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NOTES UPON CARDIAC HYPERTROPHY.

BY \

.1. G^ADAMf. :ir.A., M.D.,

ProfesEor of Pathology, MoQili University, Montreal, and Pathologist to the Royal

Victoria Hospital.

{Reprinted from the Montreal Medical Journal, May, 1895.)

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NOTES UPON CARDIAC HYPERTROPHY.

J. G. AuAMi, M.A., M.D.,

Professor of Pathology in McGill University, Mflntreul, and Pathologist to the Royal

Victoria Hospital.

I shall, I think, best satisfy you, and at the same time
myself, if what I contribute to this evening's discussion
takes the form of a series of notes upon the experimental
pathology and the anatomy of cardiac hypertrophy, rather
than that of an academic survey of the subject from the
clinical standpoint. Frequently, it is true, I must of neces-
sity illustrate what I have to say by reference to clinical
history, hut, on the whole, I shall leave the clinical aspects
to be dealt with by those more capable.

In the first place, if we study the causes of hypertrophied
heart, whether of hypertrophy of one or both sides, we see
this that reading the clinical history of these cases the
assigned causes of hypertrophy may be summed up under
the heading of increased work This one heading may be
subdivided into three, increased work due to resistance
from within, increased work due to resistance from without,
increased work due to nervous stimulation and augmentor
action. I shall not discuss this last subdivision, because
frankly we are ignorant how far the hypertrophy that
occurs in exophthalmic goitre and allied conditions is due
to heightened blood pressure, and how far it is secondary
to excitation of the accelerators or ausfmentors.

Of the increased resistance from within, or increased
tension, the main causes are, heightened pressure in the
arterial blood stream, and secondly, obstruction to the
onward passage of blood within the heart itself, by stenotic
diseases of one or other orifice. Of resistance from with-
out, the one great cause is pericardial adhesion. To-night
we have, as far as possible, to leave out the subject of
valvular disturbance, and I shall neglect nervous disturb-

ances. There is still the large field of hypertrophy due
to increased arterial pressure, and the pericardial adhesion.
In all these cases, the individual fibres of the heart muscles
of the aft'ected regions have to contract under increased
difficulty, they have to carry or contract against a greater
load, and as a result of this, just as is the case with the
skeletal muscles, with the muscles in the blacksmith's arm,
and the muscles of [the body in the all-round athlete, in-
creased work brings about increased growth — brings about,
that is to say, hypertrophy of the muscle.

• Into the subject of the nature of this increased growth I
shall enter in a few minutes' time, at present I wish to
carry a word further this parallel between the behaviour
of the cardiac and skeletal muscles, under circumstances in
which the load is increased. If you take a skeletal muscle,
for example, the gastrocnemius of the frog, so dear to the
physiologist, and observe its contraction with gradually in-
creasing loads, there are two points especially to be made
out. In the first place the greatest amount of work is not
performed with the smallest load, but there is a certain
medium load with which the distance through which the
load is pulled multiplied by the weight of the load gives
the biggest result. This product of weight moved and the
distance through which it is moved is the work done by
the muscle. The most work, therefore, is done with a
medium load. The second point is that with increasing
weights fastened or brought to bear upon the muscle, that
muscle in its resting state becomes more and more elongated,
and with regularly increasing weights attached the shorten-
ing attained by the contracted nmscle constantly diminishes.
Or, to put the matter in a slightly different light, and to
combine these two statements of fact, although with a cer-
tain medium load the greatest amount of work is done,
nevertheless with that medium load the muscle in contract-
ing does not attain to the same amount of shortening as it
does with a lesser load.

Let me now apply these observations to what is found
in the ventiicular muscles of mammals. Experimentally

the amount of work performed by the ventricles of the
mammalian heart can be increased by ligaturing the aorta
with a sliploop ligature, and drawing this ligature more
or less tight, according to need. [This in an animal that
has been narcotised and curarised and subjected to artificial
respiration, the heart l)eing exposed by making a window
in the ribs.] In such a case as this, as shown by Professor
Roy and me,* the behaviour of the cardiac muscle can be
observed and recorded by an apparatus, of which I give a
rough diagram. (See Fig. 1.) The ends of this apparatus
are attached to the surface, say of the left ventricle, by fine
threads, and ncnv it is possible to observe upon the record-
ing rlrum the extent of contraction of the portion of muscle
between the two points under different pressures within
the heart. Narrow the aorta by drawing the ligature
tight and the pressure is increased. Under these condi-
tions it is found that the ventricular muscle reacts exactly
along the same lines as does the gastrocnemius of the frog.

