of cardiac hypertrophy by DaCosta, Myers, Albutt, Seitz,[47] and
others. {622} Soldiers, blacksmiths, miners, mountaineers, and men
whose occupations call for heavy and prolonged exercise occasionally
develop hypertrophy of the heart, which it seems reasonable to connect
with the over-use of the muscles. DaCosta's irritable heart in young
soldiers appears to represent the early stage of this condition. In 38
per cent. of the cases excessive marching was the cause. He was able to
confirm the existence of hypertrophy by autopsy. It is not uncommon to
meet with cases of pronounced heart disease, with symptoms of failing
compensation, dropsy, etc., in large, powerfully-built men who have
been engaged in laborious occupations, and who are admitted to hospital
with the clinical picture of chronic valvular disease. At the autopsy
one is surprised to find an hypertrophied and dilated heart without
valve lesion, perhaps no extensive arterial degeneration, and no kidney
disease. They are called cases of idiopathic hypertrophy, but I believe
that some of them, at any rate, are instances of a condition induced by
prolonged muscular effort. I have had an opportunity of studying
carefully four such cases, and I have seen autopsies in two other
instances. As I mentioned, alcoholism may be also a factor in these
cases, as most of them occur in hard drinkers.
[Footnote 47: _Die Ueberanstrengung des Herzens_, Berlin, 1875--a
collection of six monographs on the subject.]
How muscular effort acts in inducing hypertrophy has been much
discussed. It seems rational to suppose that prolonged action of the
heart at a rate more vigorous and rapid than normal would induce
enlargement of its muscle, just as constant exercise acts with others;
and possibly within limits this does take place. Albutt speaks of the
large red left ventricles in the Leeds iron-workers killed by accident
or cut off by acute disease. No doubt the thickness of the ventricle is
measured by the muscular needs of the system. Muscular contraction
affects the heart in two ways: first, the venous flow is accelerated,
more blood reaches the right heart, and is sent to the lungs, and more
reaches the left ventricle and the systemic arteries. The fuller
inspirations also favor flow to the heart. When the exercise is
excessive the right heart and the venous system become still more
distended, and the outflow from the peripheral arteries proportionately
retarded and the tension in them increased--particularly is this the
case in efforts requiring straining, as in lifting, etc.; and,
secondly, the effect of muscular contraction has been shown by Traube
to increase very greatly the pressure in the arteries. Gaskell,
however, states[48] that when a muscle contracts its own arterioles
dilate; but however that may be, the increased tension during muscular
contraction can be determined in the radial by the finger, and still
better by the sphygmograph, during steady contraction of the muscles of
the arm. In yet a third way the blood-pressure may be increased during
violent muscular efforts, particularly when the breath is held. The
vaso-motor centre is stimulated by the lack of oxygen, and in
consequence the blood-pressure rises in the peripheral arteries. At the
end of prolonged contests we sometimes see men get pale or the left
ventricle may become so embarrassed that they faint.
[Footnote 48: _Journal of Physiology_, iii.]
(8) That the heart becomes hypertrophied during pregnancy has been
specially insisted upon by French writers, Larcher[49] and others. Many
doubt the correctness of their deductions, but the weight of evidence
seems to point unmistakably to the existence of moderate increase in
the thickness of the walls of the left ventricle.[50] Cohnstein[51]
connects it with the hydræmic and chlorotic conditions of the blood, so
liable to develop during pregnancy.
[Footnote 49: _Archives générales_, 1859.]
[Footnote 50: McDonald, _Heart Disease during Pregnancy_, London,
1878.]
[Footnote 51: _Virchow's Archiv_, lxxvii.]
(9) Hypertrophy of the right heart in disease of the lungs or of the
valves is usually followed by more or less hypertrophy of the left
ventricle as well, caused by the increased work in consequence of
retarded outflow into the venous system.
{623} Right Ventricle.--Hypertrophy of this chamber is most frequently
met with in connection with disease of the left side of the heart; next
with various chronic affections of the lungs; and lastly with valvular
affections of the right side.
(1) Mitral lesions--incompetence or stenosis--are very common causes
which act by increasing the resistance in the pulmonary veins and
obstructing the free flow of blood in capillaries of the lung. To
compensate for this defect the walls of the right ventricle increase in
size, and the hypertrophy at first may be unattended with dilatation.
