Heart Disease In Dogs Research Articles

Myxomatous mitral valve disease in dogs part 1: features and diagnosis

Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs, and potentially leads to the development of congestive heart failure. This first part of two articles discusses the features of MMVD including prevalence, aetiology and pathophysiology, and also discusses the diagnosis and staging of the condition. The management of MMVD will be discussed in part 2.

Serum proteomic profiles in CKCS with Mitral valve disease.

BackgroundMyxomatous mitral valve disease (MVD) is the most common acquired heart disease in dogs, and the Cavalier King Charles Spaniel (CKCS) is the most studied breed because of the high prevalence, early onset and hereditary component evidenced in the breed. MVD has different severity levels, and there are many practical limitations in identifying its asymptomatic stages. Proteomic techniques are valuable for studying the proteins and peptides involved in cardiovascular diseases, including the period prior to the clinical onset of the disease. The aim of this study was to identify the serum proteins that were differentially expressed in healthy CKCS and those affected by MVD in mild to severe stages. Proteomics analysis was performed using two-dimensional gel electrophoresis separation and a bioinformatics analysis for the detection of differentially expressed spots. In a comparative analysis, protein spots with a p < 0.05 (ANOVA) were considered statistically significant and were excised from the gels for analysis by MALDI–TOF–MS for protein identification.ResultsEight proteins resulted differentially expressed among the groups and significantly related to the progression of the disease.In mild affected group versus healthy dogs complement factor H isoform 2, inhibitor of carbonic anhydrase, hemopexin, dystrobrevin beta isoform X7 and CD5 molecule-like resulted to be down-regulated, whereas fibronectin type-III domain-containing protein 3A isoform X4 was up-regulated.In severe affected dogs versus healthy group complement factor H isoform 2, calpain-3 isoform X2, dystrobrevin beta isoform X7, CD5 molecule-like and l-2-hydroxyglutarate dehydrogenase resulted to be down-regulated.Complement factor H isoform 2, calpain-3 isoform X2, dystrobrevin beta isoform X7, CD5 molecule-like and hydroxyglutarate dehydrogenase were found to be down-regulated in mild affected group versus healthy dogs. All of these proteins except complement factor H followed a decreasing trend according to the progression of the pathology.ConclusionThe differential expression of serum proteins demonstrates the possibility these might be valuable for the detection and monitoring of the disease. Further longitudinal studies are required to determine whether differential protein expression occurs sufficiently early in the progression of the disease and with sufficient predictive value to allow proteomics analysis to be used as an early detection and on-line diagnostic tool.

ДІАГНОСТИКА ХРОНІЧНОЇ СЕРЦЕВОЇ НЕДОСТАТНОСТІ СОБАК – ІСНУЮЧІ МЕТОДИ ТА ПОДАЛЬШІ ПЕРСПЕКТИВИ

The article analyzes the current scientific work related to the study of processes of chronic heart failure (CHF), and the use of biomarkers in the diagnosis of heart disease in dogs. Thoracic radiography, electrocardiography, and echocardiography are used to diagnose heart disease in dogs but despite the use of non–invasive methods, there is uncertainty about the severity of the disease and prognosis for each patient individually. In veterinary practice for the diagnosis of myocardial lesions in animals are clinically valuable, highly sensitive and simple to use cardiac biomarkers. A biomarker is typically a substance in the blood that can be objectively measured and indicates a biologic or pathologic process or response to therapy.1 There are scores of cardiac biomarkers,but this article will focus on the 2 most clinically useful ones in the dog and cat:cardiac troponin I (cTnI) and N–terminal pro–B–type natriuretic peptide (NT–proBNP). The cardiac troponins I, T, and C (cTnI, cTnT, and cTnC) are thin filament–associated regulatory proteins of the heart muscle. Cardiac troponin I («I» for inhibition) is uniquely expressed in the myocardium and is a potent inhibitor of the process of actin–myosin cross–bridge formation. The molecular weight is 24.000 D. Cardiac troponin T («T» for tropomyosin binding) has a molecular weight of 37.000 D and binds the troponin complex to tropomyosin. Cardiac troponin C («C» for calcium) binds to calcium and starts, therefore, the crossbridge cycle. As with cTnI, approximately 95% of cTnT in man and dogs is myofibril bound and about 5% is cytosolically dissolved. Mechanisms for an elevation in circulating cardiac troponins include an increase of myocyte membrane permeability (initial release of the cytosolic troponin pool) or cell necrosis (release of myofibrilbound troponins). Four to six hours after acute myocardial cell injury, the cardiac troponin concentration in blood increases in a biphasic pattern. Plasma half–life of cardiac troponins is approximately two hours, and elimination mainly occurs via the reticuloendothelial system (cTnI and cTnT) and renal loss (cTnT). Cardiac troponins are phylogenetically highly preserved proteins with a more than 95% total structural agreement between mammals. Therefore, established human serologic tests for troponin analysis may be used reliably in pets as well. Myocardial cell injury, manifested anatomically as inflammation (endomyocarditis, myocarditis, perimyocarditis), acute degeneration, apoptosis, or necrosis or hemodynamically as transient or permanent cardiac contractile dysfunction, is a frequent consequence of physical myocardial trauma (cardiac contusion), cardiomyopathy, metabolic or toxic myocardial damage (anthracyclines, catecholamines, bacterial endotoxins, tumor necrosis factor), myocardial ischemia or infarction. However, early diagnosis of myocardial injury may be important from a therapeutic and prognostic perspective.