Similar results are obtainable if, instead of increasing the
pressure in the arterial system by narrowing the aorta, we
increase the work of the heart by increasing the amount
of blood passing through it, either temporarily, by pressure
upon the abdomen, vyhereby a large quantity of blood is
expelled from the abdominal viscera, or by injecting into
venous circulation some few hundred cubic c . timetres of
defibrinated blood. The results in all these . . .es are the
same. By the instrument just described it is easy to see
that the heart is more filled in diastole, so that the two
ends of the levers are pushed further apart, and that in
systole the ends do not approximate so nearly as in the
condition when there is less resistance or less blood pouring
through the organ.

It is seen from these observations that with increased
pressure within the ventricle the wall expands in diastole.
There is dilatation of the heart. But with the increased
loid to contract against the fibres do not shorten to the

•JIuirt beat anil iuI.sl' wave. /Voc<tttoner, February, 1894, p. 81.

ir .

same extent ; that is to aay, with increased work of the
heart there is, necessarily, accompanying tlie dilatation in
diastole, a dilation in systole. All the blood is not ex-
pelled in systole. There is of necessity reaidunl Mood, as
Roy and I termed it, in the ventricular chambers.
There is a general belief that the healthy heart, even

Fig. ].— Myocardiocrraph for mammalian heart shown semi-diagrammatioally. The
light vertical rod a, which for convenience of space is shown shortened in the
figure, is slung from the pivots which are represented in section as seen from
above B. This arrangement allows the rod u to swing freely, the centre of rotation
being the small hole at b (in B) The lower end. c, of this rod is fixed to the sur-
face of the heart-wall as seen in the figure. To obtain tracings of the heart- wall,
the small hook d is inserted in the visceral pericardium at a convenient distance
from the end of the rod a. To this hook ia attached a strong silken thread, «, which
after passing round the light grooved pulley f is conveyed upwards through the
small bole b to the lever g, beiof kept taut by the fine rubber thread h.

under conditions of increased work, contracts completely,
so that the chamber ia emptied at the end of systole. From
what I have said it will be seen that this is not the case.
One can go further and prove for one's self that even under
(H'dinary conditions the mammalian heart does not com-
pletely expel all the blood within the ventricles. By
taking a dog that has been curarised and subjected to arti-
ficial respiration, opening the chest wall, making an in-
cision at the very apex of the left ventricle, so as just not
to completely enter the cavity, then it is easy to push the
little finger into the cavity through the thin apex without
the loss of a drop of blood. The heart action is not re-
cognisably disturbed by this procedure, and it can be felt
that while the walls of the ventricle in the lower two-thirds
up to the apices of the papillary muscles, close completely
round the finger, there is a clear space in the upper third
which is not and cannot be emptied of blood.

Although it may seem at first sight to have no direct
bearing upon the subject of this evening's discussion,
nevertheless it is worth while to make a few remarks upon
this subject, inasmuch as it ia so intimately associated with
conditions of hypertrophy without valvular disease. It is
quite possible that where there is increased work to be per-
formed by the heart, there is some economy of the action
of the organ when there exists a certain Amount of residual
blood, in and dilatation of the ventricles. Taking the ven-
tricular chamber as a sphere,* there is this to be noted
concerning the relationship between the circumference of
the sphere and its contents, namely, that as a sphere ex-
pands its cubic contents increase out of all proportion, I
was going to say, to increase in circumference, or more
truly, the ratio between increase in cubic contents and in-
crease in circumference is by no means an arithmetic ratio.

