upon them are a deposit of fibrin from the blood, the projections
acting as foreign bodies in the blood-current. The fibrinous deposits
occur chiefly on the surface which is opposed to the current of the
circulation, and sometimes they are distinctly conical; at others they
have the shape of a raspberry. They occupy the parts most exposed to
the friction of the blood, and are arranged on the borders of the
aortic valves at a little distance from their edges, the seat being
determined by the limit of the vascular network. The band of tissue
which passes from the attached border of the valve to the Arantian body
in the centre shows the inflammatory granulations most distinctly. They
consist of a cauliflower-like bulbous extremity, connected by a
constricted neck with a firm, hard base that is intimately blended with
the subjacent tissue. A thin hyaline layer covers each mass. At first
these granulations or vegetations are very small and numerous, so that
the membrane presents a granular appearance. Later, they become larger,
reaching oftentimes the size of a small pea.
Near the insertion of the tendons upon the auricular surface of the
mitral valve are found irregular wreaths of vegetations which enclose
the attachments of the chordæ tendineæ. Moxon has shown that the
friction of the vegetations or of fibrinous clots that gather upon the
vegetations may, by the irritation it produces, excite endocarditis at
points remote from the valves.
The tendon of the mitral valve may show the effects of endocarditis by
becoming soft and friable, and even rupturing, or the chordæ tendineæ
may adhere to one another. When such adhesions occur either with
agglutinations of the flaps to each other or to the heart-walls,
stenosis or regurgitation may result.
In connection with these changes new vessels are developed in the
substance of the mitral valve, or those that already exist become more
apparent. In the semilunar valves new vessels are formed or neighboring
capillaries send out prolongations into the parts destitute of vessels.
This, according to Charcot, is one way in which arborescent vascularity
occurs. These changes are most marked in those forms of exudative
endocarditis which run an acute course.
In some instances the hyperplasia is so extensive as to interfere with
nutrition, and may lead to fatty metamorphosis. A cavity is then formed
filled with granular fat-cells, discrete fat-globules, and
blood-pigment, whose endocardial covering ruptures, and the contents
are carried into remote capillaries to cause capillary embolism and
septicæmia. This has been called ulcerative endocarditis.
{642} Ulcerative Endocarditis.
Ulcerative endocarditis occurs in those diseases where there is great
vital depression. It is met with oftenest in pyæmia, puerperal fever,
scarlatina, and diphtheria. It has been called septic, diphtheritic,
and infectious endocarditis.[1]
[Footnote 1: Jaccoud, Klebs.]
MORBID ANATOMY.--Ulcers may form in endocarditis in either one of three
ways: 1st. The exudative process may be so rapid and extensive as to
cut off the nutrition of the endocardium covering the apices of the
papillary elevations, and ulcers result in non-septic inflammation. 2d.
Degeneration of the neoplastic tissue, due either to deficient
blood-supply or other causes of impaired nutrition, may so soften the
villi or efflorescences that their apices will be swept away by the
blood-current and ulcers thus be formed. Charcot especially insists
that the ulceration of these elevations is the consequence of granular
degeneration, and not of fatty metamorphosis, with which it is often
confounded. 3d. The exudative process may be purulent in character, and
form minute abscesses in the substance of the valves beneath the
endocardium, which, rupturing, leave comparatively deep ulcers. Acute
multiple abscesses in the aortic valves are of frequent occurrence in
ulcerative endocarditis.
The margins of the ulcers are irregular, but well defined; the edges
are swollen and thick, and their floor (the muscular substance of the
heart or the fibrous layer of the valve) is infiltrated with pus.
Where there is extensive loss of substance perforation of the valve may
occur. These perforations are sometimes closed or hidden by a fibrinous
exudation.
The soft and friable vegetations may be torn into long shreds by a
forcible blood-current, and subsequently may excite endocardial
inflammation where they come in contact with the walls of the
heart-cavity, or they may break off and form emboli. A fibrinous string
upon a flap of the aortic valve is not infrequently driven down and
back by a regurgitant current, so as to excite endocarditis in the
mitral valve.
