J Vet Intern Med 2011;25:477–483

R e tro spe c t iv e Re v ie w of Co n g e n i t a l H e a r t D i s e a s e in 9 7 6 D o g s
P. Oliveira, O. Domenech, J. Silva, S. Vannini, R. Bussadori, and C. Bussadori

Background: Knowledge of epidemiology is important for recognition of cardiovascular malformations.

Objective: Review the incidence of congenital heart defects in dogs in Italy and assess breed and sex predispositions.
Animals: Nine hundred and seventy-six dogs diagnosed with congenital heart disease (CHD) of 4,480 dogs presented to
Clinica Veterinaria Gran Sasso for cardiovascular examination from 1997 to 2010.
Methods: A retrospective analysis of medical records regarding signalment, history, clinical examination, radiography,
electrocardiography, echocardiography, angiography, and postmortem examination was performed. Breed and sex predispo-
sition were assessed with the odds ratio test.
Results: CHD was observed in 21.7% of cases. A total of 1,132 defects were observed with single defects in 832 cases (85%),
2 concurrent defects in 132 cases (14%), and 3 concurrent defects in 12 cases (1%). The most common defects were pulmonic
stenosis (PS; 32.1%), subaortic stenosis (SAS; 21.3%), and patent ductus arteriosus (20.9%), followed by ventricular septal
defect (VSD; 7.5%), valvular aortic stenosis (AS; 5.7%), and tricuspid dysplasia (3.1%). SAS, PS, and VSD frequently were
associated with other defects. Several breed and sex predispositions were identified.
Conclusions and Clinical Relevance: The results of this study are in accordance with previous studies, with slight differences.
The breed and sex predilections identified may be of value for the diagnosis and screening of CHD in dogs. Additionally, the
relatively high percentage of concurrent heart defects emphasizes the importance of accurate and complete examinations for
identification. Because these data are from a cardiology referral center, a bias may exist.
Key words: Breed predisposition; Canine; Congenital heart defects; Multiple heart defects; Sex predisposition.

ardiovascular malformations represent a substantial

C cause of morbidity and mortality in dogs o1 year of
age.1 The exact prevalence of these malformations is
Abbreviations:
AS valvular aortic stenosis
difficult to determine because some do not cause audible ASD atrial septal defect
cardiac murmurs, some lead to perinatal death, and CHD congenital heart disease
regional differences in breeds affect their frequency. In PDA patent ductus arteriosus
humans, cardiovascular malformations represent the PS pulmonic stenosis
most common congenital anomalies.2 Early recognition SAS subaortic stenosis
is of great importance to achieve appropriate medical or TOF tetralogy of Fallot
surgical management, improve outcome and provide an TTE transthoracic echocardiography
accurate prognosis. For this purpose, the epidemiology VSD ventricular septal defect
of cardiovascular defects plays an important role. Several
reports exist in veterinary literature regarding the preva-
lence of congenital heart disease (CHD) in dogs, mostly
2010 were reviewed retrospectively. Cases that presented with con-
from the United States, Australia, United Kingdom, genital heart defects were identified, and information regarding
Sweden, and Switzerland.1,3–6 The most commonly re- signalment, history, clinical examination, radiography, electro-
ported defects in this species are patent ductus arteriosus cardiography, echocardiography, angiography, and postmortem
(PDA), pulmonic (PS) and subaortic stenosis (SAS), ven- examination was obtained.
tricular septal defects (VSD), tricuspid dysplasia, and A complete transthoracic echocardiographic examination (TTE)
tetralogy of Fallot (TOF).1,4,5 The aim of this study was was performed in all patients. Echocardiographic examinations
to review the incidence of congenital heart defects in a were performed with an Esaote Caris ultrasound machine with me-
large population of dogs in Italy. chanical transducers ranging from 2 to 10 MHz,a or Esaote Megas,
Esaote Mylab30Vet, Esaote MyLab60 ultrasound machines with
electronic transducers also ranging from 2 to 10 MHz.a The exams
were performed and interpreted by the authors and reviewed by an
Materials and Methods ECVIM board-certified cardiologist (C.B., O.D., or both). The pa-
The medical records of 4,480 dogs presented for cardiovascular tients were placed in right and left lateral recumbency and the
examination at Clinica Veterinaria Gran Sasso between 1997 and examinations were performed according to the American Society of
Echocardiography standards and guidelines and other published
recommendations.7 Angiographic procedures also were performed
From the Department of Cardiology of Clinica Veterinaria Gran
by the authors with a fluoroscopy systemb in cases undergoing
Sasso, Milano, Italia. The results from this study have been partially
presented as an abstract at the 20th ECVIM Meeting 2010 in Tou- interventional percutaneous procedures or when necessary for
louse, France. diagnostic purposes. Postmortem examinations were performed
Corresponding author: Pedro Oliveira, DVM, Clinica Veterinaria under the supervision of C.B., O.D., or both.
Gran Sasso, Via Donatello 26, 20131 Milano, Italia; e-mail: pedro SAS lesions were classified according to the Pyle & Patterson
[email protected]. studies as type 1, when presenting with a thickened and raised septal
Submitted November 26, 2010; Revised January 15, 2011; endocardium to form small nodules; type 2, when presenting with a
Accepted February 2, 2011. fibrous thickening and raising of the subaortic endocardium form-
Copyright r 2011 by the American College of Veterinary Internal ing a complete, or incomplete, fibrous ring below the aortic valve;
Medicine and type 3, when presenting with a concentrical ‘‘tunnel-like’’ lesion
10.1111/j.1939-1676.2011.0711.x at the left ventricular outflow tract.8
 19391676, 2011, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2011.0711.x by CAPES, Wiley Online Library on [06/11/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
478 Oliveira et al

