Magnetic Resonance Imaging of Right Ventricular Morphology and Function in Boxer Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disease characterized by fibrofatty replacement of the right ventricle and ventricular tachyarrhythmias, reported most commonly in the Boxer dog. Although ARVC is characterized as a myocardial disease, the impact of the disease on the function of the right ventricle has not been well studied.
Objective: To noninvasively evaluate the function and anatomy of the right ventricle in Boxer dogs with ARVC.
Animals: Five adult Boxer dogs with ARVC and 5 healthy size-matched hound dogs.
Methods: Magnetic resonance imaging was performed on an ECG-gated conventional 1.5-T scanner using dark blood imaging and cine acquisitions. Images were evaluated by delineation of endocardial right and left ventricular contours in the end-diastolic and end-systolic phases of each slice. Right and left end-systolic and end-diastolic volumes were generated using Simpson's rule and ejection fraction was calculated. Images were evaluated for right ventricular (RV) aneurysms and wall motion abnormalities. Spin echo images were reviewed for the presence of RV myocardial fatty replacement or scar.
Results: RV ejection fraction was significantly lower in Boxers with ARVC compared with the controls (ARVC 34%± 11 control 53%± 10, P < .01). There was an RV aneurysm in 1 dog with ARVC but not in any of the controls. RV myocardial gross fatty changes were not observed in dogs of either group.
Conclusions and Clinical Importance: These findings could be interpreted to suggest that arrhythmias and myocardial dysfunction precede the development of morphological abnormalities in dogs with ARVC.     

Omega-3 fatty acids in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy

BACKGROUND: Omega-3 fatty acids have been shown to reduce arrhythmia in animal models and people. These effects have not been studied in dogs with spontaneously occurring arrhythmia. HYPOTHESIS: Fish oil will reduce the frequency of ventricular arrhythmia in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC). ANIMALS: Twenty-four Boxers with ARVC were included in this study. METHODS: Asymptomatic Boxers not receiving antiarrhythmic medications were evaluated with echocardiogram and electrocardiogram. Dogs with at least 1 ventricular premature contraction (VPC) received 24-hour ambulatory electrocardiography (AECG) recordings. Dogs with > 95 VPCs in 24 hours were randomized to 1 of 3 treatments: (1) Fish oil, 2 g; (2) Flax oil, 2 g; or (3) sunflower oil, 2 g (Control group), for 6 weeks. Investigators and owners were blinded to the treatment groups. All baseline measurements were repeated after the 6-week supplementation. RESULTS: There were no differences at baseline for age, sex, blood pressure, weight, echocardiographic measurements, or VPCs. Median number of VPCs in 24 hours for all dogs was 543 (range, 96-40,063) at baseline and 193 (range, 6-14,825) after 6 weeks of supplementation. VPCs/24 h were reduced for the Fish oil group (baseline median = 397 [range, 249-10,587]; 6-week median = 162 [range, 16-3,781]; P = .02), but not for the Flax oil (P = .58) or Control (P = .48) groups. CONCLUSIONS AND CLINICAL IMPORTANCE: These data suggest that fish oil, but not flax oil, supplementation for 6 weeks reduces arrhythmia in Boxers with ARVC and that it could be useful in treating this common disease. Further studies are needed to determine optimal dose and duration of treatment.     

Efficacy of Benazepril Hydrochloride to Delay the Progression of Occult Dilated Cardiomyopathy in Doberman Pinschers

Background: Angiotensin converting enzyme inhibitors (ACEIs) are recommended in people to treat asymptomatic (occult) dilated cardiomyopathy (DCM). Efficacy of therapy in occult DCM in dogs is unknown.
Hypothesis: ACEIs, specifically benazepril hydrochloride (BH), will delay the onset of overt DCM in Doberman Pinschers.
Animals: Ninety-one Doberman Pinschers were studied, 57 dogs received BH, and 34 dogs no ACEI.
Methods: Retrospective study of the medical records of all Doberman Pinschers with occult DCM that received BH or no ACEI between April 1989 and February 2003. Two criteria of left ventricular enlargement were used for enrollment: one independent of body weight (BW) (C1) and the other indexed to BW (C2). Cox proportional hazards analyses were used to identify variables associated with the onset of overt DCM.
Results: On univariate analysis the median time to onset of overt DCM was significantly longer for the benazepril group (for C1: 425 days for BH, 95% confidence interval [CI] 264–625 days; 339 days for no ACEI, CI 172–453 days, P = .02; for C2: 454 days for BH, CI 264–628 days; 356 days for no ACEI, CI 181–547 days, P = .02). The hazard ratio (HR) (benazepril/no ACEI) was 0.57, CI 0.35–0.94, P = .03 for C1; HR = 0.56, CI 0.34–0.93, P = .02 for C2. On multivariate analysis, BH significantly delayed onset of overt DCM (HR [benazepril/no ACEI] = 0.45, CI 0.26–0.78, P < .01, for C1; HR = 0.36, CI 0.21–0.63, P < .01, for C2).
Conclusions: BH in particular and ACEIs in general might delay the progression of occult DCM. Prospective studies are warranted to test this theory.     

