"CARDIAC CIRRHOSIS" OF THE LIVER.

A CLINICAL AND PATHOLOGICAL STUDY.

(Abstract.)
By HERRMAN L. BLUMGART, M.D., AND (by invitation)
HERBERT KATZIN, M.D.,
From the Medical Research Laboratories of the Beth Israel Hospital, and the
Department of Medicine, Harvard Medical School, Boston.
This investigation was aided by a grant from the DeLamar Mobile Research Fund.
The term "cardiac cirrhosis" is used to denote various condi
tions; according to some authors, the term signifies any type of
hepatic fibrosis occurring in a cardiac patient; to others it signifies
that the hepatic fibrosis is due to congestive failure, while some
authors reserve the application of the term only to those cases in
which cirrhosis of the liver due to congestive failure is responsible for
clinical manifestations of portal obstruction. Thus, the varied usages
of the term imply a simple co-existence of hepatic fibrosis and cardiac
disease, a causal interrelationship between the two anatomic condi
tions, or a causal morphological interrelationship which results in
clinical manifestations of portal obstruction.
These different connotations of the term have been responsible
in part for the conflicting statements in the literature. There has also
been considerable discussion as to the site and nature of the fibrosis
in the liver, 'certain authors believing that this apparent fibrosis
represents only a simple condensation of reticular fibers almost always
confined to the centers of the lobules, whereas other investigators
attribute the changes to active proliferation of fibroblasts. Con
fronted in certain cases of congestive failure with the question of the
presence of cardiac cirrhosis and with the paucity of pertinent avail
able information, we undertook the following investigation of an un
selected series of consecutive autopsied cases in order to learn: ( 1)
the incidence of hepatic fibrosis in all cases with congestive heart
failure; (2) the types and degrees of such hepatic fibrosis found in
the cases of congestive failure of varying duration; (3) a comparison
of these findings with those found in the cases without congestive fail-
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 "CARDIAC CIRRHOSIS" OF THE LIVER 83

ure ; (4) the incidence of hepatic fibrosis in patients with congestive

failure compared to that in patients with biliary tract disease.
Such a comparison of the incidence and degrees of the various
types of hepatic fibrosis in cardiac and non-cardiac cases should indi
cate the significance of congestive failure as an etiological factor in
causing cirrhosis of the liver.
Two thousand consecutive autopsy protocols were examined, and
the following three groups of cases were selected for further study in
order to ascertain the interrelationship of chronic passive congestion,
hepatic cirrhosis and certain other possible etiological factors in the
production of this connective tissue increase. All cases in the series
of 2000 showing chronic passive congestion, all those showing hepatic
fibrosis, and all those showing disease of the biliary tract were placed
in three separate groups.
A study was made of the 95 cases in which chronic passive con
gestion coexisted with cirrhosis, to ascertain the following facts: (1)
the incidence of the types and extent of fibrosis; (2) the relation
between the incidence of cirrhosis and the duration of congestive fail
ure; (3) the relation between the degree of fibrosis and the duration
of congestive failure; (4) the relation between the duration of failure
and the presence, type and degree of fibrosis in the cases that showed
predominant ascites; (5) the incidence of ascites, anemia and
jaundice.
It was evident that the incidence of fibrosis was higher in the
cases with chronic passive congestion than in the entire unselected
series; consequently it became of interest to ascertain whether mini
mal changes in the liver were responsible for this finding. This did
not prove to be the case.

DISCUSSION OF RESULTS.

Of patients dying with congestive heart failure, approximately

one-third showed increased hepatic fibrous tissue, which was twice
the incidence found for the entire 2000 consecutive autopsies. The
proportion of cases showing the various degrees of fibrosis was, in
general, similar in the cases with and without congestive heart failure.
Further, the incidence of fibrosis in patients with chronic passive
congestion increased with the duration of failure, and the more severe
grades were found in those patients in whom the illness was of longest
84 HERRMAN L. BLUMGART AND HERBERT KATlIN

