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Hypertrophic Cardiomyopathy in the Dog

Si-Kwang Liu, DVM, PhD, Barry J. Maron, MD,


and Lawrence P. Tilley, DVM

Clinical and necropsy findings in 10 dogs with a spontaneous primarv hvpertrophic


cardiomyopathy are described. Each dog had marked cardiac hypertroph, and 8 dogs
had disproportionate thickening of the ventricular septum with respect to the left
ventricular free wall (compared with dogs with normal hearts or with cardiac hyper-
trophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in
the 10 dogs ranged from 1.1 to 1.5; 6 had ratios . 1.3. However, marked cardiac muscle
cell disorganization in the ventricular septum, characteristic of patients with hyper-
trophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most
commonly while the dogs were under anesthesia during the course of operative proce-
dures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic
manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive
heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4
dogs with heart failure and 1 dog without previous symptoms (that died during a
noncardiac operation) manifested complete heart block. It is conceivable that dogs with
spontaneous hypertrophic cardiomyopathy may prove useful in the future investiga-
tions of the clinical, hemodynamic, and pathologic features of this disease in humans.
(Am J Pathol 94:497-508, 1979)

HYPERTROPHIC CARDIOMYOPATHY is a disease of cardiac muscle


in which the most characteristic anatomic feature is a disproportionately
thickened ventricular septum `6 containing numerous disorganized car-
diac muscle cells.7 9 Since animal models of hypertrophic cardiomyopathy
wvould be useful in the studs' of this disease, identification of spontaneous
cardiac diseases in animals similar to hyrpertrophic cardiomyropathy in
humans is of particular interest. In this regard, a form of feline cardiac
disease with manv of the features of hypertrophic cardiomyopathy has
been recently reported.10 The present report describes, for the first time, a
spontaneous primary cardiomyopathy in dogs that also resembles hyper-
trophic cardiomyopathy in humans.34
Selection of Animals
The cardiovascular registry of The Animal Medical Center, 1975 to
19 7, was reviewed. During that period, 177 dogs with cardiac disease
From the Departments of Pathology and Medicine. The Animal Medical Center. New- York. New-
l'ork, and the Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of
Health. Bethesda, MIarvland
Supported in part by grant-in-aid from the New York Heart Association.
Accepted for publication Nosember 1. 1978
Address reprint requests to Dr. Si-Kwang Liu. Department of Pathology. The Animal Medical
Center. .510 East 62nd Street. Nesw York. NY 10021
0002-9440/79/0308-0497$01.00 497
( American Association of Pathologists
498 LIU ET AL American Journal
of Pathology

were examined at necropsy; 10 of those dogs were identified as having


anatomic features of a primary hypertrophic cardiomyopathy (as will be
discussed in detail below). In addition, 11 dogs with normal hearts that
died of noncardiac diseases and 84 dogs with other acquired or congenital
heart diseases were studied for comparative purposes. The latter 84 dogs
included 19 with congestive (dilated) cardiomyopathy, 18 with acquired
mitral valvular disease, 20 with congenital malformation of the mitral
valve complex," 13 with dysplasia of the tricuspid valve,12 and 14 with a
variety of other congenital cardiac malformations (including 4 with dis-
crete subaortic stenosis, 6 with patent ductus arteriosus, 2 with ventricular
septal defect, 1 with atrial septal defect, and 1 with tetralogy of Fallot).
Materials and Methods
Gross Pathology
After removal from the body, hearts (with approximately 2 cm of the great arteries
attached) were trimmed rigorously of fat and blood was removed from the chambers.
Measurements of ventricular wall thicknesses were made (in the fixed specimen) in the
following areas: a) ventricular septum in the area of maximal thickening approximately
one third to one half the distance between the aortic valve and left ventricular apex; b)
posterior left ventricular free wall directly behind the midpoint of the posterior mitral
valve leaflet and at the level of the inferior extent of the mitral leaflets; c) anterolateral left
ventricular free wall approximately 2 cm lateral to the anterior descending coronary artery;
and d) right ventricular wall near the tricuspid valve anulus. Care was taken to avoid
including trabeculae, papillary muscles, or crista supraventricularis in the measurement of
wall thickness.
Histology
Blocks of myocardium were taken from the full thickness of a) ventricular septum in the
area of maximal thickening approximately one third to one half the distance between the
aortic valve and left ventricular apex; b) posterior left ventricular wall approximately one
half the distance between the mitral valve anulus and left ventricular apex, and c)
anterolateral left ventricular free wall approximately 2 cm lateral to the anterior descend-
ing coronary artery. All tissue specimens were embedded in paraffin, sectioned at a
thickness of 6 ,, and stained with hematoxylin and eosin. The extent of disorganization of
cardiac muscle cells was initially assessed qualitatively in each tissue block. In addition,
the extent of disorganization was assessed quantitatively Is in the five tissue sections (four
of ventricular septum and one of posterior left ventricular wall) in which abnormally
arranged cardiac muscle cells were evident. Tissue sections were photographed, positive
prints were magnified to approximately 1000 times the size of the original section, and a
transparent cellulose overlay was placed over the print. Areas of myocardium occupied by
cardiac muscle cells that were cut in longitudinal or transverse section or judged to be
abnormally arranged were outlined separately on the transparent overlay. These respec-
tive areas of myocardium were quantitated utilizing video planimetry.14 The extent of
disorganization was expressed as the area of myocardium occupied by disorganized cells
divided by the total area of myocardium occupied by cardiac muscle cells viewed in
longitudinal section.
In 2 dogs with complete heart block (A17741 and A18460), tissue was removed from the
Vol. 94, No. 3 HYPERTROPHIC CARDIOMYOPATHY 499
March 1979