Severity of Mitral Valve Degeneration Is Associated with Chromosome 15 Loci in Whippet Dogs.

Mitral valve degeneration (MVD) is the most common form of heart disease in dogs, frequently leading to left-sided congestive heart failure and cardiac mortality. Although breed-specific disease characteristics and overrepresentation point towards a genetic origin for MVD, a causative mutation and complete molecular pathogenesis are unknown. Whippet dogs are overrepresented in incidence of MVD, suggesting an inherited component in this breed. Expressivity of this condition is variable with some dogs showing evidence of more severe disease at earlier ages than other dogs. This phenomenon makes a traditional case versus control genetic study prone to phenotyping error. This study sought to avoid these common pitfalls by identifying genetic loci associated with severity of MVD in Whippets through a genome-wide association study (GWAS). 138 Whippet dogs were characterized for MVD by echocardiographic examination and a novel disease severity score was developed and adjusted for age in each subject. Single nucleotide polymorphism (SNP) genotype data (170k Illumina CanineHD SnpChip) was obtained for DNA isolated from blood of each study subject. Continuous variable genome wide association was performed after correction for population stratification by efficient mixed model association expedited (EMMAX) in 130 dogs. A genome wide significant association was identified on chromosome 15 (peak locus 57,770,326; Padj = 0.049) and secondary loci of suggestive association were identified on chromosome 2 (peak locus 37,628,875; Padj = 0.079). Positional candidate genes were identified within the primary and secondary loci including follistatin-related protein 5 precursor (FSTL5) and Rho GTPase-activating protein 26 (ARHGAP26). These results support the hypothesis that severity of MVD in whippets has a genetic basis and warrants further study by either candidate gene sequencing or next-generation techniques.

Veterinary Medicine and Multi-Omics Research for Future Nutrition Targets: Metabolomics and Transcriptomics of the Common Degenerative Mitral Valve Disease in Dogs.

Canine degenerative mitral valve disease (DMVD) is the most common form of heart disease in dogs. The objective of this study was to identify cellular and metabolic pathways that play a role in DMVD by performing metabolomics and transcriptomics analyses on serum and tissue (mitral valve and left ventricle) samples previously collected from dogs with DMVD or healthy hearts. Gas or liquid chromatography followed by mass spectrophotometry were used to identify metabolites in serum. Transcriptomics analysis of tissue samples was completed using RNA-seq, and selected targets were confirmed by RT-qPCR. Random Forest analysis was used to classify the metabolites that best predicted the presence of DMVD. Results identified 41 known and 13 unknown serum metabolites that were significantly different between healthy and DMVD dogs, representing alterations in fat and glucose energy metabolism, oxidative stress, and other pathways. The three metabolites with the greatest single effect in the Random Forest analysis were γ-glutamylmethionine, oxidized glutathione, and asymmetric dimethylarginine. Transcriptomics analysis identified 812 differentially expressed transcripts in left ventricle samples and 263 in mitral valve samples, representing changes in energy metabolism, antioxidant function, nitric oxide signaling, and extracellular matrix homeostasis pathways. Many of the identified alterations may benefit from nutritional or medical management. Our study provides evidence of the growing importance of integrative approaches in multi-omics research in veterinary and nutritional sciences.

