cardiac walls, diminishes the vigor of their contractions, and is thus
the very reverse of hypertrophy. So long as compensation is maintained
the enlargement of a cavity may be considerable: the limit is reached
when the hypertrophied walls can no longer in the systole expel all the
contents, part of which remain, so that at each diastole the chamber is
abnormally full. Thus in aortic incompetency blood enters the left
ventricle from the aorta as well as the auricle, dilatation ensues, and
also hypertrophy as a direct effect of the increased pressure and
increased amount of blood to move. But if from any cause the
hypertrophy weakens, and the ventricle during systole does not empty
itself completely, a still larger amount is in it at the end of each
diastole, and the dilatation becomes greater. The amount remaining
after systole is a cause of obstruction, preventing the blood entering
freely from the auricle. Incompetency of the auriculo-ventricular
valves follows with dilatation of the auricle and impeded blood-flow in
the pulmonary veins. Dilatation and hypertrophy of the right heart may
compensate for a time, but when this fails stasis occurs in the venous
system, with dropsy. The consideration of the symptoms of chronic
valvular lesions is largely that of dilatation and its effects. Acute
dilatation, such as we see in fevers or in sudden failure of an
hypertrophied heart, is accompanied by three chief symptoms--weak
usually rapid impulse, dyspnoea, and signs of obstructed venous
circulation. Cardiac pain may be present, but it is often absent.
The physical signs of dilatation are those of a weak and enlarged
organ. The impulse is diffuse, often undulatory, and is felt over a
wide area, and an apex-beat or a point of maximum intensity may not
exist. When it does it may be visible, and yet cannot be felt--an
observation of Walshe's which is very valuable. An extensive area of
impulse with a quick, weak maximum apex-beat may be present. When the
right heart is chiefly dilated the left may be pushed over so as to
occupy a much less extensive area in the front of the heart, and the
true apex-beat is not felt; but the chief impulse is just below or to
the right of the xiphoid cartilage, and there is a wavy pulsation in
the fourth, fifth, and sixth interspaces to the left of the sternum. In
extreme dilatation of the right auricle a pulsation can sometimes be
seen in the third right interspace close to the sternum, and with free
tricuspid regurgitation this may be systolic in character. Whether the
pulsation frequently seen in the second left interspace is ever due to
a dilated left auricle is not satisfactorily determined. I have
sometimes thought it was presystolic in rhythm, though it may be
distinctly systolic. Post-mortem, it is rare in the most extreme
distension to see the auricular appendix so far forward as to warrant
the belief that it could beat against the second interspace. The area
of dulness is increased, but an emphysematous lung or the full
distended organ in a state of brown induration may cover over the heart
and limit greatly the extent. The directions of increase were
considered when speaking of Hypertrophy with dilatation.
The first sound is shorter, sharper, and more valvular in character,
and more like the second. As the dilatation becomes excessive it gets
weaker. Reduplication is not common, but occasionally differences may
be heard in the joint sound over the right and left hearts. Murmurs
very frequently obscure the sounds; they are produced by incompetency
of the valves due to the great dilatation, or are associated with the
chronic valve disease on which the condition depends. The aortic second
sound is replaced by a murmur in aortic regurgitation; the pulmonary is
accentuated in mitral regurgitation and pulmonary congestion, but with
extreme dilatation it may be much weakened. The heart's action is
irregular and intermittent, and the pulse is small, weak, and quick.
The DIAGNOSIS is generally easy when the physical signs, the history,
and {635} the general condition are taken into account. In a case of
valvular disease with hypertrophy the onset of dyspnoea and venous
stasis with dropsy tell unmistakably of cardiac dilatation. Increased
præcordial dulness, with a weak, diffuse impulse, is not simulated by
many conditions, and one only, pericardial effusion, need be specially
mentioned. This may present very serious difficulties, and indeed a
dilated heart has been aspirated under the belief that effusion was
present. The points to be attended to are--the greater lateral dulness
in dilatation and the wavy impulse which may extend over a great part
of it; in effusion the dulness extends upward and is more pear-shaped,
the impulse is not so extensive, and may be tilted up an interspace or
may not be visible. The sounds in pericardial effusion are muffled and
distant over the dull region, but at its upper limit may be clear. The
absence of friction is an important negative sign. In some cases it is
extremely difficult to determine between the conditions, and I have
known a weak, feeble, irregular heart, with cyanosis, and oedema lead
to the diagnosis of dilatation when effusion was present.