(2) Pulmonary Lesions.--The obliteration of any considerable number of
blood-vessels within the lungs by emphysema, cirrhosis, or phthisis
(sometimes), occasionally the compression of pleuritic exudation,
increases the blood-pressure in the pulmonary artery and rapidly leads
to hypertrophy of the right heart. Narrowing of the main branches of
the pulmonary artery by the growth of tumors or an aneurism of the
aorta occasionally produces the same effect.
(3) Valvular lesions on the right side are rare causes of hypertrophy
in the adult, but during foetal life, when endocarditis is more
prevalent in the pulmonary and tricuspid valve, stenosis or
insufficiency at these orifices leads to great enlargement of the
ventricle. Pulmonary stenosis is the most common lesion; incompetence
is not often met with. Lesions of the tricuspid valves in the adult are
almost always associated with mitral disease. When the dilated
hypertrophy of the right ventricle reaches a certain grade in cases of
mitral disease or pulmonary lesion, tricuspid incompetence develops.
(4) Among other causes which may be mentioned are pericardial
adhesions, which some think tend specially to the production of
right-sided hypertrophy and extensive pleuritic adhesions. Atheroma of
the pulmonary arteries is more often a consequence than a cause of
hypertrophy.
The auricles are usually dilated and hypertrophied; simple hypertrophy
is probably never seen. In the left auricle this condition develops in
lesions at the mitral orifice, particularly stenosis when it
compensates for the obstruction. In free mitral regurgitation the
hypertrophy is not so marked.
The right auricle hypertrophies when there is greatly increased
blood-pressure in the lesser circulation, whether due to mitral
stenosis or pulmonary lesions, and incompetency at the tricuspid
orifice. Stenosis of the auriculo-ventricular orifice is a less
frequent cause. The dilatation is always excessive.
MORBID ANATOMY.--In general hypertrophy the entire organ is increased
in size and weight; more commonly we find the condition limited to two
or three chambers or to one side. The estimation of slight grades of
enlargement is difficult, but where the increase is marked the process
is simple enough. The volume of the heart varies in different
individuals according to their age and size. The normal heart is about
the size of the closed fist, and, as Virchow suggests, a fair estimate
can be made by comparing the two together. By careful weighing we get
much more accurate information. The heart of an average-sized man
weighs about 9 oz., of a woman about 8 oz. In great hypertrophy the
organ may weigh three or four times the normal amount. A heart which
weighs over 12 oz. in a man, and over 10 oz. in a woman, may be
considered hypertrophied. Hearts weighing from 16 to 20 oz. are not
uncommonly met with. Weights above 25 oz. are rare. The heaviest hearts
on record are described by Beverley Robinson of New York,[52] 53 oz.;
Dulles of Philadelphia, 48 oz.; and there are several cases described
in the _Transactions_ of the London Pathological Society of the organ
weighing as much as 46 oz.
[Footnote 52: _New York Medical Record_, 1883.]
{624} Next to weighing, careful measurement of the thickness of the
walls is the best means of determining hypertrophy. When there is great
dilatation of a chamber the walls, though actually thick, may look
proportionately thin; and on the other hand, when rigor mortis is
present the cavity may be very small and the walls appear enormously
thick. In this case measurements should not be made until the heart has
been soaked in water and thoroughly relaxed. The normal thickness of
the left ventricle is about half an inch (12 or 13 millimeters), being
thicker toward the base. It is well to measure in two or three places,
not including the papillary muscles. A thickness of 10 lines or over
(20 to 25 mm.) indicates hypertrophy. It is rare to meet with the wall
thicker than 1 inch (25 mm.), even in very great hypertrophy. The right
ventricle is thinner than the left, and has an average diameter of from
2 to 3 lines (4 to 7 mm.). A thickness of from 6 to 9 lines (13 to 20
mm.) may be met with in great hypertrophy. It is very rare to see a
diameter of more than three-quarters of an inch, but cases are reported
of a thickness of over an inch. The left auricle has a normal thickness
of about a line and a half (3 mm.), which in considerable hypertrophy
may be nearly doubled. The wall of the right auricle is even thinner
than the left, rarely exceeding 1 line in diameter. In hypertrophy the
sinus does not present a marked increase in thickness, but the
appendix, particularly the musculi pectinati, may be greatly developed
and measure from 2 to 3 lines in diameter.