Double-chambered Right Ventricle with Intact Ventricular Septum in a Maltese Dog

A 6-year-old female Maltese (body weight, 3.1 kg) without clinical signs was referred for further evaluation of the cause of cardiac murmur. Thoracic radiography revealed right-sided cardiomegaly. Echocardiography showed marked hypertrophic remodeling of the right ventricular free wall and an anomalous muscular bundle and fibrous nodule near the subinfundibular portion of the right ventricular outflow tract (RVOT), indicating a double-chambered right ventricle (DCRV). The turbulent flow from the anomalous muscular bundle to the main pulmonary artery was 4.6 m/sec, in addition to the tricuspid valvular regurgitation of 4.4 m/sec and main pulmonary artery flow of 1.1 m/sec. The dog is receiving atenolol (0.5 mg/kg) to minimize the deleterious cardiac effects of the high afterload, even though she remains asymptomatic. This report describes a case of DCRV, a rare congenital heart disease in dogs in South Korea.

Predictive model for the detection of pulmonary hypertension in dogs with myxomatous mitral valve disease.

Pulmonary hypertension (PH) often occurs due to a left heart disease, such as myxomatous mitral valve disease (MMVD), in dogs and is diagnosed using Doppler echocardiography and estimated pulmonary arterial pressure. Diagnosis of PH in dogs requires expertise in echocardiography: however, the examination for PH is difficult to perform in a clinical setting. Thus, simple and reliable methods are required for the diagnosis of PH in dogs. The purpose of this study was to develop models using multiple logistic regression analysis to detect PH due to left heart disease in dogs with MMVD without echocardiography. The medical records of dogs with MMVD were retrospectively reviewed, and 81 dogs were included in this study and classified into PH and non-PH groups. Bivariate analysis was performed to compare all parameters between the groups, and variables with P values of <0.25 in bivariate analysis were included in multiple logistic regression analysis to develop models for the detection of PH. In multiple logistic regression analysis, the model included a vertebral heart scale short axis of >5.2 v, and a length of sternal contact of >3.3 v was considered suitable for the detection of PH. The predictive accuracy of this model (85.9%) was judged statistically adequate, and therefore, this model may be useful to screen for PH due to left heart disease in dogs with MMVD without echocardiography.

Valvuloplastia mitral em um cão com degeneração valvar

The myxomatous degeneration of the mitral valve is the most common heart disease in dogs. Its evolution is slow and leads to congestive heart failure, which is the main complication of the disease, often leading to death. Pharmacological therapy only slows down the course of heart failure. The only way to prevent the progression of the disease is surgery. The objective of this study is to report a case of mitral valvuloplasty by means of margin-to-margin repair associated to comissural plication annuloplasty and cardiopulmonar bypass in a canine with valvular disease. This case report describes the surgical technique used, as well as the pre-, trans- and postoperative care, demonstrating the effectiveness of this technique and supporting surgical intervention as an alternative for patients with congestive heart failure due to valvular degeneration.

Cardiovascular endocrinology in naturally occurring canine and feline models

Rodents are frequently used to study aspects of cardiovascular endocrinology. The present review focuses on opportunities offered by naturally occurring heart disease in dogs and cats, that is larger animal models. In particular, the benefits of using these species include the possibility of studying the same types of naturally occurring diseases as those occurring in humans, and carrying out studies in genetically similar individuals (i.e. breeds) sharing the same environment as humans. Recent findings in neuroendocrine hormones, that is natriuretic peptides, components of the renin–angiotensin–aldosterone system, and endothelin-1, in dogs and cats are reviewed in this article. As in humans, all these hormones have been evaluated as cardiovascular biomarkers in dogs and cats, and natriuretic peptides have shown promise in the diagnosis, staging and prognostication of heart disease. However, components of the renin–angiotensin–aldosterone system and endothelin-1 appear to be more useful as functional biomarkers for monitoring compensatory responses to naturally occurring heart diseases and their treatments.