duration. Thus, the causal significance of chronic passive congestion

in the production of hepatic fibrosis is emphasized by the increasing
incidence and severity of the fibrosis with increasing duration of con
gestive heart failure. The only type of fibrous tissue increase peculiar
to this group of patients with cardiac decompensation was central
fibrosis, for with one exception no instance of central fibrosis was
found among the 1714 autopsies not showing congestive failure.
. It should be noted that other types of fibrosis were also found
in the cases with chronic passive congestion. Indeed, the incidence of
each of the various kinds of fibrosis, except biliary, was higher in the
group with congestive failure than in the remaining 1714 cases. Of
particular interest was the finding of increased periportal connective
tissue in 23 per cent of the 286 patients with congestive failure, as
compared to 9 per cent in the 1714 cases without chronic passive con
gestion. The occurrence of but two instances of biliary cirrhosis in
the entire group of cases with chronic passive congestion indicates
the absence of etiological relationship between these two conditions;
two instances are within the expected incidence in 95 random
autopsies.
Since it is commonly accepted that diseases of the biliary tract
are an important etiological factor in hepatic fibrosis, it was of in
terest to learn that congestive failure is of comparable etiological
significance.
Clinical cardiac cirrhosis, signifying extreme fibrosis, which
clearly results from chronic passive congestion and which causes evi
dences of portal obstruction, does occur but is rare. Of the 286 cases
with congestive failure there were only 15 cases which showed
marked, but not necessarily predominant ascites requiring abdominal
paracentesis. Six of these fifteen cases on autopsy examination
showed cirrhosis of the type caused only by chronic passive conges
tion, namely, central fibrosis. Although the majority of those who had
failure one year or more showed increased fibrous tissue, they did not
necessarily show preponderant ascites. The presence of anemia or
jaundice in. congestive failure was not closely correlated with the
postmortem finding of a pathological increase of connective tissue;
these factors are consequently of no value in diagnosing hepatic cir
rhosis clinically.
 "CARDIAC CIRRHOSIS" OF THE LIVER 8S

Morphological evidence of increased fibrosis of the liver was

seen in all of the six cases that had recurrent ascites, and were in fail
ure two years or more. The clinical diagnosis of cardiac cirrhosis,
signifying increased fibrous tissue in the liver, can be made, there
fore, with considerable assurance in all cases of this type. If there is
no marked portal obstruction, the fibrosis is not clinically important.
From these studies, it would seem that cardiac cirrhosis signify
ing morphological increase in connective tissue in the liver conse
quent to congestive failure is present in approximately 50 per cent of
all patients who have had congestive failure nine months or more.
While central cirrhosis is characteristic of congestive failure and does
not occur in patients with biliary tract disease, it would appear that
other portions of the liver are also more susceptible to injury in
patients with chronic passive congestion. Thus, 48 uncomplicated
instances of periportal fibrosis were encountered in the group of 286
cases of chronic passive congestion, which contrasts with an expectan
cy of but 30 cases if congestive failure were not a contributory factor.
The occurrence of 17 additional cases in which definitely increased
fibrosis of both the central and portal areas was found is further evi
dence of an increased susceptibility of the portal areas to injury
under such circumstances.
Excluding the cases which showed increased connective tissue in
both central and portal areas, the incidence of portal fibrosis in the
286 cases of congestive failure was 17 per cent, compared to an inci
dence of central cirrhosis of 9 per cent in these cases. The significance
of alcoholism as a contributory factor could not be accurately
appraised, although increased consumption of alcohol was not appar
ent in the records of the patients with congestive failure.
From the foregoing evidence, the meaning of the term "cardiac
cirrhosis" is clarified. In the morphological sense of increased fibrosis
being due to chronic passive congestion, one may state that the
majority of patients who have suffered from even mild congestive
failure for 9 months or more show increased fibrosis of the liver,
either central or portal, or a combination of both.
Whether cardiac cirrhosis in the clinical sense of increased
fibrosis causing clinical manifestations is present or not must be
based on clinical evidence. If there is preponderant ascites, if there is
marked elevation of the venous pressure but the liver is not palpable,
86 HERRMAN L. BLUMGART AND HERBERT KATZIN

and particularly if the spleen is palpable, clinical cardiac cirrhosis may

be assumed to exist. In a patient in whom the diagnosis of clinical
cardiac cirrhosis is made, one may find portal or central fibrosis or a
combination of these types, or diffuse patchy fibrosis. A reverse
situation may be present in some patients, however. Even after the
subsidence of the elevated venous pressure, the liver may be enlarged
and ascites may be present. In such cases which represent an earlier
stage of the one previously mentioned, the sinusoids are still dilated,
increased fibrous tissue is present, and the surface of the liver is non
tender and sometimes somewhat irregular.