heart for histopathologic study of the conduction system.'5 These tissue blocks included
the junction of the interatrial and interventricular septums, from the posterior margin of
the noncoronarv sinus of the aorta to the anterior margin of the coronary sinus. Serial
sections 6 p in thickness were cut perpendicular to the line of junction of the interatrial and
interventricular septums. Every 20th section was stained with either hematoxylin and
eosin or Masson's trichrome before examination.

Results
Clinical Fkidings and Ccurnstances of Death
Clinical findings in the 10 dogs with hvpertrophic cardiomvopathy are
summarized in Table 1. At death, ages ranged from 1 to 13 years (mean, 6
years). Eight dogs were male and 2 were female. Of the 10 dogs, 4 were
German Shepherds and 1 each was a Doberman Pinscher, Airedale, Great
Dane, Boston Terrier, Poodle, and Bulldog.
Four of the 10 dogs had evidence of congestive heart failure 1 week to 1
year prior to death. In 2 dogs (A14586 and A15978) cardiac decompensa-
tion was mild and was manifested by coughing, mild dyspnea, and radio-
graphic evidence of pulmonary venous congestion. In 2 other dogs (18109
and A18460) cardiac failure was marked, as evidenced by severe dyspnea,
cardiomegaly, hepatomegaly, and pleural or pericardial effusions. Three
of the 4 dogs with heart failure died unexpectedly while under anesthesia
during operation (1 each for repair of a skin laceration, pacemaker im-
plantation, and pericardiocentesis); the remaining dog was put to death
by request of the owner.
Six other dogs with hypertrophic cardiomyopathy had no evidence of
cardiac disease prior to death, including 2 dogs that died unexpectedly
during operations for noncardiac abnormalities (A17741 and A18065) and
3 that died suddenly (A15053, A16059, and A16456). Of the latter 3 dogs,
1 collapsed while being walked and the other 2 were found dead by their
owner. The remaining dog (A16020) died of causes apparently unrelated
to heart disease, ie, renal failure of undetermined etiology associated wvith
disseminated intravascular coagulopathy.
Electrocardiographic Findings
Electrocardiographic recordings were obtained in 5 of the 10 dogs with
hypertrophic cardiomyopathy. Three dogs showed complete heart block
(Text-figure 1), including 1 with a history of syncope, that died during
implantation of a pacemaker (A14586). This latter dog and 1 other
(A18460) with complete heart block also showed evidence of bifascicular
block with left axis deviation and right ventricular conduction delay
(Text-figure 2). In 1 other dog (A17741) complete heart block wi-as noted
500 LIU ET AL American Journal
of Pathology

TEXT-FIGURE 1-Rhythm strip of Lead II, recorded in Dog A18460 1 day prior to death, showing
complete heart block. Ventricular rate is 70 beats/min. ECG recorded at 50 mm/sec.

