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The primary fibres are occasionally almost homogeneous in appear-
ance. Alongside of fibres much atrophied or degenerated there may
be others relatively healthy.

In chronic fatty degeneration of the heart muscle, especially if it is at


all advanced as to its stage, the color of the muscle is notably pale and
yellow in places. Sometimes, however, where the changes are not so
far advanced, at least in spots, but more generally disseminated, the
heart muscle, particularly of the ventricles where the degeneration is
most pronounced, is less changed in color from the normal. However,
in these instances the muscle has lost its consistence, is very flabby,
and the heart flattens out and loses somewhat its healthy outline on
the table ; beside it has lost resistance and is easily torn and lacerated.
Under the microscope the diseased fibres may show very numerous
granules, or at an ulterior stage these granules may be replaced by many
glistening, shiny, very refringent round bodies of large calibre, which
evidently are oily or fatty. Here, again, the nucleus of the muscle may
or may not have become degenerated or have disappeared entirely.
The same is true of the lateral strise and the longitudinal fibrillations.

There may sometimes be an overgrowth of pigment granules. These
granules may be deposited in the muscular fibre itself or in the inter-
stitial connective tissue between the fibres. The pigmentary granules
may be more or less irregularly placed. Usually there are a larger
number near the muscle nucleus. Occasionally the whole fibre may
be larger than normal and appear almost entirely homogeneous.

Alongside of some fibres completely degenerated there are others which
are relatively healthy or diseased only in parts. The connective tissue
between the fibres in typical fatty degeneration of the muscle is usually
not much, if at all, increased in quantity. In other cases, especially
where there are fibroid changes throughout the vascular system and in
different viscera, there may be a considerable increase of interstitial
connective tissue and pronounced fatty degeneration.

For further and more complete and accurate knowledge of the
pathology of these cases I would direct my readers to the best modern
treatises on cardiac disorders, among which that of Gibson seems to
me particularly valuable. To this author I feel especially indebted
for much valuable knowledge, which I have not hesitated to utilize
and to whom I now give full credit.


Angina pectoris, in its typical form, is in my experience a very
rare disease. Pseudo-angina, or what resembles it at times, cardiac
asthma, is not infrequent. Although angina pectoris is described
among the neuroses of the heart by authors, this view in my judgment
is frequently erroneous. In the great majority of instances where
angina is present there exist also organic changes of the coronary cir-
culation, of the cardiac muscular fibres, or a lesion of the aortic orifices.

I should be loath to admit, except in a very exceptional way, the
existence of true angina purely of neurotic origin. On the other hand,
pseudo-angina is very frequently of this provenance, accompanied by
symptoms of flatulent dyspepsia. It must be understood, however,
that there are cases on the border-line in which, during life, we have
great difficulty in pronouncing as to what symptoms are of nervous
origin and what are clearly due to organic changes of the heart or

In many such instances, unfortunately, even if death occurs, we are
uot always able to obtain verification of clinical facts by the results of
an autopsy. Hence, certain theories are brought to the front which
have no basis in actual, reliable observations from the dead-house.

One statement is certainly true of angina, viz. : that it has usually
connected with it an element of spasm or sudden intracardiac pressure
which separates it notably from conditions which, in many ways, are
similar, and yet from this stand-point differ manifestly in a greater or
less degree. Of the truth of this statement we shall be convinced later.

In general, it may be stated that pain, properly speaking, does not
characterize organic disease of the heart as we commonly meet it. Of
course, there may be more or less prsecordial anxiety or oppression, or
there may be pain in the vicinity which is of stomachal or hepatic
origin; but acute cardiac pain is very rare. For this reason it has
become almost an axiom for clinicians to say when acute cardiac pain is
complained of, it is more than likely no organic disease of the heart is
present. Perhaps this affirmation is too positive or dogmatic, since I
am confident functional distress may occur which is dependent upon
obvious tissue changes.