The PROGNOSIS depends upon the cause of the dilatation. In anæmia and
fevers the temporary dilatation may undoubtedly pass away with the
improvement of health; but when the cause is not remediable the danger
must be measured by the presence or absence of compensation. In the
majority of the cases which we see the dilatation occurs in valve
disease, and no symptoms of importance arise so long as the
compensation is perfect. Failure of this, which may result from many
causes, as already mentioned, is always serious. It may be only
temporary, and with care the compensation can be re-established and the
symptoms pass away. We constantly see this in the eccentric hypertrophy
of the right heart from mitral disease; an attack of bronchitis
suffices to disturb the compensation, and with the relief of the
catarrhal trouble the dyspnoea and heart symptoms disappear.
The TREATMENT of dilatation is virtually that of chronic valvular
disease, and we shall only refer to general indications. With the
earliest symptoms of failure the work of the heart should be reduced to
a minimum by placing the patient at rest. This in itself may suffice
without any other measures. Time and again I have seen, particularly in
cases of aortic insufficiency, the dyspnoea relieved and the oedema of
the feet disappear and the compensation re-established by placing the
patient in bed, enjoining absolute quiet and carefully regulating the
diet. The importance of rest in the early stages of heart failure
cannot be too much insisted upon.[69] Quiet and careful dieting may
suffice for the milder attacks, but we have usually even in these to
resort to heart tonics. Digitalis is the most powerful remedy we
possess in restoring and maintaining compensation. Under its use the
irregular, feeble, and frequent contraction becomes regular and
stronger, and the embarrassed circulation is relieved. In hospital
practice the same chronic heart cases may return year after year with
attacks of cardiac failure, dyspnoea, dropsy, etc., and each time the
rest in bed and digitalis may suffice to restore compensation. A fourth
or fifth, even a sixth, attack may be safely weathered, and then the
final breakdown occurs when nothing avails to combat the dilatation. Of
substitutes for digitalis, caffeine and convallaria have been much used
of late. Caffeine in some cases acts more promptly, which is an
advantage, but its action is not so certain and not so enduring.
Convallaria is very variable {636} in its action; it has succeeded in
some instances in which digitalis has failed, and in others has been
quite without effect. In extreme cardiac failure with great dilatation,
lividity, orthopnoea, and feeble pulse, stimulants must be freely
given; ether may be employed hypodermically. In this condition of final
asystolism digitalis seems to have lost its influence. In the heart
failure of pneumonia I have found camphor a valuable adjuvant to the
diffusible stimulants. To improve the general nutrition, and with it
that of the heart-muscle, iron and arsenic are most valuable adjuvants,
especially in the dilatation of anæmia. The treatment of special
symptoms, dropsy, dyspnoea, etc., is considered under Valvular
Affections.
[Footnote 69: In Ortel's system (_Ziemssen's Handbuch der Allgemeine
Therapie_, Bd. iv.) of treating heart disease exercise, particularly
climbing, forms a very important part, but an analysis of his cases
shows that most of them were instances of fatty heart in obese persons.
It would scarcely be applicable to valvular disease. The severe
exercise, he thinks, stimulates the heart-muscle and helps in the
restoration of the hypertrophy. His other suggestion, the reduction of
the liquids ingested, seems much more reasonable, as in this way the
volume of blood to be circulated may be considerably reduced.]
Aneurism of the Heart.
This term is now restricted to local or partial dilatations of the wall
of one of the cardiac cavities. Formerly, dilatation of the heart or of
one of its chambers was spoken of as aneurism. This rare condition[70]
is most frequently associated with fibroid degeneration, but other
causes of local weakness of the walls, as ulcer, acute myocarditis, and
fatty degeneration, have been present in a few cases. An instance is on
record where the aneurism followed a stabbing wound of the chest.[71]
The left ventricle is usually involved; very few cases occur in the
other chambers. The condition may be acute or chronic.