Some observers state that micrococci and bacteria are found in
ulcerative endocarditis of a septic or diphtheritic origin, and they
have given to it the name of mycosis endocardii. It is probable that
these minute organisms are developed by the septic ulcerative process
rather than that they are the cause of such processes. They appear as
spheres, highly refractive, motionless, cohering in groups, without any
stroma. Acids, alkalies, ether, and chloroform have no effect on them,
so that they are not to be regarded as vegetable products.
The valvular ulcerations in this form of endocarditis give rise to the
most diverse lesions. Masses may be detached from the diseased cardiac
orifices, either from the fibrinous deposits on the valves or from
ulcerations of the valves themselves, and, having entered the
circulation, they will produce various symptoms in the organs and
tissues to which they are carried.
It is important to make a distinction between the results produced by
displacements into the blood-current of large masses and those arising
from the entrance of molecular fragments. It is also to be remembered
that the masses from the vegetations or ulcerated valves in ulcerative
endocarditis are often stamped with a septic element which leads to the
development of suppurative infarctions in different organs.
The size and site of the emboli are important, for they may be so large
as to obstruct vessels of large size.
The femoral and even the external iliac may suddenly become impervious
to the circulatory currents, on account of the presence of a large
embolus from the heart.
{643} When the arteries in the limbs are thus plugged, the result is
generally an ischæmia, terminating often in gangrene. Capillary
embolism may occur in a number of organs at the same instant, and give
rise to a variety of lesions. When the cutaneous capillaries are
obstructed ecchymotic spots are produced, followed by cellulitis. When
the cerebral vessels are obstructed softening may occur, which, if the
vessels are very small, may be developed without any evidence of
obstruction to the cerebral circulation. If the obstructed artery is of
large size, instantaneous hemiplegia and secondary softening will
result.
Capillary emboli may have their seat in the vessels of the spleen,
giving rise to infarctions and suppuration.
The kidneys may also undergo analogous changes. Rayer, without knowing
the origin of these changes, has given an excellent description of them
under the name of rheumatic nephritis.
In addition to the local lesions arising from these arterial or
capillary emboli, the septic phenomena are most important. When typhoid
symptoms, deep jaundice, and symptomatic intermittent fever are
associated with acute endocarditis, it establishes its ulcerative
character. In acute exudative as well as in ulcerative endocarditis,
when the inflammation progresses rapidly, the valves soften and become
less resistant than normal. As a result, they are stretched, bulged, or
torn by the stream of the circulating blood-current.
A rupture of the mitral valves will open into the auricular, and that
of the aortic into the ventricular, cavity. The reason for this is to
be found in the fact that when the valves are closed the blood-pressure
is exerted from the left ventricle toward the mitral valve, and from
the aorta toward the semilunar valves. If the blood penetrates a rent
in a flap of the valves, the endocardium is puffed out, and a valvular
aneurism is formed, and round or funnel-shaped aneurismal sacs may
project from the valves. The bottom of one of these sacs may be
perforated, and long, ragged, gray shreds, covered with fibrin, may be
found hanging in the ventricular cavity.
Microscopically, the torn shreds from a valvular aneurism, the result
of acute endocarditis, consist of nuclei and round cells imbedded in a
mass of granular matter. There is neither connective fibrilla nor
elastic tissue. When the ulceration is localized in the ventricle, the
pressure of the blood may bulge out the heart-wall, and thus give rise
to a so-called partial cardiac aneurism. By rupture of such aneurism
communication between the different heart-cavities may be established,
which will vary with the seat of the ulceration.
Acute exudative endocarditis may involve the muscular structure of the
heart. Such myocarditis (or carditis) may involve the deeper
structures, weaken them, and so alter their consistence that bulging
and the formation of a ventricular aneurism may result. Usually such
myocarditis is so slight that incomplete organization of the new
embryo-plastic cells occurs and the tissue undergoes fatty changes. The
results of all forms of acute endocarditis are best studied in
connection with the morbid changes of interstitial endocarditis, into
which they so often gradually merge.
