Reprint Albany Medical Annals, June, 1888. 
CLINICAL REPORTS. 
II. 
TRA UM A TIC RUPTURE OF THE VALVES OF 
THE HEART. 
By HENRY HUN, M.D., 
Professor of Diseases of the Nervous System and of Psycho- 
logical Medicine in the Albany Medical College. 
ALBANY, N. Y., 
The question whether external vio- 
lence or a sudden strain of the body can 
cause a rupture of the valves of the 
heart is a very interesting one. Theo- 
retically it seems possible that any sud- 
den effort, which causes an intense and 
universal muscular contraction through- 
out the body, might result in such a great 
and sudden increase in arterial tension 
as to cause a rupture of the delicate 
semi-lunar valves, especially when at the 
same time the body, and in particular 
the aorta, already put on a stretch by the 
increased arterial tension, receives a vio- 
lent jar. The result of daily experience, 
however, shows that such an accident 
is very uncommon, even in the case of 2 
the aortic valves, which are much more 
exposed to such an injury than the mi- 
tral valves. Very few cases of such 
accidents have been reported, and the 
cases are extremely rare which show 
with any probability that healthy valves 
are ever the seat of traumatic rupture. 
The following case is one in which a sud- 
den muscular effort seems to have caused 
a rupture of aortic valves, which had 
previously exhibited no symptoms of 
disease. 
R. O. K., set. 40. In November, 1883, 
the patient, who was tall and thin, but 
muscular, and had always been healthy 
and had never had rheumatism, lifted a 
heavy box from a shelf on a level with 
his head and placed it on the floor. As 
he did so he felt something give way in 
the front of his chest, and felt something 
fluttering and jumping inside of him. 
He felt so faint and weak that he had to 
be taken home in a carriage, and was 
confined to his bed for a couple of weeks. 
He never was able to resume work, and 
for the most part was confined to the 
house, rarely being able to take a short 
walk. In March, 1884, he fainted and 3 
remained in a condition of collapse for 
several days, recovering from it very 
slowly. At that time his heart was ex- 
amined. The area of cardiac dullness 
was slightly enlarged, and a loud, smooth 
diastolic murmur was heard over the 
aortic valves, and was propagated down- 
wards towards the apex. No other 
murmur could be detected either over 
the heart or the vessels of the neck. 
The pulse was feeble and rapid. He had 
one or two more fainting fits, and on the 
evening of December 26, 1884 (a little 
more than a year after the accident), just 
after getting into bed, he suddenly died 
without any warning. 
Unfortunately there was no autopsy 
held in this case, but it seems very proba- 
ble that the suddenly increased arterial 
tension caused by the muscular effort of 
lifting the box down from the high shelf 
had torn one of the aortic valves; for 
immediately afterwards he had severe 
palpitation and symptoms of heart dis- 
ease, which persisted up to the time of 
his death. In accordance with this sup- 
position was the fact that the only mur- 
mur heard was that of aortic regurgita- 4 
tion, and the lesion could not have been 
of long standing, as there was no cardiac 
hypertrophy. Of course, no absolute 
proof can be offered in this case that the 
aortic valves were perfectly healthy at 
the time of the muscular exertion, but 
certainly up to that time there were no 
symptoms of heart disease, and ever 
afterwards such symptoms were ex- 
treme. The mere fact that the symp- 
toms of heart disease did not appear till 
after the accident is not in itself alone a 
sufficient proof that there was not pre- 
viously existing heart disease, as is illus- 
trated by the following case. 
J. L., set. 43. In October, 1887, the 
patient, who was a strong, muscular man, 
and had always been well, had never had 
rheumatism, and had never noticed any 
dyspnoea on exertion, was kicked by a 
horse. (The scar of the kick still re- 
mains over the middle of the left biceps 
muscle.) He was knocked about ten 
feet, striking on the right buttock. He 
was not confined to the house, but did 
not work for three weeks on account of 
his arm. At the end of three weeks he 
resumed work, and then for the first 5 
time noticed that his breath was short, 
and he found that he became so weak 
that he was unable to work. He had no 
palpitation and no pain in the chest. An 
examination of the patient was made on 
November 17, 1887, at which time the 
area of cardiac dullness was much in- 
creased, commencing above on second 
rib, running one inch to the left of the 
left nipple and one inch to the right of 
the right border of the sternum. The 
heart's action was violent. A loud 
double blowing murmur heard over the 
whole front of the chest and faintly over 
the back, being loudest in the second 
right intercostal space close to the ster- 
num. There was a strong systolic thrill 
in both subclavians, and a double mur- 
mur in the subclavian and also in the 
femoral on deep pressure. Some fine 
moist rales at base of chest on both 
sides. A sphygmographic tracing of the 
pulse is shown in the accompanying 
figure. The patient steadily failed in strength, and suddenly died without any 
warning on January 10, 1888, about 
three months after the accident. At the 
autopsy, which was held thirty hours 
after death, the heart was found im- 
mensely hypertrophied and dilated. Al- 
though greatly dilated, the wall of the 
right ventricle was more than an inch 
thick. Except for a small calcareous 
plate at the base of one of the aortic 
valves, which did not interfere with its 
function, all the valves were normal, and 
the muscular tissue seemed healthy. 
The mitral orifice was dilated, admitting 
the ends of three fingers easily, and the 
aortic orifice was decidedly dilated. The 
arch of the aorta was also the seat of a 
great but uniform dilatation, and the 
intima was everywhere yellow and irregu- 
lar, like the skin of a rough orange. 
In this case the symptoms were due to 
a dilatation and loss of elasticity of the 
aorta and an enlargement of the aortic 
orifice, which were of such old standing 
that they had caused an extreme degree 
of cardiac hypertrophy, which in turn 
had made an apparently perfect compen- 
sation for the aortic lesion until after the 
6 7 
accident, and probably in consequence of 
this latter, this compensation was de- 
stroyed. 
Although the symptoms of heart dis- 
ease in this case did not appear until after 
the accident, yet there were many things 
which made it clear that this was not a 
case of traumatic rupture of the valves. 
In the first place, dyspnoea and weakness 
made their first appearance three weeks 
after the accident; in the next place, 
there was a double aortic murmur; 
whereas, if the aortic valves had been 
torn, there should have been a regurgitant 
murmur only ; then, the sphygmographic 
tracing was not that of aortic regurgita- 
tion ; and, finally, there was an extreme 
degree of cardiac hypertrophy, which 
showed that there was a heart lesion of 
much earlier date than the time of the 
accident. 
This second case, then, teaches us that 
we must be cautious in considering car- 
diac symptoms which appear after a 
severe injury as necessarily due to the 
injury, and therefore of a traumatic 
nature, but it does not in the least invali- 
date the claim of the first case to be 8 
regarded as a case of traumatic rupture 
of the aortic valves. The question as to 
the traumatic nature of the first case has 
a decidedly practical bearing, inasmuch 
as the patient had an accident insurance 
policy on his life. The claim, I believe, 
was never pushed by the family, and was 
never paid by the company, and yet 
strong proof could have been offered 
that his death was due to an accident.