PS lesions were classified as type A when presenting with Weimaraner (OR, 9.4), French Bulldog (OR, 8.2), Stan-
pulmonic leaflet thickening and fusion, and type B when presenting dard Schnauzer (OR, 7.1), and Australian Shepherd
with pulmonic ostium hypoplasia with varying degrees of leaflet (OR, 5.6). Breed distribution and predispositions for the
thickening and fusion.8 most commonly observed defects are presented in Tables
2–7. Sex distribution was similar to that of the overall
Statistical Analysis population with males being slightly more frequent
Descriptive statistics were performed. The Kolmogorov-Smirnov
(54%) than females (46%). Specific male predisposition
test was used to assess normality. The Mann-Whitney test was used was observed for PS (OR, 1.5), SAS (OR, 1.7), and AS
to identify differences in breed distribution between the CHD group (OR, 2.6) and female predisposition for PDA (OR, 2.7).
and a reference population composed of 7,780 dogs of the same age Mean age at presentation was approximately 42 months,
range presented to Clinica Veterinaria Gran Sasso during the same ranging from 1 to 187 months.
time period. Breed and sex predilections were assessed by means of Lesion classification information was available in 333
calculation of the relative risk with the odds ratio test. Breed predi- cases of PS. Type A was most common (n 5 235, 70.6%),
lection was considered to be present if a statistically significant (P o followed by type B (n 5 84, 25.2%), mixed (n 5 13,
.05) odds ratio 4 1.5 was observed with the following classification: 3.9%), and supravalvular stenosis (n 5 1, 0.3%).9–11 In
mild increased risk if 1.5 o OR o 2.9, moderate risk if 3.0 o OR o
the case of SAS, lesion classification according to Pyle &
4.9, and marked risk if OR 4 5.0. Only breeds represented by a
minimum of 4 dogs were tested, except in the case of tricuspid dys-
Patterson8,12,13 was available in 134 cases, with type 2
plasia, in which this limit was set to 3 due the lower number of cases. being the most common (n 5 69, 51%), followed by type
Data processing and statistics were performed by commercially 3 (n 5 41, 31%), and type 1 (n 5 24, 18%).
available statistics softwarec and Microsoft Excel 2003.d Reverse PDA was observed in 6 of the 237 dogs with
this defect. Diagnosis was made with the aid of agitated
Results saline echocardiographic contrast in 5 cases and angio-
graphy in 1 case.
CHD was diagnosed in 976 (21.7%) of the 4,480 dogs.
Single defects were present in 832 cases (85%), 2 concur- Multiple Heart Defects
rent defects in 132 cases (14%), and 3 concurrent defects
in 12 cases (1%), corresponding to a total of 1,132 heart The various combinations of congenital heart defects
defects. Observed congenital heart defects are presented observed are presented in Table 8. The most commonly
in Table 1, including information regarding sex and age observed were PS and SAS (n 5 38, 26.4%), followed by
at presentation. The most common were PS (32.1%), PS and VSD (n 5 24, 16.7%). PDA was associated with a
SAS (21.3%), and PDA (20.9%), followed by VSD concurrent defect in 9.3% (n 5 22) of the cases, mostly