Losartan versus enalapril in dogs asymptomatic carriers of myxomatous degeneration of mitral valve

The myxomatous mitral valve degeneration (DMVM) is the most common heart disease in dogs. The treatment of congestive heart failure (CHF) from DMVM is based on the use of angiotensin-converting enzyme inhibitors (ACE inhibitor) Receptor antagonists of angiotensin II (ARBs) promote complete blockade of angiotensin II, and are used in the treatment of CHF in humans, but is not common in dogs. The objective of this research was to compare the clinical responses of dogs carriers DMVM treated with enalapril-ACE inhibitors, losartan-ARBs. Thirteen dogs with DMVM and ICC class Ib were randomized into two groups as follows: G1-enalapril and G2-losartan. On physical examination, electrocardiogram and blood pressure were measured on days 0, 14, 28 and 56 after the begging of treatment. Radiographic measure, Vertebral Heart Size-VHS and ecodopplercardiográficas variables were obtained on days 0 and 56. Data were subjected to analysis of variance with repeated measures. There was no difference (P&gt;0.05) for ecodopplercardiográficas, electrocardiographic and radiographic variables between the groups studied. In relation to time, there was a decrease (P &lt;0.05) of the VHS, duration of the P wave and the QRS complex variables. We conclude that losartan acts similarly to enalapril in the initial treatment (first 56 days) of dogs with DMVM class Ib and II of the CHF.

Abdominal obesity is associated with heart disease in dogs.

BackgroundThe relationship between overall obesity and fat distribution in dogs and the development of heart disease is unclear. In the present study we evaluated the association between overall obesity and fat distribution and clinical heart disease by morphometric and computed tomography (CT)-based measurements. Body condition score (BCS), modified body mass index (MBMI, kg/m2), waist-to-hock-to-stifle distance ratio (WHSDR), waist-to-ilium wing distance ratio (WIWDR), and waist-to-truncal length ratio (WTLR) were compared between dogs with (n = 44) and without (n = 43) heart disease using receiver operating characteristic (ROC) analysis. Intra-abdominal fat (IAF) and subcutaneous fat (SQF) were measured in dogs with (n = 8) and without (n = 9) heart disease at the center of the fourth and fifth lumbar vertebrae by CT.ResultsBCS was similar between heart disease and healthy groups (3.6 ± 0.2 vs. 3.3 ± 0.1, P = 0.126). The following morphometric measurements were greater in the heart disease group compared with healthy canines: MBMI (65.0 ± 4.5 vs. 52.5 ± 3.7 kg/m2, respectively, P = 0.035); WIWDR (4.1 ± 0.1 vs. 3.1 ± 0.1, P < 0.01); and WTLR (1.25 ± 0.04 vs. 1.05 ± 0.04, P < 0.01). However, there was no significant difference in WHSDR (3.6 ± 0.1 vs. 3.7 ± 0.2, P = 0.875). Interestingly, IAF was significantly increased in dogs with heart disease compared with healthy dogs (23.5 ± 1.5% vs. 19.4 ± 1.2%, P = 0.039) whereas SQF was similar between two groups (35.5 ± 2.7% vs. 38.6 ± 3.5%, P = 0.496). Of the five morphometric indices studied, WIWDR and WTLR provided acceptable discrimination for diagnosing heart disease in dogs, with areas under the ROC curve of 0.778 (95% confidence interval [CI]:0.683-0.874) and 0.727 (95% CI:0.619-0.835), respectively.ConclusionsOur data indicate that abdominal obesity, rather than overall obesity, is associated with heart disease in dogs. Measurements of both WIWDR and WTLR are particular useful for detection of an abdominal obesity in dogs.

Genomic and genetic aspects of heart failure in dogs — A review

The most common causes of heart failure in dogs are valvular disease, predominantly endocardiosis, and myocardial disease, predominantly dilated cardiomyopathy. They are related to changes in the expression of several genes in the heart muscle and in peripheral blood nuclear cells which could be considered as prognostic or diagnostic markers of heart disease in dogs. Since many human genetic markers of heart failure have turned out to be useless in dogs, the screening for genomic markers of canine heart failure could give more insight into the molecular pathology of these diseases and aid the development of new treatment strategies.