just prior to death on a cardiac monitor during a urologic operation. Of


the 2 remaining dogs with electrocardiograms, 1 (A15053) showed first
degree atrioventricular block (PR interval = 0.15 second; normal < 0.13
second) and the other (A18109) was normal.
Necropsy Data
Gross Anatomic Findings
Fresh heart weights in the 10 dogs with hypertrophic cardiomyopathy
(9.6 0.3 [SE] g/kg) were significantly greater than in dogs with normal

I II III

TEXT-FIGURE 2-Electrocar-
diogram recorded in Dog
A 14586 1 day prior to death,
showving left anterior hemi-
block and right ventricular
conduction delay (QRS dura-
tion = 0.09 second; normal
< 0.06 second). T waves are
peaked and upright in Leads
II, I1I, AVF, and V3. rV2
is obtained at right fifth inter-
space at chondrosternal junc-
tion.

A14586
Vol. 94, No. 3 HYPERTROPHIC CARDIOMYOPATHY 501
March 1979

0
S

0
0
0

S
0
0

.
I

ow - .*..._ -
-90-
0

S *
so
i_
a.

* 0

I I I I I I
Normal Acquired MV TV Other Congestive Hypertrophc
MVD Complex Dysplasia Congenital Cardio- Cdrdio-
Malformation Heart Diseases myopathy mVopdthV
TEXT-FIGLRE 3-Septalfree wall thickness ratios in 10 dogs with hypertrophic cardiomyopathy
and 95 dogs with normal hearts or with other acquired or congenital heart diseases. Group marked
with asterisk includes 4 with discrete subaortic stenosis, 6 with patent ductus arteriosus, 2 with
ventricular septal defect, 1 with atrial septal defect, and 1 with tetralogy of Fallot.

hearts (6.6 0.3 g/kg; P < 0.001); heart weights in each of the 10
individual dogs with hypertrophic cardiomyopathy were equal to or ex-
ceeded heart weights in each of the dogs with normal hearts. Heart
weights in the dogs with hypertrophic cardiomyopathy (9.6 0.3 g/kg)
did not differ significantly from those in dogs with acquired or congenital
heart diseases (12.2 0.5 g/kg).
In the 10 dogs with hypertrophic cardiomyopathy, ventricular septal
thickness ranged from 13 to 22 mm (mean, 19 mm) and posterior left
502 LIU ET AL American Journal
of Pathology

Table 1-Clinical and Necropsy Findings in 10 Dogs With Hypertrophic Cardiomyopathy


Ventricular wall CMC
Heart wt. thickness (mm) disorganization*
Necropsy Age (yr)/
No. Sex Breed g g/kg VS PW AL RV VS/PW VS LVFW
A16020 8/M Doberman 311 9.5 21 14 23 7 1.5 0 0
A15978 4/M German Shepard 266 8.5 21 15 22 6 1.4 0 0

A15053 Airedale 153 10.6 17 12 12 6 1.4 0 0


A16059 7/M German Shepard 273 8.0 20 15 24 7 1.3 0 0
A18460 13/M Poodle 98 10.8 13 10 11 4 1.3 12% 8%t
A14586 6/F German Shepard 247 9.2 21 16 18 7 1.3 0 0
A16456 1/M Great Dane 385 10.4 22 19 21 6 1.2 0 0
A17741 3/M Bulldog 193 10.1 19 16 15 7 1.2 14% 0
A18065 3/M German Shepard 269 9.1 18 16 18 8 1.1 0 0

A18109 8/M Boston Terrier 116 10.2 16 15 12 4 1.1 0 0

VS = ventricular septum, PW = posterobasal left ventricular free wall, AL = anterolateral


left ventricular free wall, RV = right ventricular wall, VS/PW = ventricular septal to
posterobasal left ventricular free wall thickness ratio, LVFW = left ventricular free wall,
0 = absent, - = data not available, CHF = congestive heart failure, 10 A-V = first degree
atrioventricular, CHB = complete heart block, LAD = left axis deviation, RVCD = right
ventricular conduction defect, RVH = right ventricular hypertrophy
* Expressed as the area of myocardium involved by disorganized cells relative to the area
of myocardium containing cardiac muscle cells viewed in longitudinal section
t Disseminated intravascular coagulopathy at necropsy
t Combined tissue sections from anterolateral and posterior left ventricular free wall
Noted just prior to cardiac arrest on monitor; a complete scalar ECG was not obtained

ventricular wall thickness ranged from 10 to 19 mm (mean, 15 mm).