[Footnote 70: In the index catalogue there are references to only 18
cases by American authors. In the museums of Philadelphia there are
only 5 specimens--3 in the museum of the College of Physicians; 1 each
in the University and Pennsylvania Hospital cabinets.]
[Footnote 71: Quoted by Legg, _Bradshawe Lecture on Cardiac Aneurisms_,
London, 1883.]
Acute aneurism is met with occasionally in ulcerative endocarditis,
more rarely as the result of local softening due to myocarditis or
plugging of a branch of a coronary artery. In severe endocarditis
perforation is, I think, more common than the production of aneurism.
In one case I saw a deep excavation at the upper part of the septum
produce a bulging the size of a marble in the wall of the left auricle,
and in another ulceration in one sinus of Valsalva had extended into
the septum, the upper part of which presented an aneurismal dilatation
which had ruptured into the left ventricle. Legg considers the
production of acute aneurism by the rupture of abscesses or cysts as
doubtful.
Chronic aneurism is almost confined to the left ventricle, and, as
Cruveilhier pointed out,[72] is the result of fibroid degeneration of
the muscle. In a few instances fatty degeneration appears to have been
the cause. The monographs of Thurnam,[73] Pelvet,[74] and Legg[75] give
the most complete account of the disease. They are more common in men
than in women, and the majority of the cases occur after middle life.
[Footnote 72: _Anatomie pathologique_, Paris, 1835-42.]
[Footnote 73: _Medico-Chirurgical Transactions_, vol. xxi., 1838.]
[Footnote 74: _Des Aneurysmes du Coeur_, Paris, 1867.]
[Footnote 75: _Loc. cit._]
The situation of the aneurism is most frequently at the apex--59 of 90
cases collected by Legg. They are usually rounded in shape, and may
vary in size from a marble to a cocoanut. The sac may be double, as in
a case described by Janeway,[76] or, as in a specimen in Guy's Hospital
Museum, the whole wall of the ventricle may be covered with aneurismal
bulgings. In the simplest form there is a rounded dilatation at the
apex, and the lower part of the septum is lined with thrombi. Often the
tumor is distinctly sacculated, and communicates with the ventricle by
a very small orifice. The pericardium is usually thickened, and
calcification may occur in the walls. Rupture seems rarely to occur--in
only 7 of the 90 cases collected by Legg. Of other {637} parts of the
ventricle, the septum and the undefended space at the highest part of
the septum just below the aortic ring are most often involved. This
latter situation is sometimes the seat of a congenital dilatation,
usually a small, thin, smooth sac without thrombi, which has no
pathological significance.
[Footnote 76: _N.Y. Med. Journ._, 1875, xxi.]
Cardiac aneurisms rarely produce any symptoms, and in the majority of
cases have been found accompanying other conditions which have proved
fatal. At the left apex the increase in dulness and area of pulsation
could scarcely be distinguished from hypertrophy unless associated with
marked bulging. They seldom perforate the chest-wall. Berthold (quoted
by Legg) has described one connected with the right auricle which
produced a pulsating tumor beneath the skin, the region of the second
and third ribs.
Adventitious Products in the Heart.
Tubercle.--In general tuberculosis and in tuberculous pericarditis
there may be nodules in the heart-substance, but, as a rule, this organ
is very rarely the seat of tubercle. Large caseous masses sometimes
occur, but unless associated with tubercle in other organs they are not
to be regarded as necessarily tuberculous. Miliary granulations have
been seen on the valves.
Cancer and sarcoma rarely are primary, and are not often met with as
secondary growths. Sometimes a mediastinal sarcoma penetrates along the
veins and involves the auricle, with or without great involvement of
the pericardium. The secondary tumors may be single or multiple. In a
case of cancer of the uterus I found a large mass in the wall of the
right ventricle, involving also the anterior segment of the tricuspid,
and partially blocking the orifice. The surface was eroded, and the
pulmonary arteries contained numerous cancerous emboli. In another
instance the heart was considerably enlarged by the presence of many
rounded masses of colloid cancer throughout the walls. In a remarkable
case of sudden death in a child I found the tricuspid orifice firmly
blocked with a sarcomatous mass which I thought at first had originated
in the heart, but dissection showed to have come from the renal vein,
which was filled with sarcoma extending from a large tumor of the
kidney. Melanotic cancer, fibromata, and myomata have occasionally been
seen, and a secondary epithelial growth has been described by Paget.
