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Objective—To evaluate the use of 24-hour ambulatory electrocardiography (AECG) for the detection of ventricular premature complexes (VPC) in healthy dogs.

Design—Case series.

Animals—50 healthy mature dogs.

Procedure—A 24-hour AECG was performed on each dog and evaluated for the presence of VPC.

Results—Fifty dogs weighing between 18.2 to 40.9 kg (40 and 90 lb) representing 13 breeds were evaluated; there were 4 sexually intact females, 21 spayed females, 4 sexually intact males, and 21 castrated males. Ages ranged from 1 to 12 years. Thirty-four dogs had no VPC; 16 dogs had between 1 and 24 VPC. The grade of arrhythmia ranged from 1 to 4, with 4 dogs having an arrhythmia with a grade > 1. Significant differences were not detected between the group of dogs with VPC and those without VPC with regard to sex, age, and minimum, maximum, or mean heart rate.

Conclusions and Clinical Relevance—We conclude that healthy mature dogs have infrequent VPC, as detected by use of 24-hour AECG. The presence of numerous or sequential VPC may be suggestive of cardiac or systemic disease and may indicate the need for thorough clinical evaluation. (J Am Vet Med Assoc 2001;218:1291–1292)

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in Journal of the American Veterinary Medical Association


Objective—To determine clinical features of dilated cardiomyopathy (DCM) in Great Danes and to determine whether DCM is familial in this breed.

Design—Retrospective study.

Animals—17 Great Danes with DCM.

Procedure—Medical records of Great Danes in which DCM was diagnosed on the basis of results of echocardiography (fractional shortening < 25%, endsystolic volume index > 30 ml/m2 of body surface area) were reviewed. Pedigrees were obtained for affected animals, as well as for other Great Danes in which DCM had been diagnosed.

Results—Dilated cardiomyopathy appeared to be familial and was characterized by ventricular dilatation, congestive heart failure (left-sided or biventricular), and atrial fibrillation. Pedigree analysis suggested that DCM was inherited as an X-linked recessive trait, but the mode of inheritance could not be definitively identified.

Conclusions and Clinical Relevance—Results suggest that DCM may be an X-linked recessive trait in Great Danes. Thus, dogs with DCM probably should not be used for breeding, and female offspring of affected dogs should be used cautiously. Male offspring of affected females are at an increased risk of developing DCM and should be evaluated periodically for early signs of disease. Results of pedigree analysis were preliminary and should be used only as a guide for counseling breeders, rather than as a basis for making breeding decisions. (J Am Vet Med Assoc 2001;218:729–732)

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in Journal of the American Veterinary Medical Association


Objective—To determine survival times in dogs with severe subvalvular aortic stenosis (SAS) treated by means of balloon valvuloplasty or with atenolol, a β-adrenoceptor blocking drug.

Design—Prospective study.

Animals—38 dogs < 24 months old with severe SAS (peak systolic pressure gradient ≥ 80 mm Hg).

Procedure—10 dogs underwent balloon valvuloplasty and were reexamined 6 weeks later to determine the feasibility of the procedure. The remaining 28 dogs were randomly assigned to undergo balloon valvuloplasty (n = 15) or to be treated with atenolol long term (13) and were reexamined annually for 9 years or until the time of death.

Results—For the first 10 dogs, mean pressure gradient 6 weeks after balloon valvuloplasty (mean ± SD, 119 ± 32.6 mm Hg) was significantly decreased, compared with mean baseline pressure gradient (167 ± 40.1 mm Hg). Median survival time for dogs that underwent balloon valvuloplasty (55 months) was not significantly different from median survival time for dogs treated with atenolol (56 months).

Conclusions and Clinical Relevance—Results suggest that balloon valvuloplasty can result in a significant decrease in the peak systolic pressure gradient in dogs with severe SAS, at least for the short term. No clear benefit in survival times was seen for dogs that underwent balloon valvuloplasty versus dogs that were treated with atenolol. (J Am Vet Med Assoc 2005;227:420–424)

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in Journal of the American Veterinary Medical Association


Objective—To evaluate the use of in-hospital electrocardiography (ECG) for detection of ventricular premature complexes (VPC), compared with 24-hour ambulatory ECG.

Design—Original study.

Animals—188 Boxers > 9 months old; 31 had a history of syncope, and 157 were healthy (no history of syncope).

Procedure—In-hospital ECG was performed on all Boxers for at least 2 minutes. Within 7 days after the in-hospital ECG was completed, 24-hour ambulatory ECG was performed.

Results—The specificity of in-hospital ECG was 100% for the detection of at least 50 VPC in a 24-hour period in dogs with syncope and 93% in healthy dogs. In-hospital ECG had poor sensitivity, although sensitivity increased as the number of VPC per 24 hours increased.