If the circumferences be taken as abscissae, and the cor-
responding volumes as the ordinates, the curve of succesive

* I'liP^phere *» the nearest geometrieal figure that can be employed here for pui-

poscs of illustration.

values is what is known to mathematicians as a cubical
paraltola. From this it follows that a dej^ree of shortening of

Fig, % •

Curve reiiTesentinK the relationship between the circumference of a sphere and ist
volume, with successive unit increments of oircumferenoet
Ordinates — volume in cubic inches.
' AbBoisxc = circumferenoe in inches,

the fibres of the heart wall sufficient, let us say, to reduce the
circumference of the ventricle onc^ inch, will cause a greater
(liuiiiuition in volume (a greater output) the more dilated
the ventricle is at the beginning of its contraction. For
example, a diminution of the circumference hy one inch of
a sphere whose circumference is ten inches causes a diminu-
tion of th(! volume or an output, in the case of the heart,
efpiul i6 Jf.5 cuhic inches, while a diminution by one inch
in the circumference of a sphere //ye inches round causes a
diminution or an output of only 1.027 cubic inches, although
in the first case the circumference was reduced only by
(me-t(^nth, while in the other case it was reduced by (me-
fifth. That is to say, if we have a dilated heart the fibres
will need to contract a very small amount, in order to
expel a given amount of blood, compared with the amount
they would have to contract in the normal undilated heart.

There are other factors to be taken into account, it is
true, and Roy and I went a little into this sulyect in our
paper published in the Philosophical Transactions* All
that I wish to do here is to point out that it is possible that
in a hard-working heart a certain amount of dilatation)
with presence of residual blood, by diminishing the extent
which each fibre is called upon to contract, may really be
an economy 'to the organ as a whole.

It follows from these observations that hypertrophy is
never primary, dilatation always precedes hypertrophy.
This was recognized as most probable by Hilton Fagge ;
few other writers have laid stress upon the point. If, how-
ever, the heart muscle is well nouri.shed, where this dilata-
tion is due to increased work, by Paget's law hypertrophy
ensues, and the numerical hypertrophy or hyperplasia of
the ventricular muscle fibre will have the effect of lessen-
ing the load of each individual fibre. Consequently, with
a lessened load, each fibre will contract more completely
and the dilatation will tend to disappear. Where this is
the case we have what is known as simple hypertrophy.

* Phil, Trans, of the Royal Society, London, 1892.

There can be no doubt that in the early stages, where
ample reserve force and good compensation are present,
this simple hypertrophy exists and may persist for years.
But I would add that in the post-mortem room it is more
rarely to l)e seen than is generally accepted. If a liyper-
trophied heart, say of Bright's disease, without valvular
lesion, be examined within a few hours after death, in very
many cases we appear to have this simple hypertrophy.
If, however, time be given for the rigour and contraction
of the muscle to pass off it is found — that at least is my
experience — that the cavity of the left ventricle is dis-
tinctly larger than the cavity of the normal heart. I
would say that only in those cases in which death has
occurred from some intercurrent disease, and not from one
of the cycle of diseases associated with cardiac hyper-
trophy — only when death occurs before the final stage of
' the disease of which cardiac hypertrophy is an integral
part — do we obtain evidence of real simple hypertrophy.
Eccentric, and not simple, hypertrophy is the rule ; that is
to say, hypertrophy associated with definite dilatation of
the ventricular cavities.

As for the concentric hypertrophy, which is said to be
observable in non-valvular disease, I feel more and more
assured that it is falsely so termed ; there is no such thing
. as true concentric hypertrophy, for the condition implies a
Jack of economy in the work of the organ, a most un-
natural lack ; it implies that the ventrical in contracting
expends a large part of its energy, after expelling the
blood, in squeezing up the more internal fibres. Only
within the last fortnight I obtained a specimen of so-called
concentric hypertrophy. The patient, an old woman of
eighty, in Dr. Stewart's ward at the Royal Victoria Hos-
pital, died from cerebral apoplexy, following upon extreme
atheroma of the aorta and the main vessels ; there was, in
addition, atheromatous stenosis of the aortic valves, both
conditions favouring the development of hypertrophy, with
dilatation of the left ventricle, ... ,. :

The old woman had lingered some days in a comatose
condition, with presumable lowering of the arterial blood
pressure. In addition the tone of ventricular muscle had
been in all probability considerably increased by digitalis.
At any rate, at the autopsy a very few hours after death
the left ventricle was found hypertrophied, and instead of
being dilated was so firmly contracted that the only cavity
left was immediately around the chordae tendineas. The
thickness of the ventricular muscle at the junction of the
lower and middle thirds was 20 mm.; that is to say, there
was moderate hypertrophy. However, on coming to
observe this heart the next day, the concentric hyper-
trophy had quite disappeared. With the passing off" of
rigidity there was a relatively large cavity left behind.

