Domestic Animals–Case Report

Veterinary Pathology
2017, Vol. 54(2) 254-257
Left Ventricular Apical Aneurysm ª The Author(s) 2016
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in a Cat With Primary Cardiomyopathy DOI: 10.1177/0300985816671378
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C. Ramı́rez-Hernández1, A. Barbosa-Quintana2,
and R. Ramı́rez-Romero1

Abstract
A 13-year-old female Persian cat died suddenly after severe respiratory distress. At necropsy, the changes were compatible with
congestive heart failure. The heart was enlarged with a flabby and puckered sac-like aneurysm at the apex of the left ventricle. The
apical zone showed a thin muscular wall arising from the free wall of the left ventricle connected to a bulged saccular area through
a wide communication. Microscopically, the wall of the aneurysm was composed of fibrous connective tissue with neovascu-
larization and sparse atrophied myocardial cells at the margins. A few isolated cardiomyocytes in the lesion stained positively for
desmin, and the inner lining of the aneurysm had immunoreactivity to von Willebrand factor and CD31. Mature fibrous connective
tissue was interspersed with degenerated and disorganized cardiomyocytes elsewhere in the myocardium, and many small
myocardial arteries were tortuous and thickened. In this case of sudden death, the diagnosis was primary cardiomyopathy, with
formation of a left ventricular apical aneurysm within an area of marked myocardial fibrosis and cardiomyocyte atrophy.

Keywords
left ventricle, apical aneurysm, cats, cardiomyopathy, heart failure, diverticulum

Primary cardiomyopathy is a term restricted to cases in which necropsy. The heart was enlarged with a flabby and puckered
there is no clear cause of the heart failure or the changes in small sac (1 cm) at the apex of the left ventricle (Fig. 1). The
myocardium.3 Originally identified in humans, cardiomyopa- apical zone had a pale and thin muscular wall arising from the
thies constitute a heterogeneous but well-characterized group free wall of the apex connected to a bulged saccular area
of pathological conditions in cats.3 Primary cardiomyopathies through a wide communication (Fig. 2). Other changes
are inherent while secondary cardiomyopathy refer to specific included acute hepatic congestion and mild ascites.
causes such as hypothyroidism, hypersomatotropism, systemic Samples of the heart, lung, liver, spleen, and kidney were
hypertension, and aortic stenosis, among others.3 Four main fixed in 10% neutral buffered formalin and processed routinely
primary cardiomyopathies are recognized: dilated or congestive, to obtain sections stained with hematoxylin and eosin and with
hypertrophic, restrictive, and arrhythmogenic right ventricular Masson’s trichrome. Additional heart sections were labeled by
cardiomyopathy (ARVC).3 The unclassified cardiomyopathy immunohistochemistry using an avidin-biotin-peroxidase
group includes cases that do not easily fit in one of the previous method (Autostainer Link 48; Agilent Technologies, Dako,
groups.3 The commonest type of cardiomyopathy in cats is Carpinteria, CA) using monoclonal antibodies against desmin,
hypertrophic cardiomyopathy (HCM).3,8 HCM is a continuum vimentin, a–smooth muscle actin, von Willebrand factor, and
that may eventually lead to an end-stage lesion (ES- CD31 (Dako, Comercial Biomédico JR, México). The chromo-
HCM).2,3,8,10 This condition parallels ES-HCM in humans, gen was diaminobenzidine, and the counterstain was Harris’s
and left ventricular apical aneurysm occurs in a subset of hematoxylin.
humans with ES-HCM.2,8,9 Similarly, cats and humans with
ARVC may develop right ventricular apical aneurysms.4
The aim of this report is to describe the gross and histological 1
Posgrado Conjunto Agronomı́a-Veterinaria, Universidad Autónoma de
findings in a case of sudden death in a cat with left ventricular Nuevo León, Ex-Hacienda el Canadá, Gral. Escobedo, N.L. México
apical aneurysm as a result of primary cardiomyopathy. 2
Hospital San José-Tecnológico de Monterrey, Laboratorio de Patologı́a,
A 13-year-old Persian female cat had received routine Monterrey, N.L., México
grooming and returned home normally. However, 2 hours later,
the owner noted sudden respiratory distress and frantic beha- Corresponding Author:
R. Ramı́rez-Romero, Facultad de Medicina Veterinaria y Zootecnia,
vior. The cat was taken to the veterinarian but collapsed and Universidad Autónoma de Nuevo León, Campus Ciencias Agropecuarias, Av.
died before receiving attention. Hydrothorax, hydropericar- Francisco Villa s/n. Escobedo, Nuevo León, México. C.P. 66050.
dium, and edematous, noncollapsed lungs were noted at Email: raramirez@prodigy.net.mx
Ramı´rez-Hernández et al 255