(7.5%), valvular aortic stenosis (AS) (5.7%), and tricus- PS (n 5 10, 45%) and SAS (n 5 7, 32%). VSD was as-
pid dysplasia (3.1%). Angiographic procedures were sociated to another defect in 48% of the cases, mostly PS
performed in 158 cases: 116 PS, 1 AS, 28 PDA, 1 VSD, (65%).
3 PS with anomalous right coronary artery, 1 PS with
anomalous right coronary artery and SAS, 3 PS with Discussion
persistent left cranial vena cava, 2 atrial septal defects
(ASD), 1 reverse PDA, 1 anomalous subclavian artery, 1 PS, SAS, PDA, and VSD consistently have been
anomalous pulmonary venous return. Postmortem reported as being the most commonly encountered
examinations were performed in 43 dogs: 4 PDA, 7 cardiac defects in previous studies.1,4,5,14 In the present
type 1 SAS, 4 type 2 SAS, 3 type 3 SAS, 6 type A PS, 8 study, PS was the most common cardiac defect, account-
type B PS, 3 muscular VSD, 4 perimembranous VSD, 2 ing for 32.1% in contrast to 18–23% reported in other
TOF, 1 case with 2 stenotic pulmonic arteries, 1 aortic- studies.1,4,5,14 This difference may be because of the fact
pulmonary window. that our center receives many referrals for pulmonary
Seventy-seven breeds were represented, with Boxer balloon valvuloplasty. The high percentage of Boxers in
(26%) and German Shepherd (10%) being the most com- our study (26%), and corresponding predisposition for
mon, followed by mixed breed dogs (9.9%), English PS (OR, 5.7), also may account for this fact. Boxer pre-
Bulldog (3.7%), and Newfoundland (3.7%). A statisti- dilection for PS has already been reported in the
cally significant difference between breed distribution in literature,13,15 as well as a male predisposition in this
the CHD group and the overall population was observed breed.15 In the present study, male predisposition was
(P o .0001). Purebred dogs showed a significantly higher observed in the overall breed population (OR, 1.5). Ad-
probability of presenting with CHD when compared ditionally, other breed predilections were identified,
with Mongrel dogs (OR, 3.3). Additionally, a mild in- some of which had already been reported previously, as
creased risk for CHD was observed for 7 breeds: is the case of the English Bulldog, West Highland White
Chihuahua (OR, 2.5), English Bulldog (OR, 2.4), Labra- Terrier, and Chihuahua.1 Lack of predisposition of
dor Retriever (OR, 2.3), Italian Mastiff (OR, 2.1), and Golden Retriever, Labrador Retriever, and Yorkshire
German Shepherd, Golden Retriever, and West High- Terrier also is in accordance with previously published
land White Terrier, all with OR of 1.8. A moderate risk results.1 According to our results, type A is the most
was observed for 3 breeds: Boxer (OR, 4.6), American common form observed, representing 70.6% of the cases
Staffordshire Terrier (OR, 4.2), and Newfoundland (OR, in this study, as compared with 25.2% with type B.
3.6). Finally, a marked risk was observed for 4 breeds: Mixed lesions (type A and B) seem to be uncommon
 19391676, 2011, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2011.0711.x by CAPES, Wiley Online Library on [06/11/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Congenital Heart Disease in 976 Dogs 479