Where the left or right ventricle alone is affected the con-
dition of the ventricle may be one of either simple or eccen-
tric hypertrophy. Where, on the other hand, as Walshe noted
more than thirty years ago, there is general hypertrophy
of the organ, there hypertrophy is always eccentric.

A little consideration shows why this must inevitably be
the case. So long as there is simple hypertrophy (hyper-
trophy without dilatation), so long the mitral valves re-
main competent, and there is no regurgitation into the left
auricle, no increased work for that organ to do, no hyper-
trophy. So soon i*s the left ventricular muscle begins to
fail and to be unable to contract properly under its load,
dilatation ensues, and with this dilatation expansion or
giving way of the muscular ring around the mitral orifice,
and with this, relative incompetence of that orifice. It is
only when this relative incompetence occurs, or when from
other causes the mitral valves fail to perform their duty,
that there is any possibility of the other chambers of the
heart being called upon to do increased work. Thus it is
that general hypertrophy of the heart demands or is asso-
ciated with eccentric hypertrophy of the left ventricle.

Time forbids that I should go more fully into this sub-
ject or do more than point out that relative incompetence

of the auriculo-ventricular valves is more frequently found
at the post-mortem than it is diagnosed during life. Rela-
tive incompetence, therefore, is not necessarily indicated by
the presence of a murmur.

I cannot here enter fully into the histological nature of
hypertrophy, although perhaps as a pathologist it might bo
expected that I should say some words upon this point. I
will only say that while one can, in certain cases of hyper-
trophy, make out clearly that the individual fibres have
undergone a definite increase in size, it is far more common
to note, and of this there can be no doubt, that there has
been an actual numerical increase in the fibres. This in-
crease appears to be general throughout the ventricular
wall and is possibly, nay probably, due not only to a new
growth beneath the endocardium especially, but also to a
splitting up or division of pre-existing fibres. It must be
remembered that the heart muscle fibre is not a single cell,
but is a compound, the result of a fusion of several cells
into one individual unit. As a consequence of this it is
possibly more easy for the fibres to split up into inde-
pendent territories without undergoing temporary derange-
ment of function than is the case with the cells of those
tissues formed of isolated cell units.

To pass on now to certain aspects of this subject of
hypertrophy more immediately in connection wath this
evening's discussion, I would point out that of the cases of
hypertrophy without valvular lesion, we have to consider
in the first place increased resistance through the column
of blood. This could be brought about by increased
amount of blood to be propelled, or, in the second, by in-
creased resistance to passage in the arterial system. Of
these two the first may exist as a constitutional condition,
but the more one studies the less assured does one become
that there is such a condition as general plethora unless
these case be regarded as true plethora in which (as in
German beer drinkers) there is oft repeated flushing of
the circulation with imbibed fluid. Of increased resist-

unce in the arterial stream the reverse would appear
to be the case, and with further studies of blood pres-
sure in the arteries one begins to see that this plays an
extremely important part. The hypertrophy following
upon not only gouty conditions and senile artero-sclerosis,
but also upon acute rheumatism, chorea and chlorosis may
be present with or without lesion of the aortic or mitral
valves of sufficient intensity to explain its extent ; so that
in all these cases we have to fall back upon increased blood
pressure as a cause of hypertrophy.

Increased blood pressure in itself is capable of setting up
a vicious circle of which one segment may be hypertrophy.

In the first place it leads to an increased nutrition of
the walls of the arteries, increased nutrition leads to in-
creased connective tissue growth of the walls, the increased
fibrous tissue of the walls leads to contraction and in-
creased rigidity of those walls, the increased rigidity leads
to increased resistance to the passage of the blood current,,
the increased resistance required increased propulsive
power on the part of the ventricular muscle, that is to say,
increased work ; the increased work of the heart leads to
overgrowth and hypertrophy, and with this, heightened
blood pressure and further increased nutrition of the walls.
And now at last the stage is reached, this vicious circle con-
tinuing, in which either the walls give way or the heart.