In the remaining portions of the left ventricle and in the

papillary muscles, fibrous connective tissue was interspersed
with degenerated cardiomyocytes. The cardiomyocytes were
hypertrophied or atrophied with hyaline, fragmented, hypereo-
sinophilic, and densely staining cytoplasm; in some areas, the
cardiomyocytes appeared disorganized with fibrous connective
tissue interspersed (Fig. 4). The diagnosis was severe left ven-
tricular fibrosis and myocardial atrophy with left ventricular
apical aneurysm.
Protruding structures in the ventricles are extremely rare in
animals and humans. Apical aneurysms in the right ventricle have
been described in cats with ARVC.4 Also, an aneurysm on
the right ventricular free wall was encountered in a cat with a large
atrial septal defect.1 Recently, a congenital aneurysm in the right
ventricle was reported in a pigeon5 and a case of diverticula in both
ventricles in a dog.6 However, to our knowledge, left ventricular
apical aneurysm has not been previously described in animals.
Ventricular diverticula, left ventricular apical aneurysm, and
ventricular pseudo-aneurysm are well-characterized conditions
in humans.6,7 Although sometimes used interchangeably, car-
diac diverticulum and aneurysm are different.6,7 In humans, left
ventricular aneurysm may be congenital or acquired. Congenital
aneurysms are rare and are characterized by a wide channel of
communication with the apical left ventricle and a limiting wall
composed of a single layer of fibroelastic tissue that is some-
times calcified and lacks ventricular muscle. The anomaly is
Figure 1. Primary cardiomyopathy with left ventricular aneurysm, isolated and originates due to structural errors during embryo-
heart, Persian cat. The heart is rounded with left atrial enlargement. genesis. The condition is diagnosed after the exclusion of other
The apex has a puckered and invaginated sac (arrow) and pallor of the
myocardium.
pathologic changes.7 Conversely, a left ventricular diverticulum
is commonly associated with other cardiac anomalies and mid-
line thoracoabdominal malformations.7 In the case of a cardiac
Microscopically, the paucity of the myocardium in the sac- diverticulum, a thin layer containing endocardium, myocardium,
cular wall of the left ventricle was obvious. In the left ventricle, and pericardium maintains contractility, whereas with an aneur-
near the sacculus, the small arteries were tortuous and thick- ysm, the fibrous tissue exhibits systolic dyskinesia/akinesia or
ened due to proliferation of the endothelium and hypertrophy paradoxical bulging.7 However, left ventricular aneurysm may
of the tunica media (Fig. 3). No Purkinje fibers were recog- be acquired, in which case the most plausible origin is a myo-
nized, and few infiltrating lymphocytes were noted. Further- cardial infarct, with replacement by fibrous tissue.6,7,9 The apical
more, there were several foci of myocardial ischemic necrosis location is attributed to the thinness of the myocardium at this
and occasionally large areas with scarring, suggesting previous site. Systemic causes of acquired left ventricular apical aneur-
infarcts (Fig. 4, upper inset). The saccular lesion was composed ysm in humans include Chagas disease, mucopolysaccharidosis,
of abundant fibrous connective tissue, sparse and atrophied and sarcoidosis, among others.7 Ventricular pseudo-aneurysm
cardiomyocytes, and neovascularization (Fig. 4, lower inset). (also called false aneurysm) is a similar condition but represents
Sections of liver and lung confirmed acute centrilobular con- a rupture of the ventricular wall that is contained by adhesion of
gestion and alveolar edema with numerous hypertrophied the pericardium.7
macrophages, respectively. The lesion encountered herein differs in several ways
By immunohistochemistry, there was strong staining for from those previously described in animals. In the cats with
desmin in isolated cardiomyocytes in the lesion (Fig. 3, ARVC, the lesion occurs only in the free wall of the right ven-
upper inset) and in the remaining myocardium. The immu- tricle.4 Similarly, the right ventricular aneurysm reported in a cat
noreactivity to vimentin was moderate and was encountered was likely a consequence of a large atrial septal defect.1 Con-
in the fibrous connective tissue in the lesion but not in the versely, in the dog, several lesions occurred in both ventricles,
cardiomyocytes. a–Smooth muscle actin staining was mark- but not in the apex, and these had a narrow ventricular commu-
edly positive in the walls of the new vessels and in vessels nication in contrast with the wide passage in our case.6 Finally,
in the remaining myocardium. Finally, the cells lining the the apical lesion in this cat was accompanied by the presence of
inner surface of the sacculus were positive for von Will- disorganized cardiomyocytes in the myocardium as well occlud-
ebrand factor (factor VIII) and CD31 (Fig. 3, lower inset) ing changes in the small arteries, which are evidence of primary
similar to the endocardial lining. cardiomyopathy.2,3,8 Based on the absence of left ventricular
256 Veterinary Pathology 54(2)