Conclusions and Clinical Relevance—Use of in-hospital ECG is highly specific for detection of at least 50 VPC during a 24-hour period. However, in-hospital ECG is insensitive, and a lack of VPC does not suggest that the dog does not have a substantial number of VPC during that same period. The use of in-hospital ECG appears to be inadequate for screening purposes and therapeutic evaluations in mature Boxers with ventricular arrhythmic disease. (J Am Vet Med Assoc 2001;218:222–224)

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in Journal of the American Veterinary Medical Association


To determine whether prevalence of naturally developing chronic infection with Trypanosoma cruzi in dogs in Texas changed between 1987 and 1996 and to characterize clinical aspects of the disease.


Retrospective study.


11 dogs with chronic infection with T cruzi.


Number of positive serologic test results for T cruzi obtained between 1987 and 1996 were compared with the number of tests for T cruzi performed during the same period. Survival time, signalment, and clinical signs of dogs and results of thoracic radiography, electrocardiography, and echocardiography were evaluated. The Mann-Whitney test was used to assess the association between age at time of initial examination and survival time.


The proportion of positive test results increased, compared with the number of tests submitted, during the 9-year period. Clinical signs in affected dogs were consistent with right-sided cardiac disease. Results of thoracic radiography were nonspecific. Conduction disturbances and supraventricular and ventricular arrhythmias were evident. Echocardiographic abnormalities, including chamber enlargement and functional impairment, were detected. Dogs were characterized on the basis of survival time; group-1 dogs (n = 6) survived 0 to 5 months, and group-2 dogs (5) survived 31 to 60 months. Age at time of initial examination was associated with survival time.

Clinical Implications—

Clinical course of disease varied. Electrocardiographic and echocardiographic changes may be detected. Clinicians should be aware of the potential for T cruzi infection in dogs with clinical signs of right-sided cardiac dysfunction and unexplained conduction disturbances and arrhythmias. Prevalence of this disease may be increasing in some regions of Texas. (J Am Vet Med Assoc 1998;213:497-500)

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in Journal of the American Veterinary Medical Association


Objective—To compare plasma fatty acid concentrations and the relationships of fatty acids to arrhythmias in Boxers versus Doberman Pinschers.

Animals—38 Boxers and 13 Doberman Pinschers.

Procedures—Boxers and Doberman Pinschers evaluated via Holter recording and for which a blood sample was available were included. Echocardiograms were performed in 49 of 51 dogs. The number of ventricular premature complexes (VPCs)/24 h was counted and fatty acids analyzed. Plasma fatty acid concentrations and VPCs/24 h, as well as correlations between the 2 variables, were compared between the 2 breeds.

Results—Compared with the Doberman Pinschers, Boxers had significantly higher plasma concentrations of γ-linolenic acid but lower concentrations of arachidonic acid. Total n-6 fatty acids and total polyunsaturated fatty acid concentrations were higher in Doberman Pinschers. There were significant, but weak, positive correlations between VPCs and oleic acid, total n-3 fatty acids, and total n-9 fatty acids in Boxers but not in Doberman Pinschers.

Conclusions and Clinical Relevance—Data suggested that plasma fatty acid concentrations may differ between Boxers and Doberman Pinschers and that the relationship between fatty acid concentrations and VPCs may be different between these 2 breeds.

Full access
in American Journal of Veterinary Research


Objective—To evaluate the coding region of the cardiac actin gene in Doberman Pinschers with dilated cardiomyopathy (DCM) for mutations that could be responsible for the development of the condition

Animals—28 dogs (16 Doberman Pinschers with DCM and 12 mixed-breed control dogs).

Procedure—Ten milliliters of blood was collected from each dog for DNA extraction. Polymerase chain reaction (PCR) primers were designed to amplify canine exonic regions, using the sequences of exons 2 to 6 of the cardiac actin gene. Single-stranded conformational polymorphism analysis was performed for each exon with all samples. Autoradiographs were analyzed for banding patterns specific to affected dogs. The DNA sequencing was performed on a selected group of affected and control dogs.

Results—Molecular analysis of exons 2 to 6 of the cardiac actin gene did not reveal any differences in base pairs between affected dogs and control dogs selected for DNA evaluation.

Conclusions—Mutations in exons 5 and 6 of the cardiac actin gene that have been reported in humans with familial DCM do not appear to be the cause of familial DCM in Doberman Pinschers. Additionally, evaluation of exons 2 to 6 for causative mutations did not reveal a cause for inherited DCM in these Doberman Pinschers. Although there is evidence that DCM in Doberman Pinschers is an inherited problem, a molecular basis for this condition remains unresolved. Evaluation of other genes coding for cytoskeletal proteins is warranted. ( Am J Vet Res 2001;62:33–36)

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in American Journal of Veterinary Research


Objective—To measure QT interval duration and QT dispersion in Boxers and to determine whether QT variables correlate with indices of disease severity in Boxers with familial ventricular arrhythmias, including the number of ventricular premature complexes per day, arrhythmia grade, and fractional shortening.

