As theirname implies, they are capable of expansion such the media, from those in which the

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CHANGES OCCURRING IN THE ELASTIC FIBERS OF THE AORTA
WITH ADVANCING AGE.*
*L. S.FOSTER.
(From thePathologicalLaboratory, Royal Victoria Hospital,Montreal.)
The aortas described in this series were examined mainly
forthe purpose ofstudyingthe progressive changes occurring
in the middle coat, with respect to the nature of the elastic
fibers at successive life periods.
Experience has taught us thatthe elastic fibersin the arte-
rial coat areofgreat importance. In health this tissue repre-
sents that structure in the artery which maintains the size of
the vessel and does not allow it to become over-expanded.
As their name implies, they are capable of expansion such
as occurs with each pulsation of the vessel during systole of
the heart, while during diastole they regain their former
length. Diseased conditions and changes occurring in the
elastic media are very liable to alter the capabilities of this
tissue and thus seriously impair the normal function of the
vessel.
It is unnecessary to give more than a brief review of the
observations already made upon elastic tissue under various
conditions, more particularly with regard to the changes
occurring in the process of arteriosclerosis.
From the work of Thoma and his pupils the part played
by the media and, more particularly, by the elastic tissue in
the process of arteriosclerosis has been fully demonstrated.
However, with the further researches on the etiology and
progress of arterial disease we have come to distinguish so
many forms and types of arteriosclerosis that it has become
necessary to segregate those diseases which arise from pure
incompetence, consequent upon degenerative processes of
the media, from those in which the causative agent directly
and in itself produces a lesion which we must still consider
arteriosclerosis.
*ReceivedforpublicationJuly2,I909.
(297)
298 FOSTER.
Abundant evidence has been brought forward to indicate
that infectious diseases of various kinds produce certain and
definite lesions in one or other of the arterial coats. Such
lesions are not necessarily primary in the media. Itbecomes
essential, therefore, to distinguish between that type of arte-
rial disease which is primary in the arterial wall and has a
definite etiological factor and those which arise in conse-
quence to a weakness or change in one or other ofthe coats.
As far as we know at the present day, the secondary lesions
mostly ofthe nature ofrepair are consequent to changes in the
media, and in this respect this group upholds the theory of
Thoma that certain intimal thickenings result in consequence
of medial weakening. Thoma and his pupil, Kaefer, found
that in the early stages of arteriosclerosis the vessel wall is
weaker and allows agreater dilatation than is normal, while in
the later stages, in which thickened plaques and fibroses are
present, it isnotso readilydilated and thus presents a "higher
degree of elasticity or resistance." Unfortunately, as G. A.
Gibson has pointed out, Thoma in making this statement has
misused physical terms. The essential conception of elastic-
ity is not resistance to pressure: it is, on the contrary, that of
capacity to return to its previous dimensions after having
undergone forcible expansion. The thickened fibrotic artery
shows, it is true, a greater resistance but a lessened elasticity;
the force necessary to cause expansion is greater but when
that expansion is brought about there is not necessarily a
complete contraction and return to the previous dimensions
when the distending or expanding force is removed. What
Thoma's experiments proved is that the fibrosed artery
presents "a higher degree of resistance coupled with a les-
sened elasticity." The same criticism applies to the obser-
vations of Luck, a pupil of Thoma, who found that in dis-
eases with disturbed nutrition, as in cancer, tuberculosis, and
sepsis, a weakening of the vessel wall with diminished elas-
ticity is evident. This weakening continues until endarteritic
processes appear, when, with the development of new con-
nective tissue in the artery, "the elasticity increases" (i.e.,
the resistance increases), and the vessel is not so easily
dilated.
CHANGES OCCURRING IN THE AORTA. 299
Wertheim was the first to point out the importance of the
inherent elasticity of certain body cells and tissues. It is
evident that the strength and elasticity of different cells and
tissues is dependent upoIl their character of structure, and,
for each type of tissue, a mathematical curve can be plotted,
indicating its elastic powers.