The shape of the heart is much affected by the degree of hypertrophy in
different cavities. Great enlargement of the ventricles broadens the
apex, and the conical shape is lost. In the enormous hypertrophy and
dilatation of aortic insufficiency the increased breadth and rotundity
of the apex becomes very marked. When the right ventricle is chiefly
affected, it occupies a large share of the apex, and the transverse
diameter of the organ is increased. When due to mitral stenosis the
contrast between the large broad right ventricle extending well to the
apex and the small left chamber is very striking.
When not degenerated the muscle-tissue of an hypertrophied heart is of
a deep-red color, firm, and usually cuts with slightly increased
resistance. The right ventricle often has a peculiarly hard, leathery
feel, which was noticed by Rokitansky. In simple hypertrophy of the
left ventricle the papillary muscles and columnæ carneæ may be
increased in size, but the former often appear flattened in great
eccentric enlargement. The trabeculæ are usually much more developed in
the right ventricle and in the appendix of the right auricle than in
the left chambers. Very often the tissue looks pale, and may be soft
from the occurrence of fatty degeneration.
The histological characters of the changes in hypertrophy have been
much studied, particularly with a view of determining the question of
numerical increase. Hepp[53] described an increase in the thickness;
but most recent observers regard the hypertrophy as due to numerical
increase, resulting from the development of new fibres, either by the
splitting of the old ones (Rindfleisch) or their growth from
interfibrillar nuclei.[54] Wilks and Moxon[55] and Gowers[56] find that
the fibres are not increased in size. Letulle[57] thinks that there is
a process of progressive hyper-nutrition of the fibres.
[Footnote 53: _Henle's Zeitschrift_, 1854.]
[Footnote 54: Zielonko, _Virchow's Archiv_, lxii.]
[Footnote 55: _Pathological Anatomy_, London, 1875.]
[Footnote 56: _Reynolds's System_.]
[Footnote 57: Quoted by Peter, _loc. cit._, p. 280.]
The toughness of the hypertrophied muscle is due to the increase in the
connective tissue, which is more marked as a rule in the right than the
left ventricle. Sometimes, indeed, it is not at all noticeable in the
latter, which may be soft and tears readily with the finger.
SYMPTOMS.--Hypertrophy is a conservative process, usually secondary to
some valvular or arterial lesion, and is not necessarily accompanied by
any {625} symptoms. So admirable is the adjusting power of the heart
that, for example, an advancing stenosis of aortic or mitral orifice
may be for years perfectly counterbalanced by a progressive
hypertrophy, and the subject of the affection be happily oblivious to
the existence of heart trouble. Particularly is this the case with
mitral stenosis and the consequent hypertrophy of the left auricle and
right ventricle. While leading quiet lives and not straining the heart
with violent exertion, such persons may not suffer in any way, or
perhaps only experience a little shortness of breath when going up
stairs. Indeed, the hypertrophy is in almost all instances an unmixed
good, and many of the symptoms which arise are to be attributed to its
failure, or, as we say, disturbance of compensation.
The left ventricle is most often involved, and the clinical features of
hypertrophy are best seen when it is affected. Inspection may reveal
decided bulging of the præcordia, producing in extreme instances marked
asymmetry of the chest. This is most frequent in persons under twenty
years of age, and it may occur without any pericardial adhesions, which
Shroetter[58] thinks are invariably associated with this condition. The
intercostal spaces may be widened, and the area of visible impulse is
much increased. On palpation the character and position of the
apex-beat give most important results. It is stronger, more forcible
and heaving, and may lift the chest-wall. With each systole the hand or
the ear applied over the heart may be visibly raised. A slow heaving
impulse is one of the best signs of simple hypertrophy; when there is
large dilated hypertrophy the forcible impulse is often more sudden and
abrupt. A second, weaker, impulse can sometimes be felt, due possibly
(as Gowers suggests) to a rebound from the aortic valves. The area of
impulse is greatly increased, and the beat may be felt in the sixth,
seventh, or eighth interspace from an inch to three inches outside the
nipple. The downward dislocation of the apex is an important sign in
hypertrophy of the left ventricle; simple outward displacement may be
due to enlargement of the right ventricle.