Table 1. Congenital heart defects.

Heart Defect N Isolated Associated Male Female Age (Months)a
Pulmonic stenosis 363 (32.1%) 271 (75%) 92 (25%) 216 (60%)b 145 (40%)b 40 (1–161)
Subaortic stenosis 241 (21.3%) 195 (81%) 46 (19%) 150 (62%) 91 (38%) 52 (1–187)
Patent ductus arteriosus 237 (20.9%) 215 (90.7%) 22 (9.3%) 83 (35%) 153 (65%) 38 (2–155)
Ventricular septal defect 85 (7.5%) 45 (52%) 40 (48%) 39 (46%) 46 (54%) 40 (3–157)
Aortic stenosis 64 (5.7%) 52 (81%) 12 (19%) 45 (70%) 19 (30%) 78 (4–158)
Tricuspid dysplasia 35 (3.1%) 26 (74%) 9 (26%) 17 (48.5%) 18 (51.5%) 41 (2–124)
Mitral dysplasia 21 (1.9%) 13 (62%) 9 (38%) 10 (48%) 11 (52%) 21 (4–94)
Double chamber right ventricle 14 (1.2%) 9 (64%) 5 (36%) 6 (43%) 8 (57%) 24 (4–69)
Atrial septal defect 12 (1.1%) 8 (67%) 4 (33%) 3 (27%) 8 (73%) 47 (10–128)
Tetralogy of Fallot 11 (1.0%) — — 6 (55%) 5 (45%) 14 (1–33)
Aortic hypoplasia 9 (0.8%) 0 (0%) 9 (100%) 5 (56%) 4 (44%) 51 (29–103)
Anomalous right coronary artery 9 (0.8%) 2 (22%) 7 (78%) 7 (78%) 2 (22%) 38 (17–66)
Persistent left cranial vena cava 9 (0.8%) 0 (0%) 9 (100%) 6 (67%) 3 (33%) 18 (44–110)
Cor triatriatum dexter 3 (0.3%) 3 (100%) 0 (0%) 1 (33%) 2 (67%) 37 (10–60)
4th right aortic arch 3 (0.3%) 2 (67%) 1 (33%) 2 (67%) 1 (33%) 10 (2–19)
Peritoneal-pericardial diaphragmatic hernia 3 (0.3%) 2 (67%) 1 (33%) 0 (0%) 3 (100%) 49 (7–84)
c
Patent foramen ovale 2 (0.2%) 0 (0%) 2 (100%) 0 (0%) 2 (100%)
Situs inversus 2 (0.2%) 0 (0%) 2 (100%) 0 (0%) 2 (100%) 62 (28–95)
Supravalvular aortic stenosis 1 (0.1%) 1 (100%) 0 (0%) 0 (0%) 1 (100%) 3,6
Anomalous pulmonary venous return 1 (0.1%) 1 (100%) 0 (0%) 1 (100%) 0 (0%) 42
c
Truncus arteriosus 1 (0.1%) 1 (100%) 0 (0%) 0 (0%) 1 (100%)
Aortic-pulmonary window 1 (0.1%) 1 (100%) 0 (0%) 1 (100%) 0 (0%) 45
Bicuspid aorta 1 (0.1%) 0 (0%) 1 (100%) 1 (100%) 0 (0%) 65
Quadricuspid aorta 1 (0.1%) 0 (0%) 1 (100%) 0 (0%) 1 (100%) 49
Anomalous subclavian artery 1 (0.1%) 0 (0%) 1 (100%) 0 (0%) 1 (100%) 113
Two stenotic pulmonary arteries 1 (0.1%) 0 (0%) 1 (100%) 0 (0%) 1 (100%) 24
Pericardial cyst 1 (0.1%) 0 (0%) 1 (100%) 1 (100%) 0 (0%) 31
Total 1132 (100%) 42 (1–187)
a
Age at presentation.
b
Information relative to sex was unavailable in 2 cases.
c
Unavailable.