Septal:free wall thickness ratios ranged from 1.1 to 1.5; 8 dogs had ratios
> 1.1 and 6 had ratios > 1.3 (thereby meeting the diagnostic criterion for
disproportionate septal thickening in human patients 1,6) (Text-figure 3
and Figure 1). In none of the 95 control dogs (11 normals and 84 with
acquired or congenital heart disease) did the septal:free wall thickness
ratio exceed 1.1. Mean septal:free wall thickness ratio in the 10 dogs with
hypertrophic cardiomyopathy (1.3 i 0.04) was significantly greater than
in dogs with normal hearts (1.0 0.01; P < 0.001) and in dogs with
acquired or congenital heart disease (0.9 0.01; P < 0.001).
In 2 (A15053 and A16020) of the 10 dogs with hypertrophic cardiomy-
opathy, a fibrous endocardial plaque was present on the ventricular sep-
Vol. 94, No. 3 HYPERTROPHIC CARDIOMYOPATHY 503
March 1979

Clinical history Circumstances of death Electrocardiogram


No cardiac symptoms 1-week history renal failuret
2-week history mild CHF During surgery for repair of
skin laceration; under
anesthesia
No cardiac symptoms Sudden; found dead by 1 A-V block
owner
No cardiac symptoms Sudden; while being walked
1 -year history progressive Euthanasia CHB; LAD, RVCD,
CHF; syncope possible RVH
1-month history mild CHF; During pacemaker implan- CHB; LAD, RVCD,
syncope tation, under anesthesia possible RVH
No cardiac symptoms Sudden; found dead by
owner
No cardiac symptoms During surgery for urethral CHB
calculi; under anesthesia
No cardiac symptoms During surgery for repair
of fractured mandible;
under anesthesia
1-week history severe CHF; During pericardiocentesis Normal
pericardial, pleural effu-
sions, ascites

tum in the left ventricular outflow tract adjacent to the anterior mitral
leaflet (Figure 1). These endocardial plaques were similar in appearance
to those in patients wvith hypertrophic cardiomyopathy.4 In 2 other dogs
(A17741 and A18109) more diffuse fibrous tissue formation was present on
the ventricular septum in the left ventricular outflow tract. In each of the
10 dogs, the left ventricular cavity was moderately or severely reduced in
size; in 2 of these dogs the left atrium was moderately- dilated. The cardiac
valves appeared normal in each dog.
Histologic Findings
In 8 of the 10 dogs with hypertrophic cardiomyopathy and each of the
95 control animals studied, virtually all cardiac muscle cells in the ven-
tricular septum were in normal parallel alignment. However, in the
ventricular septum of the 2 remaining dogs, foci wvere present in which
cardiac muscle cells wvere arranged perpendicularly or obliquely to each
other (Figure 2). In quantitative terms, these areas of disorganized cardiac
muscle cells were marked, ie, occupied 14% (A17741) or 12% (A18460)
of the total area of mvocardium in which cardiac muscle cells were
viewved in longitudinal section.
All cardiac muscle cells in the left ventricular free wall of 9 of the 10
504 LIU ET AL American Journal
of Pathology