Syphilis of the heart is met with in the form of gummata or as a
specific arteritis leading to patches of fibroid induration. The
gummous growths form tumors of variable size, which usually occupy the
septum or the ventricles. Possibly many of the caseous and calcified
masses not infrequently met represent obsolete gummata. The syphilitic
myocarditis probably originates in an affection of the arteries, and
leads to patches of fibroid induration more or less extensive. Many
authors hold that syphilis plays a very important rôle in the
production of fibroid heart.
Cysts.--Simple cysts are rare in the heart. I have met with two
instances--one, the size of a marble, situated in the wall of the right
auricle near the septum, was filled with a brownish fluid; the other,
the size of a small walnut, occupied the base of the posterior segment
of the mitral, and was filled with a clear fluid. Blood-cysts
occasionally occur.
Parasites.--The Cysticercus cellulosæ, the larva of Tænia solium, and
the hydatid or echinococcus, the larva of Tænia echinococcus of the
dog, are sometimes found in the heart. The former, usually single, is
extremely rare; in the hog and calf the measles, as the cysts are
called, very often exist in the heart-muscle. In the recent paper by
Mosler[77] references are given to 13 cases of cysticerci in the heart.
The greatest number present was 19. The {638} hydatid is more common:
25 instances are mentioned in the statistics of Devaine and Cobbold,
and Mosler's more recent figures only give 29. They occur in the right
ventricle more frequently than in the left. Occasionally they attain a
larger size and compress the heart and push back the lungs. The cyst
may burst and the contents be discharged into the pulmonary artery or
aorta, as in a case given by Osterlen,[78] in which gangrene of the
right leg followed the plugging of the femoral by hydatid vesicles
discharged into the blood by the bursting of a cyst in the left
auricle.
[Footnote 77: _Zeitschrift für klinische Medicin_, Berlin, Bd. vi.,
1883.]
[Footnote 78: _Virchow's Archiv_, xlii.]
{639}
ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.
BY ALFRED L. LOOMIS, M.D.
Endocarditis.
DEFINITION.--Endocarditis is an inflammation of the endocardium, and
may be either exudative, neoplastic, or ulcerative in character. While
its different varieties are closely connected in their etiology, they
are distinct in the extent, duration, character, and course of their
pathological changes. They cannot be classified as acute and chronic in
the ordinary acceptation of these terms, for they often so merge into
each other as to render it difficult, if not impossible, to determine
when they cease to be acute and become chronic; and some cases are at
no time acute. It has been claimed that an acute endocarditis becomes
chronic when its course is prolonged, but the advanced changes are only
a stage of the acute process.
So-called acute endocarditis is accompanied by a fibro-cellular
exudation into the substance of, and underneath, the endocardium,
causing elevations of its surface. The better term for this variety is
exudative endocarditis, it being borne in mind that the exudation does
not take place upon the free surface of the membrane, but into its
substance and underneath it. This form of endocarditis may be entirely
recovered from, or it may lead to interstitial changes in the
endocardial and myocardial tissue which will correspond to the changes
usually described as those of chronic endocarditis.
Interstitial endocarditis is a better term for these changes. The
disease may be the sequela of exudative endocarditis, or may be
interstitial from its commencement, for the valvular changes of
interstitial endocarditis are often found in those who never have had
either acute articular rheumatism or exudative endocarditis, but have
been the subjects of chronic rheumatism or gout.
Acute exudative endocarditis may, in certain cases, be stamped with an
ulcerative process, the result of septic infection, giving rise to
those pathological changes which have been described as acute
ulcerative endocarditis.
HISTORY.--The history of endocarditis is restricted to modern
pathology. It is not spoken of by the older medical writers. Before the
sixteenth century knowledge of the structure and functions of the heart
was imperfect and scanty, and its diseased conditions were altogether
unknown.