In true angina the pain is very characteristic, and as I have said,
ordinarily means organic changes of the heart structure. First of all,


the pain of angina is marked by its great intensity. In no other dis-
ease, perhaps, is this so true. When the anginoid attack occurs, if the
patient is walking or exercising in any way, he stops immediately and
holds himself as quiet as possible, only taking hold almost involun-
tarily at times, so great is his distress, of the nearest object which will
give him support. Otherwise, he may merely stand rigidly, having
come to a short stop, with his arms lying unconsciously by his side, or
else one hand is pressed firmly in the precordial region, as if to
ameliorate in a measure the subjective agony by so doing. During the
attack the pectoral and other muscles of respiration scarcely move, and,
indeed, breathing comes almost to a stand-still for a while. In this
we perceive at once the great dissimilarity with an attack of cardiac
asthma, in which the efforts to breathe are so forcible and striking.
And yet there are numerous instances in which the cardiac asthmatic
features are most notable and where the "angina sine dolore" of
Gairdner is also present, 1 as Osier states, after a masterly summary of
the differential diagnosis of these two states, " when we recall to mind
the features of the attack in cardiac asthma and in certain anginal
seizures, the similarity of the condition, as Huchard remarks, to an
acute emphysema, the views of Von Basch 2 appear to possess at least a
reasonable probability " (p. 85).

The locality of the pain in angina is not always the same. Fre-
quently it is located over the precordial region. At times, however, it
may be situated in the upper portion of the chest, or again, but in rela-
tively few instances, it may stretch like a heavy bar across the xiphoid
cartilage and the adjacent structures. Under these circumstances the
pain may radiate directly through the chest and be felt even in the
back. The pain has been likened to a heavy weight or crushing
pressure, as though the thoracic parietes must almost meet. The pain
is also said to resemble that of some terrible griping, as though the heart
were held firmly in the clutch of some terrible monster. All these sen-
sations, and numerous others, have been described and dwelt upon by
writers, who doubtless have used their imagination at times to supply the
descriptive powers of the patient. Suffice it to add that the pain is of
a frightful sort and quite unlike any other we are familiar with. Often
the radiation of the pain is toward the left arm, and in that case is
usually carried through the forearm also and to the fingers. The ring
and little fingers are said to be usually affected. Very rarely the pain
extends to the right arm. When it does it radiates likewise in one or
other direction mentioned.

According to Broadbent, the pain of angina often originates in the

1 Osier. Angina Pectoris and Allied States, p. 82.

* These are : " Cardiac dyspnoea follows swelling and diminished elasticity in the lungs."


left wrist, and from there travels upward through the left arm and
toward the chest вАФ or again, as Osier states, although originating in the
chest, 1 " was felt very severely about both wrists." This must be an
extremely rare expression of the pain. I have never met it, nor do I
find it mentioned by others. It is clear that the relations of brachial
symptoms 2 (neuralgia) to angina pectoris are various. Sometimes,
though infrequently, there are no pains in the arms, even in quite severe
attacks of angina. Again, the brachial symptoms are very prominent,
begin the attack of angina, and last longer than it does. The fact is,
however, that the description of pain and its radiation, especially
where it has the remarkable intensity of that belonging peculiarly to
angina, must be somewhat inaccurate at times. In any event, it could
only be obtained after the attack has passed, and I am inclined to
believe that only exceptionally the patient could give any graphic and
truthful description of it. What is literally true is that the patient
has the impression vividly marked of impending dissolution, and it is
this sense, together with the character, site, and evident intensity of the
pain, which are almost pathognomonic of angina.

I know of few things more remarkable in descriptive medicine than
the account given in the life of Dwight L. Moody by his son, of the
anginoid attack near the close of the life of the great evangelist. In
this case there was no terror or mental distress, as I believe, because his
faith and works fixed him, as it were, on a rock. But in very many
instances there is unquestionably great terror and mental distress.
This is pictured often in the countenance which has that gray, ghastly,
drawn look which once seen leaves an indelible impression upon the
observers who may be near. The different radiations of the pain in
angina are, no doubt, reasonably explained by the position of the car-
diac plexus. The site of this plexus near the heart would serve to
strengthen this view. In addition, we have its divisions and communi-
cations which appear to justify this interpretation.