[Footnote 58: _Ziemssen's Encyclopædia_, vol. vi.]
In moderate grades of hypertrophy, as seen in chronic Bright's disease,
the apex-beat may be in the sixth interspace in the nipple-line or a
little outside it.
Percussion gives an area of increased dulness, due to the much larger
portion of the heart which comes in contact with the chest-wall. The
dulness in the parasternal line may begin at the third rib or in the
second interspace, and the transverse limits extend from half an inch
to two inches beyond the nipple-line, and an equal distance beyond the
middle line of the sternum. The dull region is more ovoid than in
health. When carefully delimited and measured, there may be in the
colossal hypertrophy of aortic valve disease an area of dulness from
seven to eight inches in transverse extent. In moderate grades a
transverse dulness of four inches is not uncommon.
On auscultation the heart sounds, when there is no valve disease, may
not present any special changes, but the first is often prolonged and
dull; but when there is dilatation as well, it may be very clear and
sharp. Reduplication is not uncommon, particularly in the hypertrophy
of renal disease. A peculiar clink--the tintement métallique of
Bouillaud--may sometimes be heard, with the impulse most frequently
just to the right of the apex-beat. The second sound is clear and loud,
sometimes ringing in character or reduplicated. When the hypertrophy
depends upon valvular lesions the sounds are of course much altered,
and replaced or accompanied by murmurs.
The pulse of simple hypertrophy not dependent on valvular lesions is
usually firm, full, and strong, of high tension, and regular. It may be
increased {626} in frequency, but often is normal. In eccentric
hypertrophy the pulse is full, but softer, and usually more rapid. So
long as the hypertrophy is maintained the pulse is regular; one of the
earliest signs of failure and dilatation is irregularity and
intermittence. The various modifications of the pulse in connection
with valve disease are considered elsewhere.
Among symptoms which patients complain of most frequently are
unpleasant sensations about the heart--a sense of fulness and
discomfort, rarely amounting to pain. This may be very noticeable when
recumbent and on the left side. Actual pain in simple hypertrophy is
rare, but in the irritable heart from tobacco and in neurasthenics with
slight enlargement it is often a very troublesome symptom. Palpitation
is not often complained of, nor do patients always have sensations from
the violent shocks of a greatly hypertrophied organ; others, again,
will have very uneasy feelings from a moderately exaggerated pulsation.
The general condition of health has much to do with this: we are not in
health conscious of our own heart's action, but one of the very first
indications of nervous exhaustion from excesses or over-study is the
consciousness of the heart's action, not necessarily accompanied by
palpitation. Flushings of the face, noises in the ear, flashes of
light, and headaches are not uncommon.
There are certain untoward effects of long-continued hypertrophy of the
left ventricle which must be mentioned, chief among which is the
production of atheromatous degeneration of the vessels. Particularly is
this the case when the hypertrophy results from increased peripheral
resistance. The heightened blood-pressure in the arteries (which is
expressed by the word strain) gradually induces an endarteritis and a
stiff, inelastic state of those vessels most exposed to it--viz. the
aorta and its primary divisions. In overcoming the peripheral
obstruction the hypertrophy "ruins the arteries as a sequential result"
(Fothergill). It is in this way that prolonged muscular exertion acts
injuriously, and leads to two common morbid conditions in athletes and
persons whose employment necessitates violent exercise of the
muscles--viz. aneurism and sclerosis of the aortic semi-lunar valves,
with incompetency. Syphilis certainly does not embrace the entire
etiology of aneurism, the occurrence of which in soldiers, strikers,
foundrymen, etc. can be traced to arterial strain. So also with the
sclerosis of the semi-lunar valves--just enough, perhaps, to produce
incompetency; how common it seems to be in strong, well-built men whose
excesses have been on the cinder-path or on the river! The increased
aortic tension, with the more forcible recoil and closure of the
semi-lunar valves, would seem to be factors in the production of this
condition. Aortic incompetency is the special danger of athletes, and
no inconsiderable number of the cases of this lesion occurring in men
without rheumatic or syphilitic history may be traced to over-use of
the muscles.