Animals—25 Boxers were evaluated by ECG and echocardiography.

Procedure—The QT interval duration was measured from 12-lead ECG and corrected for heart rate (QTc), using Fridericia's formula. The QT and QTc were calculated for each lead, from which QT and QTc dispersion were determined. Echocardiography and 24-hour ambulatory ECG were performed to evaluate for familial ventricular arrhythmias. Total number of ventricular premature complexes, arrhythmia grade, and fractional shortening were determined and used as indices of disease severity.

Results—There was no correlation between any QT variable and total number of ventricular premature complexes, arrhythmia grade, or fractional shortening. No difference between QT dispersion and QTc dispersion was identified, and correction for heart rate did not affect the results.

Conclusions and Clinical Relevance—QT interval duration and dispersion did not correlate with indices of disease severity for familial ventricular arrhythmias. Heart rate correction of the QT interval did not appear to be necessary for QT dispersion calculation in this group of dogs. QT dispersion does not appear to be a useful noninvasive diagnostic tool in the evaluation of familial ventricular arrhythmias of Boxers. Identification of affected individuals at risk for sudden death remains a challenge in the management of this disease. (Am J Vet Res 2001;62:1481–1485)

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in American Journal of Veterinary Research


Objective—To perform polymerase chain reaction (PCR) analysis on paraffin-embedded myocardium from dogs with dilated cardiomyopathy (DCM) and dogs with myocarditis to screen for canine parvovirus, adenovirus types 1 and 2, and herpesvirus.

Sample Population—Myocardial specimens from 18 dogs with an antemortem diagnosis of DCM and 9 dogs with a histopathologic diagnosis of myocarditis were evaluated.

Procedure—Paraffin-embedded myocardial specimens were screened for viral genome by PCR analysis. Positive-control specimens were developed from cell cultures as well as paraffin-embedded tissue specimens from dogs with clinical and histopathologic diagnoses of viral infection with canine parvovirus, adenovirus types 1 and 2, and herpesvirus. The histologic characteristics of all myocardial specimens were classified regarding extent, location, and type of inflammation and fibrosis.

Results—Canine adenovirus type 1 was amplified from 1 specimen from a dog with DCM. Canine parvovirus, adenovirus type 2, and herpesvirus were not amplified from any myocardial specimens. Histologic analysis of specimens from dogs with DCM revealed variable amounts of fibrosis; myocardial inflammation was observed in 1 affected dog. Histopathologic analysis of specimens from dogs with myocarditis disclosed variable degrees of inflammation and fibrosis.

Conclusions and Clinical Relevance—Viral agents canine parvovirus, adenovirus types 1 and 2, and herpesvirus are not commonly associated with DCM or active myocarditis in dogs. Additional studies evaluating for nucleic acid from viruses that less commonly affect dogs or different types of infectious agents may be warranted to gain insight into the cause of DCM and myocarditis in dogs. ( Am J Vet Res 2001;62: 130–135)

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in American Journal of Veterinary Research


Objective—To determine whether plasma concentrations of tumor necrosis factor-α (TNF-α) are increased in cats with congestive heart failure (CHF) secondary to cardiomyopathy.

Animals—26 adult cats with CHF and cardiomyopathy and 9 healthy control cats.

Procedure—Plasma concentrations of TNF-α were measured in cats with CHF and cardiomyopathy. Tumor necrosis factor-α was measured by quantifying cytotoxic effects of TNF-α on L929 murine fibrosarcoma cells.

Results—Concentrations of TNF-α were increased (0.13 to 3.6 U/ml) in 10 of 26 cats with CHF but were undetectable in the other 16 cats with CHF and all control cats. In 20 of 26 cats with CHF, right-sided heart failure (RHF) was evident; TNF-α concentrations were increased in 9 of these 20 cats. The remaining 6 cats had left-sided heart failure (LHF); TNF-α concentrations were increased in only 1 of these cats. Age of cats with LHF (mean ± SD, 12.1 ± 6.2 years) was not significantly different from age of the cohort with RHF (10.5 ± 5.2 years). Body weight of cats with increased TNFα concentrations (5.4 ± 1.8 kg) was not significantly different from body weight of cats with CHF that did not have measurable concentrations of TNF-α (4.7 ± 1.6 kg).

Conclusionss and Clinical Relevance—Concentrations of TNF-α were increased in many cats with CHF. Cats with RHF were most likely to have increased TNF-α concentrations. Increased plasma concentrations of TNF-α in cats with CHF may offer insights into the pathophysiologic mechanisms of heart failure and provide targets for therapeutic interventions. (Am J Vet Res 2002;63:640–642)

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in American Journal of Veterinary Research