mitral Insufficiency.--In extreme grades of mitral stenosis the
left ventricle is usually small, but when the curtains are curled and
the patent auriculo-ventricular orifice large, there may be very great
hypertrophy. Free regurgitation is always accompanied by considerable
eccentric hypertrophy, due to the distension of the chamber by the
extra quantity of blood forced in at each auricular systole.
(4) Pericardial adhesions, particularly when in addition to union of
the layers the parietal membrane is firmly united to the pleura or to
the sternum, may cause hypertrophy of the left ventricle alone, but
more commonly of the whole heart.
(5) Abnormal Conditions of the Aorta.--_(a)_ Atheroma, with or without
dilatation of the arch, is a cause of hypertrophy, for the heart has to
{621} compensate for the loss of arterial elasticity, an important
factor in the onward movement of the blood during the diastole; and,
again, there is increased resistance in the wider tube. _(b)_ Great
narrowing, as in the congenital coarctation just beyond the ductus
arteriosus, which may produce colossal hypertrophy. Pressure upon the
large vessels in the thorax by tumors may act in the same way. _(c)_
Aneurism of the aorta is not often accompanied by hypertrophy unless
the valves are affected. Theoretically, it might be expected, as a
large saccular dilatation would certainly appear to be a cause of
increased resistance, but in uncomplicated cases the experience of most
observers appears to accord with that of Stokes,[42] who states that we
usually find a small heart. Occasionally, however, there is marked
hypertrophy even without valvular disease.
[Footnote 42: _Loc. cit._]
(6) Kidney disease, acute and chronic, is very frequently accompanied
with hypertrophy of the left ventricle. Indeed, simple hypertrophy is
more often met with in chronic Bright's disease than under any other
conditions. Increased blood-pressure in the smaller arteries throughout
the body is now very generally acknowledged to be the immediate cause.
But how this is brought about is a question not yet satisfactorily
determined.
We have to deal with two sets of cases. There is the cardiac
hypertrophy accompanying acute or subacute nephritis, particularly the
scarlatinal. Here there are no chronic arterial changes, and the
increased arterial tension appears to be due to contraction of the
smaller arteries under the influence of retained excreta, which may act
through the vaso-motor centre, as Ludwig observes, or possibly directly
upon the unstriped fibres of the tunica media of the arteries. Bright's
original explanation still holds good, I think, when he says that the
altered quality of the blood "so affects the minute and capillary
circulation as to render greater action necessary to send the blood
through the distant subdivisions of the vascular system."[43]
[Footnote 43: _Guy's Hospital Reports_, 1836.]
The hypertrophy of the left ventricle in connection with contracted
kidneys is more frequent and more marked. Traube suggested[44] that the
interference with the local circulation in the kidneys by the
obliteration of vessels increased the work of the heart and induced the
hypertrophy, but it is much more probable that the change is a
widespread one throughout the body. Gull and Sutton hold[45] that in
these cases there is a condition of arterio-capillary fibrosis in which
the small arteries are thickened and their calibre diminished, leading
in time to a more or less widespread sclerosis in various organs,
particularly the kidneys. As a result of this fibrosis, the movement of
blood in the smaller vessels is much impeded, the arterial tension
increased, and the work of the heart greatly augmented. On the other
hand, George Johnson[46] maintains that the muscular coat of the
arterioles becomes thickened under the influence of retained excreta,
and they are in a state of spasm which increases the tension and
heightens the blood-pressure in the left ventricle.
[Footnote 44: _Gesammelte Beiträge_, Bd. ii.]
[Footnote 45: _Medico-Chirurgical Transactions_, lv., 1872.]
[Footnote 46: _Ibid._, vol. xxxiii.]
The question can scarcely be considered settled as regards details, but
the general fact of increased peripheral resistance is well
established, and it is one of the most frequent causes of non-valvular
hypertrophy. It may be quite marked in persons without positive
evidence of renal disease as indicated by albumen or casts in the
urine, but in whom the condition of arterio-capillary fibrosis is
evident from the thickened state of the small arteries, the increased
tension, and the firm dislocated impulse of the heart.