(3.9%) and supravalvular stenosis is a rare occurrence

Table 2. Breed distribution and predisposition— (0.3%). The presence of an associated anomalous right
pulmonic stenosis. coronary artery was suspected in 8 cases by TTE, and
Pulmonic Stenosis (363 cases)
confirmed by angiography in 4 cases and by TEE in 1
case. Angiographic classification was available in only 3
N % Odds Ratio P cases, all presenting with type R2A anomaly.16 Half of
Boxer 116 31.9 5.27 o .0001 these dogs were English Bulldogs, a fact that is in agree-
Mongrel 35 9.6 0.32 o .0001 ment with previous reports of predisposition for this
English Bulldog 27 7.4 3.16 o .0001 breed.17,18
French Bulldog 21 5.8 19.1 o .0001 The 2nd most commonly observed CHD in this study
Pinscher 14 3.8 3.1 .0001 was SAS (21.3%), similar to what has been reported
German Shepherd 11 3.0 0.44 .0085
Beagle 10 2.7 2.66 .003
West Highland White Terrier 9 2.5 2.91 .003 Table 3. Breed distribution and predisposition—
American Staffordshire Terrier 8 2.2 16.9 o .0001 subaortic stenosis.
Chihuahua 8 2.2 3.11 .003
Cavalier King Charles Spaniel 6 1.6 1.62 NS Subaortic Stenosis (241 Cases)
Cocker Spaniel 6 1.6 1.1 NS
Breed N % Odds Ratio P
Pitbull Terrier 6 1.6 4.48 .0009
Rottweiler 6 1.6 0.91 NS Boxer 121 49.8 9.4 o .0001
Newfoundland 5 1.4 0.81 NS German Shepherd 24 9.9 1.8 .0166
Golden Retriever 5 1.4 0.97 NS Dogue de Bordeaux 18 7.4 11.2 o .0001
Shih-Tzu 5 1.4 0.78 NS Newfoundland 23 9.5 7.0 o .0001
Yorkshire Terrier 5 1.4 0.23 .0013 Rottweiler 16 6.6 4.5 o .0001
Italian Mastiff 4 1.1 2.1 NS Golden Retriever 13 5.3 3.6 .0001
Poodle 4 1.1 0.23 .0062 Mongrel 5 2.1 0.1 o .0001
Standard Schnautzer 4 1.1 16.7 o .0001 Labrador Retriever 4 1.6 0.6 NS
Others 48 13.2 Others 18 7.4
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480 Oliveira et al

Table 4. Breed distribution and predisposition— Table 6. Breed distribution and predisposition—
valvular aortic stenosis. ventricular septal defect (VSD).
Aortic Stenosis (64 Cases) VSD (85 Cases)