Polotebnow made a right use of terms: he determined
the relative elasticity of normal and sclerosed vessels and
showed that the former were four times as elastic as the
latter. He further found that a sclerosed vessel when
relieved of its tension was not able to return to its original
condition. These experiments, which were carried out by
attaching a given weight to a vesselimmediately after removal
from the body, determined the longitudinal elastic powers.
A lateral distensibility was determined by immersing the
distended vessel in a cylinder of mercury and then increas-
ing the internal pressure by a second column of fluid.
Israel's observations on the elasticity of vessels were similar
to those of Polotebnow. He further found that the aortas
of chlorotics were still less resistant and more elastic than
those of normal individuals.
Luntz, another pupil of Thoma, determined the normal
elasticity of the vessels of cats and then compared the
results with those obtained in cats poisoned with phosphorus,
mercury, and lead. His conclusions are parallel to those of
Thoma in showing that these poisonings during the subacute
stage render the arteries less elastic (i.e., less resistant to a
distending force). He does not find, however, that patho-
logical changes are evident to the eye.
Aschoff believes that mechanical irritation of the blood
vessels plays a verydecided part in the production ofarterio-
sclerosis, though he admits that at the present time we are
not in a position to make any very decided statements on
this question. He suggests that our examinations of blood
vessels have not taken into account the "progressive develop-
ment" of elastic tissue in the media up to a definite period
of life. The " progressive changes," as noted by Aschoff,
consist of an increase in the elastic fibers, wvhich this author
300 FOSTER.
believes to be the result of increased pressure on the arterial
wall. It would appear from Aschoff's conclusions that the
blood pressure or rather arterial tension, increases up to the
thirty-fifth year. He furtherpoints out that there are certain
degenerative changes which take place in old age. These
are sometimes of the nature of fatty, hyaline, or calcareous
degenerations.
The fine elastic fibrils become loosened and more spread
out, and he believes that there is a certain amount of loss of
the elastic tissue as a result ofthe wear and tear of life.
The histological changes that occur in elastic fibers during
the process of disease and arteriosclerosis have been much
studied, but the inferences drawn by some of the older
observers do not bear criticism. The histological technic
then in use, particularly the use of certain fixing fluids and
copious alcohol, made it possible that artefacts were not
infrequently produced and observed as pathological changes.
Manchot,Weissmann, and Neumannhave laid greatstress on
the fragmentation of the elastic fibers which was observed in
sclerotic vessels. This lesion is also noted by Zwingmann,
who notes the possibility that rupture of the elastic fibers
may occur in the process of the preparation of the speci-
mens. This is later emphasized by Schulmann, who notes
that fragmentation is evident in hardened preparations under
both normal and pathological conditions.
In one form of degeneration the elastic fiber is represented
by a line of irregular granules which take the elective elastic
stains. Weissmann, Neumann, and Manchot observed this
form of degeneration in the early stages of arteriosclerosis
and aneurism. Dmitrijeff concludes that in arteriosclerosis
there is both disappearance and new growth ofelastic tissue;
the former, essentially a degeneration, is seen in the early
stages and primarily is marked by changes in tingibility,
followed by morphological alteration and eventuallynecrosis.
The newly formed elastica, like some other young tissues,
possesses less resistance to noxious influences and hence
yields readily before excessive pressure or deleterious
bodies.
CHANGES OCCURRING IN THE AORTA. 301
Jores has described a fatty degeneration of elastic fibers
occurring in the absence of other signs of a degenerative
process. In association with this condition, he has noticed
granulation of neighboring fibers and for this reason believes
that both these changes are due to the same cause.
Methods. - In order to study the progressive develop-
ment and regressive changes occurring in the elastic tissue of
the media a series ofsections was prepared from the thoracic
and abdominal aortas of persons ranging in age from six
months up to eighty years of life. The sections were taken
from apparently healthy portions ofthe aortic wall and never
from localized areas showing atheromatous ulceration, fatty
streaks or plaques of degeneration.
Histological technic. - The tissues were fixed in five per
cent formalin and the sections cut on the freezing micro-
toime.
The stains employed were hematoxylin (Boehmer's) and
eosin, Sudan III., Weigert's elastic tissue stain, Van Gieson's
and five per cent silver nitrate solution.