According to one eminent observer, the pain originates probably in
the central nervous system. This writer also explains its radiation and
extension by affirming that it proceeds from the spinal cord. One
thing is pretty certain, if we may judge by the few thorough observations
we have recorded of these cases, and it is that there is no pressure out-
side of the heart on the plexus from any form of aneurism or other
kind of tumor. While the heart may or may not be enlarged accord-
ing to circumstances, this enlargement, even though present, does not
explain rationally the anginoid symptoms.

Cardiac hypertrophy and cardiac dilatation are very frequently met

1 "Angina Pectoris and Allied States," p. 42.
1 Boston Med. and Surg. Journ., March 14, ]901, pp. 256, 257.


with, and yet in the vast majority of these cases there are no anginoid
symptoms, properly speaking. Leaving aside these instances, there are
a few where the heart is seemingly of normal size and volume, and we
must, therefore, seek an explanation of anginoid pains in some other
direction. Even in acute cardiac dilatation, no intense pain is felt,
and yet we should have in just such cases pressure on or distention of
nervous fibres under the endocardium. Moreover, this pressure or dis-
tention must be very much greater in patients thus affected than in
those suffering with angina where no similar condition exists. During
the attack the patient is usually very pale, and the pallor has a certain
gray, ashy hue which is indicative of the serious condition which occa-
sions it. Together with this pallor there is extreme weakness, and a
faint feeling, which cannot be resisted, overwhelms the individual wha
is attacked. The pulse shows by its character, oftentimes upon what
this weakness in part depends. It is frequently small, feeble, irregular,
as though the poorly acting heart could not send the blood to the
extremities. Again, singular' to say, it is almost unchanged, at least so
far as we can appreciate by our tactile sensations. In the former
instance, it is probable that there is present a spasmodic contraction of
the peripheral arteries; in the latter, we must assume that no' such
spasm exists, or, indeed, that arterial changes are so advanced that no
marked impression is made upon their contractibility even by the most
intense pain and disturbance of the central organ of circulation.

Frequently an attack of angina terminates by the sudden explosion of
gas from the stomach. Hence it is often stated and familiarly accepted
that flatulent dyspepsia is an immediate and efficient cause of a true
attack of angina. In my experience this is scarcely true, and I am
more inclined to the belief that it is especially in cases of pseudo-angina,
that we should expect to find symptoms of stomachal weakness or
intolerance. While admitting this, we should also not completely
ignore the fact that the stomachal conditions which occasion flatulence
may at times appear to be of considerable importance, taken with other
exciting factors, in bringing on an attack. There may be, as Broad-
bent points out, a certain sympathetic relationship between the terminal
fibres of the vagi in the stomach and those in the heart. Many facts
would serve to demonstrate this possibility. Certainly, even in cases of
marked cardiac weakness, where there has never been a true anginoid
attack, dyspepsia of an acute and very distressing type will frequently
follow undue fatigue of any sort or any severe shock to the nervous
system such as distressing or alarming news may readily excite.

A phenomenon which is somewhat curious is the fact of an intense
desire to urinate during the period of an attack, even though the effort
is vain, simply because the bladder is frequently entirely empty.
This statement may not invariably be true. I have known many a


time emotional excitement to prevent absolutely for a while the con-
tractile power of the bladder being exerted, and where, as was proven
later, the bladder contained a considerable quantity of urine. It
requires a very slight degree of annoyance or mental disturbance in
men past middle life to prevent frequently their power to void their
urine. Of course, the contrary of this is true, especially among women
of a neurotic type, and who are still relatively young. The quality of
urine of low specific gravity passed by them at times, in a very brief
period, is often very great. In the differential diagnosis of true angina
with pseudo-angina this point should be borne in mind. During the
attack where it is severe, perspiration will flow almost constantly from
the patient. His face and neck and hands may be covered with it. It
is cold and clammy, and lends additional significance to the gravity of
the other symptoms.