Figures 2–4. Primary cardiomyopathy with left ventricular aneurysm, heart, Persian cat. Figure 2. Section from the left ventricle taken through
the aneurysm in the free wall. The apical aneurysm is composed of a thin wall of fibrous connective tissue (evident as blue staining, arrow). A wide
communication (asterisk) was observed between the aneurysm and the left ventricle. The papillary muscles are enlarged. There is multifocal fibrosis
of heart muscle (blue staining). Masson’s trichrome. Figure 3. Left ventricle, at the boundary of the thinned wall. The arteries are partially
obliterated due to proliferative changes in the media and intima. There is also extensive neovascularization. Masson’s trichrome. Inset, lower right:
the endocardial lining of the aneurysm exhibits immunoreactivity to CD31. Immunohistochemistry (IHC) for CD31. Inset, upper right: isolated and
atrophied cardiomyocytes stain strongly positive for desmin. IHC for desmin. Figure 4. Focal interstitial fibroplasia and disordered cardiomyocytes.
Hematoxylin and eosin. Inset, upper right: locally extensive scarring at the boundaries of the aneurysm. Masson’s trichrome. Inset, lower right: isolated
and atrophied cardiomyocytes surrounded by fibrous connective tissue at the base of the aneurysm. Masson’s trichrome.

hypertrophy, we considered ES-HCM, restrictive cardiomyopa- cause for development of aneurysm. We suggest that these
thy, and unclassified cardiomyopathy as possible differential lesions may have arisen from a myocardial infarct.
diagnoses in this case, and cardiac ultrasound would be neces- This report describes a left ventricular aneurysm in a cat
sary to distinguish these possibilities.3,10 There was also atrophy with primary cardiomyopathy that is considered to be an
and scarring of the left ventricle adjacent to the aneurysm, sug- acquired lesion resulting from a localized area of myofiber
gesting these more severe localized myocardial changes as the atrophy and replacement fibrosis.
Ramı´rez-Hernández et al 257

Declaration of Conflicting Interests 4. Fox PR, Maron BJ, Basso C, et al. Spontaneously occurring arrhythmogenic
right ventricular cardiomyopathy in the domestic cat: a new animal model
The author(s) declared no potential conflicts of interest with respect to
similar to the human disease. Circulation. 2000;102(15):1863–1870.
the research, authorship, and/or publication of this article.
5. Gal AF, Tăbăran F, Taulescu M, et al. The first description of a congenital right
ventricular cardiac aneurysm in a pigeon (Columba livia domestica, Cluj blue
Funding tumbler pigeon). Avian Dis. 2012;56(4):778–780.
The author(s) disclosed receipt of the following financial support for 6. Herráez P, Rodrı́guez F, Aguirre-Sanceledonio M, et al. Congenital biventricu-
the research, authorship, and/or publication of this article: C. Ramı́rez- lar cardiac diverticula in a dog. Vet Pathol. 2011;48:456–459.
Hernández received a graduate studies scholarship from CONACYT. 7. Makkuni P, Kotler MN, Figueredo VM. Diverticular and aneurysmal structures
of the left ventricle in adults: report of a case within the context of a literature
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