Breed N % Odds Ratio P Breed N % Odds Ratio P

Boxer 40 62.5 17.9 o .0001 Mongrel 13 15.3 0.6 NS
Bull Terrier 5 7.8 41 o .0001 Pinscher 5 5.9 39 o .0001
German Shepherd 5 7.8 1.14 NS French Bulldog 4 4.7 7.2 .0003
Others 14 21.9 German Shepherd 4 4.7 3.7 .001
Labrador Retriever 4 4.7 0.8 NS
Others 55 64.7
previously in the United States,1,14 but in contrast to
other European studies in which it was the most common
cardiac defect, accounting for 31.55 and 35%4 of all car- referred for surgical ligation or transcatheter embolizat-
diac defects. In this study, subvalvular and valvular ion, therefore increasing its apparent incidence in
lesions were considered separately, with aortic valvular comparison with what would be expected in a first opin-
stenosis accounting for an additional 5.7% of the cases, ion practice center. For the same reason, the observed
and comparison between study results should take this incidence of reverse PDA probably is an underestimate
fact into account. Nevertheless, combined SAS and AS of the real incidence, because this condition is not suit-
still account for the 2nd most common congenital pathol- able for occlusion. Females are consistently reported as
ogy with an incidence of 27%. Males seem to be pre- being more often affected than males,1,4,19–21 and the re-
disposed (OR, 1.7) in contrast to previous reports in which sults of our study support this predilection, indicating a
sex predilection had not been confirmed,1 except in the female predisposition for PDA (OR, 2.7). Considering
Boxer breed.1,15 This breed represented, however, almost breed incidence and predilections, the results of this
half (49.8%) of the cases of SAS in the present study and study are slightly different from those of other reports.
influenced the results. Data were reanalyzed excluding The German Shepherd was the most commonly affected
this breed and, although males were still more prevalent breed and a markedly higher risk was observed (OR, 5.2),
than females (63 versus 37%), a statistically significant in contrast to previously published results in which a
higher relative risk for males was not confirmed (OR, 1.1; higher risk was not identified (nonsignificant odds ratio
P 5 .7). Breed predilections observed for SAS, except for of 1.2), although this breed was among the most common
Dogue de Bordeaux (OR, 11.2), had already been de- breeds with PDA.1 Furthermore, Poodle, Pomeranian,
scribed and are in agreement with a previous study.1 and Yorkshire Terrier predisposition reported by the
Regarding PDA, its prevalence in the United States same study1 was not confirmed in the present study. This
seems to be higher1,14 than in Europe.4,5 In the present might be because of differences in breed popularity and
study, it was the 3rd most common defect (20.9%), incidence between the 2 geographic areas. The same ap-
slightly more prevalent than in previous European re- plies to Chihuahua and Australian Shepherd for which a
ports (4th most common, 11–13.7%)4,5 and less common statistically significant higher risk was observed in this
than in USA reports (most common, 27.7–32%).1,14 Sim- study in contrast to the other study.1 In both studies, the
ilar to PS, many PDA cases received by our center are Maltese breed was found to be at a markedly higher risk
for PDA.
Table 5. Breed distribution and predisposition—patent VSD was the 4th most common cardiac defect in our
ductus arteriosus (PDA). study, with a lower incidence (7.5%) than reported
previously (9.8–14.4%).1,4,5 Interestingly, VSD was ob-
PDA (237 Cases) served in conjunction with another cardiac defect in
almost half of the cases (48%) and usually with PS
Breed N % Odds Ratio P
(65%). This association was observed in 23 dogs, of
German Shepherd 58 24.5 5.2 o .0001 which 19 were presented with a type A PS and a peri-
Mongrel 41 17.3 0.65 .018 membranous VSD (n 5 9) or a muscular VSD (n 5 8).
Newfoundland 13 5.5 4.65 o .0001
Maltese 12 5.1 4.14 o .0001
Dobermann 12 5.1 2.8 .0007 Table 7. Breed distribution and predisposition—tricus-
Poodle 12 5.1 1.18 NS pid dysplasia.
Yorkshire Terrier 9 3.8 0.71 NS
Cavalier King Charles Spaniel 9 3.8 3.7 .0006 Tricuspid Dysplasia (35 Cases)
Dachshund 6 2.5 0.42 .0372
Breed N % Odds Ratio P
Chihuahua 6 2.5 3.66 .0028
West Highland White Terrier 4 1.7 1.93 NS Labrador Retriever 9 25.7 11.13 o .0001
Pomeranian 5 2.1 2.5 NS Boxer 5 14.3 1.96 NS
Irish Setter 5 2.1 0.94 NS German Shepherd 5 14.3 2.24 NS
Belgian Shepherd 4 1.7 4.38 .0059 English Bulldog 3 8.6 6 .0035
Australian Shepherd 4 1.7 27.3 o .0001 Golden Retriever 3 8.6 6.6 .0022
Others 37 15.6 Others 10 28.5
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Congenital Heart Disease in 976 Dogs 481