The longer I study the pathology of the circulation — and
during the last eight years I have given more time and
thought to this than to any other branch of my subject —
the more assured do I feel that increased blood pressure
alone (however it be primarily brought about) is sufficient
to explain the anatomical changes so constantly seen in
arteries, valves and heart walls, without of necessity call-
ing in chronic inflammation or specific agency. The changes
I refer to are arterio-sclerosis, atheroma, and general fibroid
thickening of the valves. Perhaps here again I am diverg-
ing from the main subject of this evening's discussion, but
I say this as a connecting link with what I have just re-
uiarked and with what is about to follow.

While I am far from wishing to indicate that this is to
be regarded as the sole cause of atheromatous and arterio-
sclerotic changes, I hold that the changes I have mentioned
can one and all he explained by the increased pressure
within the vessels leading to an increased passage of fluid
from the blood into the sub-endothelial layers of the intima,
to an increased nutrition, and as a cohsequence to a pro-
liferation of connective tissue in this region, which in itself
as it contracts cuts off its own supply of nutrition, de-
generates, and what is more, leads to degeneration of sur-
rounding parts by cutting off their nutrition. The evil
effects in arterio-sclerosis, with all its combined lesions, are
not necessarily of an inflammatory origin.

Let us take now the hypertrophied heart. Time per-
mits me to refer but briefly to the anatomical changes that
may occur in it in the cases before us.

1. The overgrowth of the arterial walls may be asso-
ciated with an increased tendency to the development of
fibrous tissue in the immediate neighbourhood of the
arteries, and thus a condition of so-called interstitial myo-
carditis may be set up ; or

2. With an increased fibrosis of the arteries the narrow-
ing of the channel may lead to incomplete nutrition of the
territory supplied by each arterial twig, and as a conse-
quence the muscle fibres at the periphery of the territory
may be atrophied through lack of nutrition and be replaced
by fibrous tissue. This is the so-called dystrophic sclerosis
of the French school, and can frequently be seen more espe-
cially in the papillary muscles.

3. With the arterial disturbance there may be actual
blocking of the atheromatous arteries, and so infarctous
areas may originate, may undergo softening, may cause
rupture of the heart or aneurism of the wall, or if the
period of softening be successfully tided over, the replace-
ment of the necrosed tissue leads to cicatricial development
and disturbance of the normal contraction. ' ^

All these cases here mentioned inevitably cause interrup-

tion to the proper action of the remaining fibres and lead
towards a final failure of the ortran.

Another set of causes would seem to act alono- rather
difl'erent lines, riot so much of disturbances in the coronary
arteries as disturbance in the quality of the nutrition,
whereby the heart muscle tends to undergo fatty degenera-
tion. In the uncomplicated case of hypertrophy, without
valvular lesion, however, this fatty degeneration is rare ;
more frequent, according to the observations of Renaud,
Browicz and Von Recklinghausen, there is a tendency for
a sudden rupture of the heart fibres, from segmentation or
fragmentation. It would seem as though, from the \ei'y
careful observations of the last two, the weakened condi-
tion of the muscles permits some slight increase in the
work done by the organ to bring about, not a local rupture,
but a generalized separation of the fibres.

Possibly this segmentation may explain the suddenness
of many cases of death in those with atrophied and dilated
hearts. For my own part I cannot as yet see that it has
been proved with absolute satisfaction that the fragmenta-
tion of the fibres is agonal or pre-agonal. Nor, looking
back, does it seem to me that the most strongly marked
cases that I have encountered of this fragmentation have
been in cases of sudden death.

Lastly, to round off* this paper, it is necessary to say a
word concerning the hypertrophy that follows pericardial
adhesion. Of this I may say that I cannot recall any case
seen by me in which the hypertrophy was not markedly
eccentric. Most frequently the hypertrophy has disap-
peared with, in its place, peculiarly extensive degenerative
change.