Material. - The age, sex, cause of death, macroscopical
and clinical findings of the cases examined were as follows:
Sex. Age. CauseofDeath. IntiMmaacroofscA.orta ClRiandiciaalllsy.
Female ... 6 mos. Inanition ............ Normal.... Normal.
Male..... 4yrs. Appendicitiswith perf.. Normal......... Normal.
Female ... 7 yrs. Acute lobar Pneumonia. Normal......... Normal.
Female ... Ioyrs. Gangrenous Appendix
withperforation. Normal.... Normal.
Male ..... 14yrs. Acutelobar Pneumonia. Recent fatty
streaks. Normal.
Male . 17 yrs. Gangrenous appendix
withperforation ..... Recent fatty
streaks .. Normal.
302 FOSTER.
Sex. Age. CauseofDeath. IntiMmaacroofscA.orta ClRiandiicaalllsy.
Female I9yrs. Chronicsclerotic Aortic
... and Mitral Endocar-
ditis................ Fattyplaques on
intima ....... Normal.
I2I Pancarditis: Chr. scle-
Male yrs.
rotic Endocarditis.... Fattyplaques on
intima........ Normal.
Female 23yrs. Hyperemesis Gravido-
... rum (acouchement
force) .............. Recent fatty
streaks ....... Normal.
Female 24yrs. Typhoid feverwithPeri-
... tonitis.............. Recent fatty
streaks....... Normal.
Female 25 yrs. Acute cardiac Dilata-
... tion (alcoholic)...... Fatty streaks,
early Monke-
berg ......... Normal.
Male ..... 27yrs. Acutelobar Pneumonia. Recent fatty
streaks ....... Normal.
Male ..... 30yrs. Typhoid fever......... Normal ........ Normal.
Female 32yrs. Puerperalsepticemia Normal ........ Normal.
... ...
Female 34yrs. Typhoid fever with per-
... foration ............ Recent fatty
streaks ...... Normal.
Female 136yrs. Pregnancy with rupture
... of Vagina (puerperal
state) ............. Recent fatty
streaks....... Normal.
Male ..... 38yrs. Acuteepidemic cerebro-
spinal Meningitis..... Recent fatty
streaks ....... Normal.
Male ..... 39 yrs. Acuteplastic Peritonitis. Normal ....... Normal.
Female ... 40yrs. Mitral stenosis with se-
quelae .............. Fatty change of
intima.. ...... Normal.
Male 42yrs. D.T. with heart failure,
. (chr. sclerotic endo.) EarlyA.S....... Slight
thickening.
Male ..... 45 yrs. Typhoid fever ......... Recent fatty
streaks....... Normal.
CHANGES OCCURRING IN THE AORTA. 303
Sex. Age. CauseofDeath. IntiMmaacroofscA.orta ClRinaidciaalllsy.
Male ..... 47yrs. Acute lobar Pneumonia. A.S.withath.ulc. Normal.
Female ... 48yrs. Acutelobar Pneumonia. Fatty streaks
along intercost. Normal.
Female ... 49 yrs. Mitral stenosis with ac.
lobar Pneumonia .... Fatty streaks
along intercost. Normal.
Female ... 50yrs. Emabrotl.i.s.m...o.f...c.e.r.e.b.r.al. Slight fatty
change....... Slight
thickening.
Male . 5i yrs. RecwiutrhreTnbtc.h.e.a.r.t.d.i.s.e.as.e. Fatty calcareous
plaques ...... Marked
thickening.
Male .152yrs. Disaenadsekiodfnehyesa.r.t,...ve.s.s..,. A.S.with ath. ul-
ceration.... Marked
thickening.
Male ' 5 yrs. Duodenal ulcer with
perf.and Sequele Slight A.S. with
.... cal. plaques ... Slight
thickening.
Male 56yrs. Epithelioma complicat-
. ing Diabetes........ A.S.with ath. ul-
ceration ...... Marked
thickening.
Male 58yrs. Typhoid feverwith mul-
. tiple thromboses Recent fatty
... streaks ....... Normal.
Male ..... 6oyrs. Chr. mixedNephritis .. A.S. with calc.
plaques....... Marked
thickening.
Male ..... 62yrs. Uremia (chr. mixed
nephritis) ......... A.S. with ath. ul-
ceration ...... Normal.