Table 8. Multiple heart defects. and right aortic arch.23 Additionally, a possible associa-
tion between PS and VSD has been suggested because
Associated Pathologies N
their incidence was found to be more common than
PS 1 SAS 34 would be expected by chance.24 A possible relationship
PS 1 VSD 19 between these defects and TOF also has been proposed
PS 1 PDA 8 but not proven.24 If the pulmonary valve gradient is high
PDA 1 SAS 6
enough, right ventricular hypertrophy, another charac-
SAS 1 Mitral dysplasia 5
teristic of TOF, may occur. This was observed in most of
SAS 1 Perimembranous VSD 4
PS 1 Anomalous right coronary artery 4 the cases in the present study, however, without aortic
SAS 1 Aortic stenosis 3 overriding, and therefore not true TOF. Evidence of con-
SAS 1 Aortic root hypoplasia 3 otruncal development abnormality must be present in the
PS 1 2 Muscular VSD 3 case of TOF. No differences were identified in breed or
PS 1 AS 3 sex incidence between these subpopulations and the over-
PS 1 Persistent left cranial vena cava 3 all population of dogs with PS. Pinscher, French
PS 1 Tricuspid dysplasia 3 Bulldog, and German Shepherd seem to be at higher
AS 1 Aortic root hypoplasia 2 risk. Other breed predilections have been described else-
SAS 1 Situs inversus 2
where.1
VSD 1 Double chambered right ventricle 2
The incidence of tricuspid dysplasia (3.1%) also was
VSD 1 Mitral dysplasia 2
PS 1 AS 1 Aortic hypoplasia 2 slightly lower than reported previously (5.1–7.5%).1,4,5
PS 1 Persistent left cranial vena cava 1 Anomalous right 2 With the exception of English Bulldog, the predilections
coronary artery observed in the case of Labrador Retriever and Golden
AS 1 Bicuspid aorta 1 Retriever had already been previously reported and are
PDA 1 4th right aortic arch 1 in agreement.1 A previously observed higher female inci-
PDA 1 Anomalous Subclavian 1 dence was not confirmed in the present study.4
PDA 1 AS 1 ASD represented 1.1% of cardiac defects, a result in
PDA 1 Mitral dysplasia 1 agreement with most previously published reports1,4,25
PDA 1 Tricuspid dysplasia 1
but much lower than in 1 other study.26 Additionally, no
PDA 1 VSD 1
breed predilection was observed in contrast to other pre-
SAS 1 Muscular VSD 1
SAS 1 Persistent left cranial vena cava 1 vious reports in which Boxers were at higher risk.1,26 The
SAS 1 Persistent left cranial vena cava 1 VSD 1 diagnosis of ASD was achieved by echocardiographic
SAS 1 Persistent left cranial vena cava 1 mitral stenosis 1 examination, as in the case of the studies mentioned
SAS 1 Bicuspid aorta 1 above.4,26 In the past, it has been shown that the risk of
SAS 1 Quadricuspid aorta 1 overlooking cardiac defects with echocardiography was
SAS 1 Tricuspid dysplasia 1 greater than the risk of overdiagnosing them.27 This
SAS 1 Double chambered right ventricle 1 Mitral stenosis 1 report, however, relied on the use of 2-dimensional echo-
SAS 1 Aortic root hypoplasia 1 Supravalvular stenosis 1 cardiographic imaging, and since it has been published,
Tricuspid dysplasia 1 Patent foramen ovale 1
substantial advances have been made in echocardio-
Tricuspid dysplasia 1 ASD 1
graphic imaging that in combination with Doppler
Tricuspid dysplasia 1 Cor triatriatum dexter 1
Tricuspida dysplasia 1 Double chambered right ventricle 1 technology have rendered this diagnostic method much
VSD 1 ASD 1 more sensible and reliable.26 Additionally, all echocar-
VSD 1 ASD like Sinus Venosus Coronaricus 1 diographic examinations in this study were performed by
VSD 1 Persistent left cranial vena cava 1 experienced operators with a combination of 2D and
PS with 2 stenotic pulmonary arteries 1 Doppler techniques, and therefore, in our opinion, ASD
PS 1 ASD 1 were not underdiagnosed. TOF and persistent right aor-
PS 1 Double chambered right ventricle 1 tic arch were less frequent in the present study than
PS 1 PDA 1 Peritoneal-pericardial-diaphragmatic hernia 1 reported previously.1
PS 1 Pericardial cyst 1
In previous reports, the incidence of multiple heart de-
PS 1 Patent foramen ovale 1
fects was 7–8%,4,5 approximately half that of the present
PS 1 SAS 1 PDA 1
PS 1 SAS 1 Anomalous right coronary artery 1 study (15%). From the analysis of the results of this
PS 1 SAS 1 Aortic hypoplasia 1 and other studies, the association between PS and SAS
PS 1 SAS 1 VSD 1 seems to be one of the most common associations
PS 1 VSD 1 Anomalous coronary trunk 1 between heart defects in dogs.4,15 The frequent associa-
tion between VSD and other defects, and the presence of
AS, valvular aortic stenosis; ASD, atrial septal defect; PDA, concurrent PS and PDA in some dogs, emphasizes
patent ductus arteriosus; PS, pulmonic stenosis; SAS, subaortic the importance of performing a complete echocardio-
stenosis; VSD, ventricular septal defect.
graphic examination in all dogs, even when an anomaly
possibly explaining the clinical findings has already been
Only 4 cases were presented with a type B PS, 3 with a identified.
perimembranous VSD and 1 with a muscular VSD. In Considering the breed predispositions observed in this
humans, VSD may coexist with nearly all varieties of study, we believe that it is prudent to advise systematic
CHD22 and often is associated with ASD, PDA, PS, screening for congenital cardiac defects before breeding,
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482 Oliveira et al