Clinical implications of measurement of plasma atrial natriuretic peptide concentration in dogs with spontaneous heart disease

To determine whether measurement of plasma atrial natriuretic peptide (ANP) concentration could be used to identify heart disease in dogs and to assess disease severity in affected dogs. Cross-sectional study. 37 healthy dogs and 78 dogs with heart disease. Dogs were divided into 5 groups on the basis of plasma ANP concentration: healthy, ANP-1 (< 50 pg/mL; n = 19), ANP-2 (50 to 100 pg/mL; 24), ANP-3 (101 to 200 pg/mL; 20), and ANP-4 (> 200 pg/mL; 15). All dogs underwent physical examination, echocardiography, thoracic radiography, and blood sampling before treatment. Compared with healthy dogs, dogs with increased plasma ANP concentration had significant concomitant increases in heart rate, cardiothoracic ratio, vertebral heart score, fractional shortening, ratio of left atrial-to-aortic root diameter, and mitral early diastolic flow (E wave) velocity and a significant decrease in relative wall thickness. Use of plasma ANP concentration > 25 pg/mL to identify dogs with heart disease (International Small Animal Cardiac Health Council class > I) had a sensitivity of 91.0% and specificity of 94.7%. Use of plasma ANP concentration > 100 pg/mL to identify dogs with International Small Animal Cardiac Health Council class IIIb heart disease had a sensitivity of 81.0% and specificity of 81.1 %. Results may provide reference values for plasma ANP concentration in dogs and suggest that plasma ANP concentration may help to distinguish dogs with cardiac disease from clinically normal dogs. Measurement of plasma ANP concentration may be a useful marker for predicting the severity of heart disease in dogs.

Identification of 2 Loci Associated with Development of Myxomatous Mitral Valve Disease in Cavalier King Charles Spaniels

Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs. It is characterized by chronic progressive degenerative lesions of the mitral valve. The valve leaflets become thickened and prolapse into the left atrium resulting in mitral regurgitation (MR). MMVD is most prevalent in small to medium sized dog breeds, Cavalier King Charles Spaniels (CKCS) in particular. The onset of MMVD is highly age dependent, and at the age of 10 years, nearly all CKCS are affected. The incidence of a similar disease in humans-mitral valve prolapse-is 1-5%. By defining CKCSs with an early onset of MMVD as cases and old dogs with no or mild signs of MMVD as controls, we conducted a genome-wide association study (GWAS) to identify loci associated with development of MMVD. We have identified a 1.58 Mb region on CFA13 (P(genome) = 4.0 × 10(-5)) and a 1.68 Mb region on CFA14 (P(genome) = 7.9 × 10(-4)) associated with development of MMVD. This confirms the power of using the dog as a model to uncover potential candidate regions involved in the molecular mechanisms behind complex traits.

Motion Mode and Two Dimensional Echocardiographic Measurements of Cardiac Dimensions of Indonesian Mongrel Dogs

Prevalence of heart disease in dogs was very high and required early diagnosis through physical examination, electrocardiogram, and echocardiography. Normal reference values of echocardiography are highly breedspecific and need for comparison and evaluation of dogs suspected with heart disease. Therefore the aim of this study was to establish normal reference echocardiographic values for Indonesian mongrel dogs, specifically to find out intracardiac dimensions, wall thickness, and fractional shortening. Motion-mode and two-dimensional echocardiography from right parasternal short axis and long axis view were performed on nine clinically healthy dogs consisting of five males and four males. The results showed that wall thickness and fractional shortening of Indonesia mongrel dogs were higher compared with those in the other breed that have the same average weight. As opposite, the intracardiac dimensions and lumen dimensions of aorta and left atrial diameter were smaller. These differences might occur due to factors other than the dog’s habits and functions such as working and hunting, but can also be caused by the existence of breed differences. There was no significant difference between male and female dogs in terms of intracardiac dimension systole (P = 0.53), diastole (P = 0.38), fractional shortening (P = 0.053), and the ratio of aorta and left atrial diameter (P = 0.06).