The time during which an attack lasts is very variable. Sometimes
it is over after a few seconds, although during this short period the
agony is fearful. Again, the attack is prolonged for several minutes.
Some authors state that the attack may occasionally last throughout an
entire night, and that during all this time the patient is unable to move
at all on account of the intense pain, and, moreover, is perspiring pro-
fusely the entire period. I must confess that I have never seen any
attack of this sort, and am inclined to consider them very infrequent.

It is highly probable, moreover, that in a case of true angina depend-
ing upon advanced degeneration of the coronary circulation, which
would probably be present under such circumstances, the intense pain
of anginoid character would terminate life more rapidly. Here, again,
I should be disposed to hold the view that a neurasthenic or hysterical
element was present, which gave strength and exactness to the true
diagnosis, viz., pseudo-angina.

It must be admitted, of course, that there are instances in which the
attacks are certainly anginoid in character, although they do not reach
their complete development. This fact may be explained by stating
that the patient, having suffered from attacks previously, so soon as he
fully appreciates that one is coming on simply stops still and avoids all
possible exertion until the attack has completely passed away. In these
examples there may be pain in the chest, but without radiations toward
the arms or fingers. Of course, if the pain is diminished in violence,
there is less dread attached to the seizures, and the patient does not
expect to die at any moment. Broadbent and others speak of anginoid
attacks sine dolore. In some instances the chief danger arises from a
syncopal attack in which a patient may suddenly expire. It may be
that these attacks had been originally painful, and it was only subse-
quently that they lost this characteristic feature entirely. I should
expect, in such an instance, to find at the autopsy either marked fatty


degeneration of the heart walls independent of coronary changes, or else
advanced aortic regurgitation. Wherever the coronary circulation is
suddenly obstructed with an embolus or thrombus, the breast pang
seems to be almost an invariable accompaniment. In those cases where
the attack has evidently been brought on by exposure or exertion, it
does not usually last long, and when the accidental occasion of the
attack has disappeared, the seizure itself is apt to dissipate itself rapidly.
Wherever the attack comes on spontaneously, as it were, without any
accidental efficient cause being evident, it is apt to last a longer time,
and only to pass away little by little and slowly. Occasionally these
attacks are the most alarming in reality, and herald a fatal termination
in the not distant future.

Among the causes which act efficiently in bringing on an attack of
angina are primarily exertion. We are apt to say over-exertion when
the attack has taken place. This over-exertion may be a brisk, rapid
walk, or the patient may be walking leisurely and without effort when
the seizure occurs. Usually, however, it is when a walk has been pro-
longed and there is already a feeling of fatigue that the angina is felt.
It has been noticed that whenever exertion takes place soon after a
meal an attack is more apt to occur. It may be because digestion, if
slow and torpid, is thus interfered with, and gases which are generated
and accumulate in the stomach press against the diaphragm and indi-
rectly against the heart, and thus, by causing some displacement of this
organ, may occasion notable interference with the circulation.

One reason, no doubt, why attacks occur at times during sleep, is

because flatus is prone to accumulate in the stomach and intestines

during sleep, and considering this together with the fact that in the

horizontal position we have more pressure of the abdominal viscera

upward, we realize readily conditions which are powerful in causing


The liability, under these circumstances, to an attack is increased

notably by a feeble circulation. Moreover, as we know, the circula-
tion is always less active in repose, and this state is what prevails
during sleep. A loaded rectum is, also, a condition to be avoided, and
anyone subject to constipation must see to it that the bowels are properly
evacuated. The distended bowel may perhaps act in a reflex manner,
as well as by direct pressure.