in order to decrease their prevalence, especially in breeds 2. Hoffman JI, Kaplan S. The incidence of congenital heart
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breeders of these breeds should be appropriately in- for standards in transthoracic two-dimensional echocardiography
formed of this fact, and clinicians should have a high in the dog and cat. Echocardiography Committee of the Specialty of
Cardiology, American College of Veterinary Internal Medicine.
index of suspicion when examining individuals of these
J Vet Intern Med 1993;7:247–252.
breeds, and promptly inform breeders of the existence of
8. Bussadori C, Amberger C, Le Bobinnec G, et al. Guidelines
cardiac defects. for the echocardiographic studies of suspected subaortic and
From an analysis of Table 1, it can be seen that the av- pulmonic stenosis. J Vet Cardiol 2000;2:15–22.
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defects. These results are influenced by late diagnosis in vuloplasty in 30 dogs with pulmonic stenosis: Effect of valve
some mild cases. Nevertheless, ideally we would expect morphology and annular size on initial and 1-year outcome. J Vet
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7–11.
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viously observed tendencies, and may be of value for 15. Bussadori C, Pradelli D, Borgarelli M, et al. Congenital
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valvuloplasty for treatment of pulmonic stenosis in English Bull-
a
ESAOTE S.p.A., Firenze, Italy dogs with an aberrant coronary artery. J Vet Intern Med 24:354–
b
Villa Sistemi Medicali S.p.A., Buccinasco (MI), Italy 359.
c
MedCalc 10.2.0.0, Mariakerke, Belgium 19. Van Israel N, Dukes-McEwan J, French AT. Long-term fol-
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Microsoft Office Excel 2007, Microsoft Corp, Redmond, WA low-up of dogs with patent ductus arteriosus. J Small Anim Pract
2003;44:480–490.
20. Campbell FE, Thomas WP, Miller SJ, et al. Immediate
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