Interstitial Endocarditis.
MORBID ANATOMY.--Interstitial (or chronic) endocarditis may be a
continuation of a process which commenced in an acute exudative
endocarditis, or it may be interstitial from its commencement, and be
so insidiously evolved as to escape notice. The anatomical changes may
sometimes be confined to the edges of the valves, at others to their
base, or they may involve the entire valves, which become thickened,
indurated, contracted, degenerated, and {644} adherent. It is more
closely allied to rheumatism, gout, and chronic interstitial changes in
other organs than either of the other varieties.
There is no part of the endocardium which is exempt from interstitial
inflammation. The favorite place for its development is the endocardium
of the valves and that at the apex of the left ventricle. The
thickening at first may be either translucent or opaque, and the valves
may become three or four times thicker than normal. In some instances,
although the valves are thickened and indurated, their functional
activity is not interfered with, and they offer no obstruction to the
blood-current.
White, thickened, opaque spots are often irregularly scattered over the
internal wall of the heart. The vegetations met with in interstitial
endocarditis differ from those of the acute exudative variety in that
they are less prominent and firmer. They rest upon an indurated base.
Their cartilaginous consistency is due to the fact that their cellular
elements are not round (as in acute exudative endocarditis), but
elongated and flattened, possessing an abundant intercellular
fibrillated tissue.
In and underneath the endocardium there is an increase of tissue, and
upon any prominence arising from the thickening of the endocardium
occur fibrin deposits. These fibrinous efflorescences assume a variety
of forms, and sometimes string out into the adjacent vessels and
cavities for half an inch or more. Their usual form is globular or
wart-like, and their seat is on the ventricular surface of the aortic
and upon the auricular surface of the mitral and tricuspid valves.
In interstitial endocarditis the cell-development is far less rapid and
abundant than in the acute exudative form, and this very slowness
accounts for the greater induration and thickening.
A microscopical examination of a cross-section of an indurated valve
shows a number of flat cells arranged in irregular layers, having
between them a fibrinous material which has in it here and there a few
elastic fibres. The new formations always originate in the layer of
flat cells. These changes are best marked in the fibrous zone at the
valvular orifices, upon the surfaces of the valves themselves, and in
the chordæ tendineæ. The new tissue, whether developed rapidly as in
acute exudative, or slowly as in interstitial endocarditis, becomes
fibroid and contracts, and this contraction is progressive.
As a consequence, the rigid valves, whose edges are round and hard, are
drawn toward their base, and thus are made to assume a puckered
appearance. A similar process in the chordæ tendineæ causes them to
become hypertrophied, rigid, and cartilaginous, while they are
diminished in length. In this way the valves are not only diminished in
depth, but not infrequently have their free edges approximated to the
cardiac walls, so that extensive valvular insufficiency is the result.
This, however, does not always happen, for a thickened cartilaginous
valve may have such abundant fibrinous or papillary excrescences upon
it that the onward current is obstructed and extensive stenosis
results.
As the thickening and rigidity of the flaps of a valve increase, their
mobility is diminished, and adhesions take place between their edges
which begin at their bases and progress toward their apices: so
thoroughly do they become adherent that in some cases all evidence of a
valvular outline is lost, and a fibrinous diaphragm is formed across
the valvular orifice having only a small slit at its centre, looking
and feeling like a buttonhole; hence the term buttonhole slit. The
mitral opening, which will usually admit the ends of three fingers, may
be so narrowed that the end of the little finger will scarcely pass
through it, and the aortic opening may become so diminished as not to
admit a small quill. These retractions and adhesions cause the mitral
valves, with their columns and cords, to assume the form of a
perforated cone.
{645} Long stringy masses of fibrin, when located on the aortic valve,
sometimes form adhesions with the aortic walls, and thus is induced a
sudden and extensive regurgitation.
Insufficiency and stenosis are often found at the same valvular orifice
as the result of the thickening, adhesion, and retraction.