The Cardiac Biomarker NT‐proBNP Is Increased in Dogs with Azotemia

Amino-terminal probrain natriuretic peptide (NT-proBNP) has been proposed as a useful biomarker for heart disease in dogs. In humans, decreased glomerular filtration rate (GFR) increases NT-proBNP. To investigate whether decreased GFR as indicated by plasma creatinine concentration is associated with increased NT-proBNP in dogs without heart disease. Four groups of dogs: healthy (n= 39), azotemic (n= 36), heart disease (n= 37), and congestive heart failure (CHF) (n= 7) presented to 2 teaching hospitals. Prospective observational cohort study. Plasma creatinine concentration and NT-proBNP were measured in every dog. Nonparametric tests were used to compare the differences among groups. The median and actual results for each group were compared with the manufacturer's recommended and previously published suggestions for cut-off values for diagnosis of heart disease. Median (range) plasma creatinine concentration was 1.47 (1.06-1.70), 4.36 (1.74-15.6), 1.22 (0.69-1.91), and 1.45 (0.63-1.64) mg/dL and median (range) NT-proBNP was 118 (2-673), 556 (37-1,819), 929 (212-5,658), and 3,144 (432-5,500) pmol/L for the healthy, azotemic, heart disease, and CHF groups, respectively. Pair-wise comparison indicated a significant difference among all groups for NT-proBNP (P< or = .049). Plasma creatinine concentration was significantly higher in the azotemic group compared with other groups (P < .001) but there was no significant among other groups. Application of 3 recommended cut-off values led to misclassification of dogs with azotemia as having heart disease. Azotemia results in NT-proBNP being increased to concentrations reported as diagnostic of heart disease or heart failure in dogs. Care should be employed when interpreting the results of NT-proBNP in patients with known or possible increased plasma creatinine concentration.

Canine heart disease: progress and promise

Canine heart disease: progress and promise

Decision making in suspected congenital heart disease in dogs and cats

CONGENITAL heart defects, such as subaortic stenosis, pulmonic stenosis and patent ductus arteriosus, are relatively common in dogs, but rarely seen in cats. Such defects are usually suspected following the...

CLINICAL VALUE OF CARDIAC TROPONIN I (CTNI), CARDIAC TROPONIN T (CTNT), SERUM B‐TYPE NATRIURETIC PEPTIED (BNP) AND PRO‐BNP IN DOGS WITH CLASS IV CONGESTIVE HEART FAILURE DUE TO MITRAL REGURGITATION

Introduction: Mitral valve disease (MVD) is the most common acquired heart disease in dogs. When it results in congestive heart failure (CHF), MVD becomes an important cause of morbidity and mortality in dogs. Markers for determining the severity of cardiac injury and the heart's response to therapy might provide valuable information regarding the overall prognosis early in the course of CHF. This information might also provide a means for identifying those dogs with MVD that are at risk for CHF and those that might benefit from specific therapeutic interventions. In this study, we propose to investigate markers of cardiac myocyte injury in dogs that present in advanced (or Class IV) CHF due to MVD. Cardiac troponin I (CTnI) and cardiac troponin T (CTnT) are markers specific for cardiac myocyte damage, and serum B‐type natriuretic peptide (BNP and pro‐BNP), for myocyte stretch. These markers have shown predictive value in human and veterinary medicine, however further investigation is required. It is our hypothesis that one or more of these markers will be elevated at presentation compared to established laboratory normal values.Methods: Fifteen dogs that presented with Class IV CHF due to MVD based on physical examination findings, thoracic radiographs, and cardiac ultrasound had a blood sample drawn to measure serum levels of CTnT, CTnI and BNP, and pro‐BNP at a commercial laboratory using immunoassays.Results: Our results show that 1 of 15 dogs had an elevated CTnT, 6 had an elevated CTnI, 0 had an elevated pro‐BNP, and 3 had and elevated BNP level above laboratory normal values.Conclusions: There was no consistent elevation of CTnI, CTnT, BNP or pro‐BNP in dogs with class IV CHF due to MR at time of presentation. Further studies need to be performed to evaluate these makers in dogs with CHF due to MR at varying intervals after admission to determine their potential benefits as markers of cardiac injury and response to therapy.

Etiology of patent ductus arteriosus in dogs.

Patent ductus arteriosus (PDA) is the most common congenital heart disease in dogs and usually causes heart failure and death unless corrected at a young age. Previous histologic studies in a line of dogs derived from Miniature Poodles with hereditary PDA identified varying degrees of hypoplasia and asymmetry of ductus-specific smooth muscle and the presence of aortalike elastic tissue in the ductus wall sufficient to cause patency. To determine if similar structural abnormalities cause PDA in other dogs, serial-section, 3-dimensional histology of ductal architecture was studied in 8 non-Poodle purebred dogs with PDA with no immediate family history of PDA. Morphologic abnormalities were observed in 7 of 8 dogs with PDA and essentially were the same as those in dogs known to have a hereditary form of PDA. These findings suggest that apparently sporadic PDA in these breeds is caused by a genetic defect in the structure of the ductus arteriosus that is similar or identical to that in the Poodle. The relatives of dogs with PDA, particularly parents, offspring, and siblings, should be screened for evidence of PDA. Dogs with PDA should not be used for breeding, regardless of breed.