The history of the pathology of cardiac disease commenced with Harvey,
Lancisi, Vesalius, and Vieussens. They investigated not only the normal
structure of the heart and the mechanism of the circulation, but
accurately described a few of its valvular diseases.
There is little doubt but that Laennec, Senac, and Morgagni were quite
familiar with the valvular diseases of the heart, but Kreisig first
traced the relationship between valvular diseases and inflammation of
the lining membrane of the heart.
{640} The term endocarditis was first used by Bouillaud, who had the
advantage of Laennec's discovery of auscultation. Corrigan first
discovered the physical signs of aortic insufficiency. The most
important advance in the pathology of endocarditis is due to the
investigations of Virchow and Luschka, the former developing its
sequelæ or results, the latter its histological changes. Ulcerative
endocarditis is of modern date, and its literature scarcely extends
back twenty years. The labors of Kirk, Virchow, Charcot et Vulpian,
Moxon, Eberth, and Lancereaux are all connected with the etiology and
anatomical changes of ulcerative endocarditis.
The relationship of interstitial endocarditis to valvular diseases of
the heart and to cardiac murmurs is a subject which at present is
engaging the attention of many medical observers.
I shall describe endocarditis under three heads:
1st, Exudative endocarditis;
2d, Ulcerative endocarditis;
3d, Interstitial endocarditis.
That the pathological changes which I shall describe may be readily
appreciated, I will briefly review the anatomical structure of the
endocardium.
The endocardium consists of connective tissue, with numerous elastic
fibrils, covered by and continuous with a layer of flattened cells.
Upon this lies the endothelial layer, which disappears in twenty-four
hours after death.
Luschka regards the endocardium as continuous with all the arterial
tissues, but the majority of histologists consider it a continuation of
the internal membrane. Some regard the endocardium and inner coat of
the arteries as analogous, since both are non-vascular and have an
endothelial covering upon a connective-tissue base. As endocarditis is,
for the most part, limited to the valves of the heart, a knowledge of
their anatomical arrangement is important.
A transverse section of a segment of an auriculo-ventricular valve
shows that upon the superior or auricular surface and upon the inferior
or ventricular surface there are flattened cells and endothelium, and
that next to each lies a fibro-elastic layer, the superior being the
thicker. These two layers are separated by connective tissue.
The layer of flat cells is thickest on the ventricular surface. The
fibro-elastic tissue is thickest at the base of the valve. The
semi-lunar valves have endocardium on one side and the tunica intima on
the other.
Although the endocardium has no vessels of its own, the capillaries
upon the cardiac walls are in contact with it. The arrangement in the
valves is different, as only a few vessels ramify between the layers of
the mitral valve, and none are found, normally, in the sigmoid valves.
Acute Exudative Endocarditis.
This variety of endocarditis is met with most frequently in connection
with acute articular rheumatism.
In adults it usually has its seat in the left heart; in intra-uterine
life it occurs in the right heart. The inflammation commences in, and
seldom extends beyond, the valves and the valvular orifices, but it may
involve the whole or any part of the ventricular or auricular portions
of the endocardium.
MORBID ANATOMY.--The endocardium becomes infiltrated with young cells,
the process beginning in the layer of flat cells. The new formative
cells are developed not only from the cells of the layer immediately
underneath the endocardium, but also from leucocytes. This hyperplasia,
this heaping up of embryo-plastic cells, is accompanied by softening of
the deeper {641} layers of the intercellular structure, and as the
softening goes on the intercellular substance is destroyed.
The endothelial elements also play an active part in the processes. The
masses of new cells push out the endocardium, and papillary elevations
are formed, filled with a fluid whose chemical properties resemble
those of mucin, since it coagulates into threads when acetic acid is
added. The cone-like vegetation is surrounded in the deeper layers of
the endocardium by a zone of proliferation which is never distinctly
limited, but which exhibits progressive hyperplasia from the periphery
toward the centre.
All these changes may have taken place in non-vascular tissue. Where
the capillaries are most numerous a punctuate or arborescent
vascularity is seen, and this is followed by opacity of the part which
is the seat of the inflammation. After death the endocardium and lining
membrane of the vessels are often stained; this staining is produced by
the coloring matter from the red corpuscles, and is the result of
post-mortem change.