Changes at the aortic orifice usually occur after middle life, and
induce more insufficiency, retraction, and adhesion than those which
are limited to the mitral valve. The mitral valves are the most
frequent seat of interstitial endocardial changes in early and adult
life. These lesions are analogous to those characteristic of
endarteritis deformans. The tendency of the lowly-organized tissue
which results from interstitial endocarditis is to undergo fatty and
calcareous changes.
The minute patches of fatty degeneration in the imperfectly organized
tissue underneath the endocardium sometimes form atheromatous masses
containing more or less granular débris. The endocardium over these
patches may be destroyed, or the patches may soften and ulcerate and
cause extensive destruction of the valves. Valvular aneurism may form
in the same manner as has been described in exudative endocarditis. The
formation of calcareous granules and plates is a very frequent
termination of interstitial endocarditis.
The aortic orifice is the most frequent seat of calcareous
degeneration. It is rarely associated with mitral stenosis. So
extensive may this process be that little beads of chalky material may
be seen studding the free edges of the valve and even extending into
the cardiac cavities.
When interstitial endocarditis has its seat in the endocardium of the
cardiac cavities, the endocardium will undergo changes similar to those
of the valves, and the muscular walls of the heart will be the seat of
interstitial myocarditis. As a result, the walls of the heart become
thinner and less resistant than normal, and depressions are formed on
its inner surface. The process is in reality a fibrous overgrowth,
which occurs in spots varying in size from half an inch to one inch in
diameter. When it extends through the entire heart-wall the columns and
cords may be so shortened as to cause valvular insufficiency.
If the cardiac walls yield so that a well-defined pouch is produced, a
condition results which is called aneurism of the heart. Cardiac
aneurism, thus induced, is usually seated at the apex of the left
ventricle; the aneurismal sac may vary in size from that of a marble to
that of a closed fist, and may communicate with the ventricle by a
funnel-shaped or ring-like aperture. The walls of the sac are solid and
rigid; the internal surface is smooth, but it may be anfractuous. In
the latter case clots adhere to its wall. Cardiac muscular fibres are
found here and there in the aneurismal walls. They are mostly, however,
made up of layers of flat cells, their flatness being the result of
pressure.
Aneurisms at the base and in the inter-ventricular septum may result
from the extension of a valvular aneurism.
ETIOLOGY.--In most instances endocarditis depends upon a constitutional
dyscrasia characterized by alterations in the vital, physical, or
chemical properties of the blood.
Acute exudative endocarditis rarely, if ever, occurs as a primary or
idiopathic affection. It seems to have a direct connection with those
diseases and dyscrasiæ in which the blood is altered either in the
relative proportions of its constituents or in its physiological
elements. So frequently is acute exudative endocarditis associated with
acute articular rheumatism that they have often been described as one
disease.
It is generally stated that acute endocarditis occurs in 50 per cent.
of those who suffer with acute articular rheumatism, but the statistics
of Bellevue {646} Hospital show that endocarditis complicates
rheumatism in only 33 per cent. of the cases. From these statistics it
is evident that a majority of the cases of acute rheumatism run their
course without endocardial complication.
The irritant action of the blood, the salts of which are changed or
which contains excrementitious products or a specific poison, is shown
most markedly upon the valvular surface of the endocardium; and it is
for this reason that the parts which are most exposed to friction of
the blood-current are those which first and most extensively exhibit
the pathological changes of endocarditis.
Charcot records a large number of observations in which endocarditis
developed in patients with chronic rheumatism and in which it never
assumed an acute form. It therefore seems evident that organic lesions
of the valves from endocarditis may occur in the course of chronic as
well as of acute rheumatism.
There is no disease in which a morbid blood-state exists in which
endocarditis may not occur. The essential fevers, the exanthemata,
diphtheria, septicæmia, pyæmia, and Bright's disease, are all
conditions in connection with which endocarditis is frequently
exhibited. It is met with occasionally in secondary syphilis.