Male ..... 64yrs. Myocarditis with A.S. A.S.withath.ulc. Normal.
..
Male ..... 66yrs. PerniciousAnemia .... A.Sc.erwaittihona.th....u.l.- Marked
thickening.
Female ... 72yrs. Strhaenrgnuilaawtietdhfpeermitoonirtais1 Slight fatty
plaques....... Normal.
Male 76yrs. General A.S. of median
. vess. and Kidney A.S. with ath. ul-
.... ceration ...... Marked
thickening.
Male 80yrs. Heart disease (mitral
. stenosis) and A.S.... A.S. withath.ul-
ceration ...... Marked
thickening.
304 FOSTER.
HISTOLOGICAL FINDINGS.-Aorta ofsix months' oldchild: The sec-
tion shows that the intima is fairlywell developed. With nuclear stains
one is particularly struck with the cellular character ofthe media. In this
tunic the muscle nuclei are closely packed and arranged in concentric
lamell] about the lumen ofthe vessel. The vasavasorum penetrateup to
the middle third ofthe muscularis.
The internal elastic lamina stains more deeply and forms a strand a
little more prominent than the other elastic fibers. Occasionally it is
found that this innermost fiber splits into two layers.
The concentric elastic fibers of the media proper separate the muscle
lamellze by narrow wavy strands placed at regular intervals from the
internal lamina to the adventitia. The structure of the fibers is uniformn
and their staining qualities appear equal. Each fiber consists of a well-
defined thread wavy in character, with sharp borders and a homogeneous
structureless body. It is not possible to distinguish fibrils in the main
body ofthe fiber. There is no evidence ofa collagenousnetworkbetween
the main concentric fibers.
As one passes from the media into the adventitia the elastic fibers
become broken up into fine threads, which are woven about muscle and
connective tissue strands. The concentric arrangement is lost and many
fibers pass in a longitudinal direction with the vessel. There is no evi-
dence of rupture of the main fibers of the media. In bulk the elastic
fibers of the media form much the lesser quantity of the tissue of this
tunic.
Artery, age4years: The intimais fairly welldeveloped. The general
character of the elastic fibers of the media is like that in the above
described artery. It is to be noted, however, that fine threads of elastic
tissue occasionally cross the muscle bundles and,joining the main elastic
fiber, are lost in its substance.
Artery, age 7 years: The elastic structure of the media differs very
little from that at four years. The fine elastic threads crossing the
muscle bundles are somewhat increased in number. At intervals the
main fibergives offa branch almost equal in size to itselfand of the same
structure. Such branches pass to the neighboring fiber and intimately
fuse with it.
The elastic lamellae still retain their homogeneous character and well-
defined borders.
The material difference in the structure of the media at this age and
during the first year oflife is a noticeable increase in the elastic fibrils.
Artery, age io years: The intima is narrow and of constant width
throughout. The internal elastic lamina occasionally splits into two
layers, the main fiber usually keeping the outer course, while fine fibrils
pass into the developing intima. In otherplaces, however, the reverse is
seen.
The general character ofthe elastic fibers ofthe media differs from that
in the preceding sections in showing a more decided character to the
newly-formed elastic tissue. Whereas these fine elastic fibrille coursed
CHANGES OCCURRING IN THE AORTA. 305
through the muscle bundles as insignificant threads, these have now
developed into structures like the twigs of a tree.
Artery, age 14years: The intima is well developed and of constant
width throughout. The internal elastic lamina has sent numerous fine
branches into the intima. These branches have no arrangement in com-
mon with the structures in the media, though their general direction is
circular.
The elastic fibers of the media have the same general characters as
found at ten years. The cross fibersjoining the main elastic lamellae are
somewhat increased insize and number.
The main features at this age are the strengthening ofthe cross fibers
in the mediaand the development of an elastic network in the intima. It
is also to be noted that inagiven section the muscle tissue is apparently
reduced.
Aorta, age 17 years: The intima ofthe aorta is well developed and of
normal width throughout. The internal elastic membrane is less defined
than in the previous aorte. There is no longer a single strand; in its
place are a number of parallel fibers, with a considerable numberoffine
elastic threads springing from theirborders. These fine fibrilloe runboth
into the intimaand towards the other elasticlaminae ofthe media.