The influence of cold is sometimes very evident. This is particularly
true when a patient is walking against a cold wind. Nothing more is
required than this sometimes to precipitate an attack. On the other
hand, mild, warm weather is conducive to well-being, and sufferers
from angina will often escape attacks during long periods when the
weather is free from rapid changes and remains relatively balmy. It
is essential at night for a patient to see that the bed is. comfortably


warm and that no chilling of the surface ensues; otherwise, an attack
will often follow. This precaution may be readily attended to with a
hot-water bottle or heated bricks. Gentle friction of the surface of the
body, perhaps, before the patient retires, is also a proper precaution to
take. The wearing of long woollen stockings, and particularly those
which are somewhat loosely knit and allow free transpiration, is espe-
cially desirable, so as to keep the extremities suitably warm. I know
of no small detail so important as this in all affections in which the cir-
culation is notably impaired, and, of course, it becomes doubly impera-
tive in warding off painful attacks which are too frequently occasioned
by local chilling of the feet.

In view of the fact that dyspepsia is such a frequent symptom of
angina, and appears as an efficient cause, in the judgment of a few
writers, quite as often as an effect, it is important to avoid all late or
too abundant dinners. The food at this meal should be of the simplest
kind, and no overloading of the stomach should be permitted. In a
similar way, no sauces, condiments, or insufficiently cooked food should
be tolerated.

Whenever an attack has occurred, it behooves the patient to be more
than usually circumspect in all his doings, not to bring on another one.
This is especially true of any exertion which seemingly has been the
direct cause of an outbreak. And yet this counsel is sometimes almost
unnecessary, because the patient's own feebleness, which follows a pri-
mary attack, will compel him almost to walk very slowly and deliber-
ately, even if he walks at all, for some hours or days subsequently.
No doubt these anginoid attacks would not occur if the heart had suffi-
cient reserve force to respond adequately to the call made upon it.
Unfortunately, it has not, and it is therefore evident, in many instances,
that the attack is directly occasioned when we reach final causes, by the
manifest inability of the heart to respond to the call made upon it for
increased vigor.

Angina pectoris is not necessarily connected with any special lesion.
Practically, it is almost unknown to have either stenosis or incompe-
tence of the mitral valve appear as a direct, efficient cause of it. It is
true, however, when there have been several attacks of angina, it is
not infrequent to observe mitral incompetence arise subsequently. In
some of these instances it has been noted, where aortic incompetence
already existed, that this affection was ameliorated as regards its symp-
toms, and that the anginoid attacks also became less severe. The
explanation appears to be in the lessened blood pressure thus brought
about, as shown in the arterial pulse and in the diminished accentuation
of the aortic second sound. Musser 1 has insisted upon the importance

' Transactions of tbe Association of American Physicians, vol. x. p. 85.


of this finding, and has reported several examples in his own experience.
Broadbent 1 has also specially emphasized similar instances.

Angina is frequently connected with fibrous myocarditis, and at the
autopsy such organic change in the heart muscle is apt to be found.
So usual is this condition that Gibson states it is almost a surprise not
to find it. When fibrous myocarditis is noted, it is frequently accom-
panied with evidences of arterial degeneration. The coronary arteries
are usually implicated. Especially is this true where aortitis is present.
The lesion may be limited to their origin, which is sometimes narrowed
and thickened. The arteries may also be affected in a considerable
extent, and the organic changes may be considerably advanced. Occa-
sionally they have merely lost elasticity ; in more pronounced alteration
they may have become markedly atheromatous, or, indeed, calcified.

According to Douglas Powell, fatty degeneration of the heart walls
often exists. Sometimes, indeed, the heart is so much degenerated that
it is easily torn, and the finger sinks into it on slight pressure. Some-
times, to the naked eye, the fat exists only in patches, affecting merely
the papillary muscles or different areas of the ventricles. Even in these
instances, however, if we make use of the microscope, we are apt to find
considerable degeneration of the walls, where there has been no real
change of coloration. In a few instances the microscope shows almost
complete disappearance of the muscular fibres.

As a concurrent condition with fatty degeneration, we discover more
or less advanced changes of the coronary arteries, very similar to those
already mentioned in connection with fibrous myocarditis. These evi-
dences of fatty degeneration are particularly found, of course, where

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