Acute and chronic Bright's disease are often complicated by it. When an
individual who is already the subject of valvular disease of the heart
is attacked with acute rheumatism, the liability to endocarditis is
much increased.
Even when rheumatism and chorea are absent, endocarditis is liable to
occur when valvular disease exists. Some regard myocarditis,
pericarditis, pleurisy, and pneumonia as capable of exciting
endocarditis by the extension of the inflammatory process from the
surface of the heart; it is questionable if it ever results from such
extension. That it can be the result of traumatism is possible:
Bamberger records two cases of traumatic endocarditis. Wunderlich ranks
measles, next to rheumatism, as a cause of endocarditis.
In estimating the etiological importance that any disease bears in the
production of endocarditis, we must remember that not every blowing
sound or murmur is indicative of an inflamed endocardium. Bamberger and
Niemeyer think that the excited and irregular action of the heart in
children, by inducing irregular tension of the valves, may bring about
a blowing sound during the course of acute rheumatism.
Acute ulcerative endocarditis is met with in pyæmia, puerperal fever,
and endometritis, scarlatina, and diphtheria: it may occur as a
secondary affection to some inflammatory focus located in the
body--septic endocarditis.
Again, this form of endocarditis may appear without obvious
cause--spontaneously or in connection with some specific form of
inflammatory disease, as croupous pneumonia. Wilks calls it then
arterial pyæmia. Primary ulcerative endocarditis is a name recently and
perhaps more aptly given it.
Finally, ulcerative endocarditis may appear as a graft (recurrent
endocarditis) upon a valve the seat of interstitial endocarditis, and
have all the pathological appearances of the septic form, but none of
its clinical aspects.
The majority of cases of interstitial endocarditis are the sequelæ of
the exudative form. It is far more frequently associated with articular
rheumatism than with any other condition. In a certain proportion of
cases the process is interstitial from its onset, especially when it
occurs with gout, chronic rheumatism, in alcohol-drinkers, or in the
aged.
SYMPTOMS.--The subjective symptoms of acute exudative endocarditis are
more obscure than those of any other disease. They are not only few and
ill-defined, but they have no regular order of development. When the
muscular tissue of the heart is not involved the disease may run its
entire course without exhibiting a single subjective symptom.
{647} The urgent symptoms of acute rheumatism, the different phases
assumed by the dyscrasiæ and acute infectious diseases in which this
condition is liable to occur, so mask those of the endocardial
inflammation that they are often overlooked.
When the endocardial inflammation is extensive and the muscular tissue
of the heart is involved, the patient will complain of palpitation and
a sense of discomfort in the region of the heart; not infrequently
cardiac palpitation is accompanied by dyspnoea, and decubitus on the
left side is noticed. In a small percentage of cases the palpitation is
appreciable to the physician. The heart may beat with great force and
its action be tumultuous, and yet the pulse not be altered in
character.
The pulse, at first, is usually strong and forcible; later, it becomes
rapid, small, feeble, and irregular. In some cases it is very frequent
from the onset of the disease. As a rule, the force of the pulse will
not correspond to the cardiac activity; for, as the muscular fibres of
the heart become involved, its propelling power is diminished, and the
pulse is correspondingly feeble and compressible. It may be dicrotic.
The respirations are more or less accelerated, and sometimes labored,
and there may be paroxysmal dyspnoea. The face may be flushed and
covered with a profuse perspiration, or it may assume a dusky, pallid,
ashy-gray, or slightly cyanotic hue. In rare cases there may be
sleeplessness or nocturnal delirium of a typhoid type. If the muscular
tissue of the heart is extensively involved, nausea, vomiting,
giddiness, and syncope may be present.
When there is pain in the cardiac region, especially if it is augmented
by pressure, pericarditis is usually present, and slight pain or
tightness in the cardiac region is not an infrequent symptom, and is
quite common when endocarditis occurs in those who are the subjects of
chronic valvular disease.
The temperature in acute exudative endocarditis seldom exceeds 103° F.