The main elastic fibers of the media still retain this wavy character and
concentric arrangement, but the increased number ofcross fibers and fine
fibrilla springingfrom their borders somewhat impairs their well defined
clear-cutoutline andgives to the edges a raggedappearance.
It would appear that the larger fibers of the newly developed elastic
tissue between the lamelle were the more mature production ordevelop-
ment of this network. It is quite evident that the newly formed elastic
fibrils have theirorigin from the larger strands.
Aorta, age igyears: The main elastic fibers of the xnedia and the
newly formed interlacing network between the concentric lamellae have
much the same characters as found at the age of seventeen. Notinfre-
quently centers of distribution of elastic fibers with spider-like processes
are seen. These centers are located on the sides of the main elastic
trunks.
Artery, age 19 years: This section shows a little thickening of the
intima with a fatty change of its deep tissues. There isalso some fatty
infiltration ofthe adjacent muscle bundles ofthe media.
The elastic fibers of both intimaand mediaappear unchanged by these
recent conditions, save that in places the fatty infiltration of the muscle
has caused the elastic fibers to be pushed apart. In general, the elastic
fibers of the media simulate very closely those described at seventeen
years.
Artery, age 21 years: This section also shows a slight thickeningof
the intima andthe same fattychanges as noted in the previous artery.
The elastic fibers of the media are not so regularand smooth in their
contour as seen at earlier ages. Occasionally some of the concentric
fibers are seen to split up into several fine strands and continue on inan
306 FOSTER.
arborescent manner, interlacing with neighboring fibers. In places the
concentric arrangement is notso readily apparent, because of the splitting
up ofthe mainelastic bandsand the richlydeveloped elastictissuenetwork
between the main fibers.
In roughly judging this specimen one would say that the amount of
elastic tissue is equal to the amount ofmuscle tissue in the media.
Artery,age 23years: The character ofthe elastic fibers in this section
is very similar to that at twenty-one years, but when compared with the
fibers in the first year there is avast difference in appearance. The main
fiber has doubled in size and its borders are rough and ragged. In many
places the fibers split up into small fibrils and there separate and arborize
around neighboring strands. The number of cross fibers is markedly
increased. The concentric arrangement of the main fibers is even more
impaired than in the previously described sections.
Artery, age 24 years: There is evidence of change in the media
which, however, does not appear to affect the elastic fibers. The muscle
bundles seem to show aconsiderable amount of fatty change. At certain
points there is the appearance that someofthe muscle tissue has been lost
with a corresponding increase in the elastic tissue ofthe part.
Artery, age 25years: The elastic fibers ofthe mediatake afairly even
coursebetween the muscle bundles. The numberof cross branches link-
ing neighboring lamello together has materially increased. The network
ofnewly formed elastic tissue has become a very prominent structure; the
larger fibrils, apparently springing from the main fiber, have developed
into quite significant strands and have a concentric arrangement in
common with the main band.
Artery, age 27 years: Similar features to those noted at the age of
twenty-five.
Artery, age 30years: Theintima isrelativelythickened. The internal
elastic lamina stains deeply, its borders are rough and have a moth-eaten
appearance. Atcertain points this strand becomes fibrillated and sends
branches into the intima and media.
The elastic fibers ofthe media have lost their wavy character, and much
of their concentric arrangement. The cross fibers joining neighboring
lamellke together have increased in number and are quite as stout and
rough as the main fiber. This fact, together with the increased size of
the strands making up the interlamellar network, impairs the even course
and concentric arrangement ofthe circular lamelle and gives to the whole
the irregular roughened character ofcoral branching.
The spaces occupied by the muscle bundles are encroached upon and it
would appear that there was a relative decrease in the muscle element.
Aorta, age34years: The intima is relatively thickened and shows
evidence offatty change. There is also some fatty degeneration of the
muscle bundles, more especially those nearest the intima. The elastic
fibers appearunaffected by this change, and the general characters of the
elastic tissue in the media are as described under the age ofthirty.
Theconcentric arrangement is markedly impaired, save fora few ofthe