dogs were normally arranged. In the remaining dog (A18460) with a


septal:free wall ratio of 1.3, marked disorganization of cardiac muscle cells
was present in the anterolateral and posterior left ventricular free walls
(8% of the combined tissue sections), similar in extent to that in the
ventricular septum. This pattern of distribution of myocardial dis-
organization is characteristic of human patients with hypertrophic car-
diomyopathy who do not have obstruction of left ventricular outflow.8
Conduction System Findings
In the 2 dogs with complete heart block in which conduction tissue was
studied (A17741 and A18460), similar morphologic abnormalities were
identified. In these dogs, degenerative changes (ie, granularity, coagu-
lation necrosis, and lysis of the sarcoplasm) were evident in numerous
conduction cells of the atrioventricular node, His bundle, and the proxi-
mal right and left bundle branches and were associated with increased
amounts of fibrous connective tissue and infiltration of mononuclear cells.
Discussion
The present report describes, for the first time, the spontaneous occur-
rence of a primary hypertrophic cardiomyopathy in dogs. The clinical and
pathologic findings in these dogs are similar in many respects to the
manifestations of hypertrophic cardiomyopathy in humans. First, each of
the dogs showed marked cardiac hypertrophy, ie, increased cardiac mass,
compared with dogs with normal hearts. Second, the mean septal:free
wall thickness ratios in the dogs judged to have hypertrophic cardiomy-
opathy were significantly greater than those of dogs with normal hearts or
with acquired or congenital heart disease. It should be emphasized that
only 6 of the 10 dogs with hypertrophic cardiomyopathy had septal:free
wall thickness ratios of > 1.3, thereby meeting the diagnostic criterion
generally utilized to identify disproportionate septal thickening in hu-
mans." 6 However, septal:free wall ratios in 8 of the 10 dogs exceeded the
greatest ratio observed in the control animals, ie, 1.1. Hence, our data
suggest that a septal:free wall thickness ratio of > 1.1 may be more
appropriate than . 1.3 as a diagnostic criterion for disproportionate septal
thickening (and, therefore, hypertrophic cardiomyopathy) in dogs.
Only 2 of the 10 dogs with hypertrophic cardiomyopathy showed
marked disorganization of cardiac muscle cells in the ventricular septum.
In these 2 dogs, the area of myocardium involved by disorganized cardiac
muscle cells was considerable, ie, 12% and 14%. This degree of in-
volvement is typical of patients with hypertrophic cardiomyopathy 7 9,13
and is distinctly uncommon in patients with concentric cardiac hyper-
Vol. 94, No. 3 HYPERTROPHIC CARDIOMYOPATHY 505
March 1979

trophy due to other forms of heart disease.13 How%ever, the relative in-
frequency wvith which marked disorganization of ventricular septal archi-
tecture occurs in dogs with hypertrophic cardiomryopathy underlies the
fact that this disease does not resemble in all anatomic respects hyper-
trophic cardiomyopathy in humans.
Certain clinical features of hypertrophic cardiomyopathy in the dogs
described in this report were similar to those of human patients with this
disease.16" 7 These points of similarity include predominance of the disease
in males,'6 the occurrence of sudden and unexpected death 16-18 even in
patients without a previous symptomatic manifestation of cardiac dis-
ease,19 and the development of marked cardiac failure in some pa-
tients.6,"7 However, one feature of hypertrophic cardiomyopathy in dogs
that is distinctly uncommon in humans is complete heart block.20 Diffuse
degenerative changes were present in the conduction system of 2 of our
dogs w%ith hvpertrophic cardiomyropathy and may have been responsible
for the complete heart block in these animals. However, such histopatho-
logic abnormalities are not unique to dogs -ith hvpertrophic cardiomv-
opathv and complete heart block since similar alterations have also been
described in dogs with complete heart block that did not have a cardiomv-
opathyv 21 and in dogs without cardiac disease that either died suddenly or
were put to death by request of the owner.2
In conclusion, it is evident from the data presented in this report that a
primary mvocardial disease, with certain pathologic features similar to
those of hvpertrophic cardiomyopathy in humans, also occurs spontane-
ously in dogs. The existence of this canine disease may prove to be a
valuable aid in the investigation of human cardiomvopathies.
References
1. Epstein SE, Henry WL, Clark CE, Roberts WC, Maron BJ, Ferrans VJ, Redwood
DR, Morrow AG: Asymmetric septal hypertrophy. Ann Intern Med 81:650-680.
1974
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diagnosed by echocardiography. N Engl J Med 289:118-121, 1973
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logic diagnosis of muscular subvalvular aortic stenosis. Circulation 24:1126-1136.
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4. Roberts WC: Valvular, subs al% ular and supravalvular aortic stenosis: Morphologic
features. Cardiovasc Clin 3:97-126, 1973
5. Abbasi AS, MacAlpin RN, Eber LM, Pearce ML: Echocardiographic diagnosis of
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506 LIU ET AL American Journal
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hypertrophic subaortic stenosis: A study of operatively excised left ventricular out-


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2

4. - ;. W

Fgure 1-Heart of Dog 15053 showing disproportionate thickening of the ventricular septum (VS) with respect to
the left ventricular free wall (LV). Fibrous plaque is evident on the left ventricular outflow tract (arrow). RV, right ven-
cricular wall. Fgr 2-Histologic section of ventricular septal myocardium from Dog 18460 showing area of
cardiac muscle cell disorganization. (H&E, x 100)
508 LIU ET AL American Journal
of Pathology

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