Another special danger is rupture of the blood-vessels, particularly of
the brain. In the condition of general arterial degeneration associated
with contracted kidneys and hypertrophied left heart apoplexy is
common; indeed, we may say that in the majority of cases of cerebral
hemorrhage there is sclerosis of the cerebral vessels, often with the
development of miliary aneurisms, and the rupture is directly induced
by the forcible action of the heart.
Hypertrophy of the right ventricle in the adult is rarely induced by
valvular disease on the right side, but is a result of increased
resistance in the pulmonary circulation, as in cirrhosis of the lung
and emphysema, or in stenosis of the mitral orifice. When the
compensation is perfect, and the hypertrophy fully maintains the
equilibrium of the circulation, there are no symptoms. Extra exertion,
as in ascending stairs or running, may induce shortness of breath, but
in many respects hypertrophy of {627} the right ventricle is the most
enduring and salutary form in the whole range of cardiac affections.
For long periods of years the effects of mitral stenosis may be
counterbalanced completely, and only sudden death by accident or an
acute disease reveals the existence of extensive unsuspected heart
disease. In the hypertrophy secondary to pulmonary disease,
particularly emphysema and cirrhosis, there may be sensations of
uneasiness in the cardiac region, with cough and shortness of breath;
but so long as the dilatation is moderate the symptoms are not marked.
With great dilatation and tricuspid regurgitation come the venous
engorgement, oedema, and pulmonary troubles. The increased pressure in
the lesser circulation not uncommonly leads to atheroma of the
pulmonary artery, and the full state of the capillaries leads
ultimately to a deposition of pigment and increase in the fibrous
elements in the lung--the brown induration. Pulmonary congestion and
apoplexy from thrombosis or embolism are more often associated with
dilatation. Hæmoptysis may result from rupture of vessels during sudden
exertion.
The physical signs of hypertrophy of the right ventricle are not so
marked as those of the left. Bulging of the lower part of the sternum
and left cartilages is occasionally met with. The apex-beat is forced
to the left, but is not so often displaced downward. The most marked
impulse may be in the epigastrium, in the angle between the ensiform
cartilage and the seventh rib or beneath the cartilages of the sixth
and seventh ribs. The pulsation is rarely the strong heave of
left-sided hypertrophy, and is apt to be diffuse, not punctuate,
particularly if there is much dilatation. In thin-walled chests there
may be pulsation in the third and fourth right interspaces. The area of
dulness is increased in the transverse direction, particularly toward
the right, where it may extend an inch or more beyond the border of the
sternum. On auscultation the first sound at the lower part of the
sternum is louder and fuller than normal, but the differences are not
very marked unless there is much dilatation, when it is clearer and
sharper. The second sound is accentuated in the pulmonary artery on
account of the increased tension, and there may be reduplication. The
pulse at the wrist is usually small. The jugular pulsation occurs when
there is tricuspid incompetence, which arises when the eccentric
hypertrophy reaches a certain grade.
Hypertrophy of the auricles is always associated with dilatation. It is
most common in the left chamber, which hypertrophies in mitral stenosis
and incompetency, and assists materially in restoring the balance of
the circulation and protects the lungs. There are no special physical
signs, and we usually can only infer its presence by the existence of
mitral stenosis and a presystolic murmur. Increased dulness may be
determined at the left of the sternum, and there may be a presystolic
wave in the second left interspace.
Hypertrophy and dilatation of the right auricle occur not infrequently,
and are almost invariably associated with a similar condition in the
right ventricle, and incompetency of the tricuspid. In emphysema,
cirrhosis of the lung, chronic bronchitis, and in mitral disease, it is
very common, much more so than the statement of some authors would lead
us to expect. In comparison with the left auricle the greater
development and hypertrophy of the appendix and its musculi pectinati
is very striking. The latter may be distributed over the anterior wall
of the sinus to a much greater extent than in health. There may be
increased dulness in the third and fourth interspaces, with pulsation
presystolic in rhythm. Usually there are signs of venous engorgement,
jugular pulsation, and other evidences of dilatation of the right
heart.