Serum Cardiac Troponin I Concentration in Retired Racing Greyhounds

Background: Cardiac troponin I (cTnI) is a polypeptide found specifically in cardiac muscle tissue that has been used as a diagnostic and prognostic indicator of cardiomyopathy. Increases in cTnI are associated with myocardial pathologic processes. However, high serum cTnI concentrations have been observed in normal Greyhounds.
Hypothesis: We hypothesized that Greyhounds have cTnI concentrations higher than non-Greyhound dogs, and that a separate reference range should be established for Greyhounds.
Animals: Blood samples were collected from the jugular vein from a group of 20 healthy Greyhound blood donors.
Methods: Analysis of serum cTnI was performed with an immunoassay system with a detection level of 0.01 ng/mL, as described previously. The Greyhound values were compared with 2 groups of Boxers with and without arrhythmogenic right ventricular cardiomyopathy (ARVC), and to a group of non-Boxer control dogs from a previous study.
Results: The mean cTnI concentration in Greyhounds was significantly higher ( P < .0001) than that in non-Greyhound control dogs, although not significantly different from normal Boxers ( P = .50), or Boxers with ARVC ( P = .58). Greyhound serum cTnI concentrations were in the range found in Boxers with ARVC. The proposed reference range for cTnI in Greyhounds is 0.05–0.16 ng/mL.
Conclusions and Clinical Importance: Greyhounds have a reference range for serum cTnI concentrations that differs from that of other previously published reference ranges for dogs of other breeds. Until a broader database and more precise reference range can be established, caution should be exercised in interpreting serum cTnI concentrations in Greyhounds with suspected cardiac disease.     

Remission of Histiocytic Ulcerative Colitis in Boxer Dogs Correlates with Eradication of Invasive Intramucosal Escherichia coli

Background: Historically, histiocytic ulcerative (HUC) (or granulomatous) colitis of Boxer dogs was considered an idiopathic immune-mediated disease with a poor prognosis. Recent reports of dramatic responses to enrofloxacin and the discovery of invasive Escherichia coli within the colonic mucosa of affected Boxer dogs support an infectious etiology.
Hypothesis: Invasive E. coli is associated with colonic inflammation in Boxer dogs with HUC, and eradication of intramucosal E. coli correlates with clinical and histologic remission.
Animals: Seven Boxer dogs with HUC.
Methods: Prospective case series. Colonic biopsies were obtained at initial evaluation in 7 dogs, and in 5 dogs after treatment with enrofloxacin. Biopsies were evaluated by standardized histopathology, and fluorescence in situ hybridization (FISH) with probes to eubacteria and E. coli .
Results: Intramucosal E. coli was present in colonic biopsies of 7/7 Boxers with HUC. Clinical response was noted in all dogs within 2 weeks of enrofloxacin (7±3.06 mg/kg q24 h, for 9.5±3.98 weeks) and was sustained in 6 dogs (median disease-free interval to date of 47 months, range 17–62). FISH was negative for E. coli in 4/5 dogs after enrofloxacin. E. coli resistant to enrofloxacin were present in the FISH-positive dog that relapsed.
Conclusions and Clinical Relevance: The correlation between clinical remission and the eradication of mucosally invasive E. coli during treatment with enrofloxacin supports the causal involvement of E. coli in the development of HUC in susceptible Boxer dogs. A poor response to enrofloxacin treatment might be due to colonization with enrofloxacin-resistant E. coli .     

Arrhythmogenic right ventricular cardiomyopathy in Boxer dogs is associated with calstabin2 deficiency

ObjectiveTo examine the presence and effect of calstabin2-deficiency in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC).AnimalsThirteen Boxer dogs with ARVC.Materials and methodsTissue samples were collected for histopathology, oligonucleotide microarray, PCR, immunoelectrophoresis, ryanodine channel immunoprecipitation and single-channel recordings, and calstabin2 DNA sequencing.ResultsIn cardiomyopathic Boxer dogs, myocardial calstabin2 mRNA and protein were significantly decreased as compared to healthy control dogs (calstabin2 protein normalized to tetrameric cardiac ryanodine receptor (RyR2) complex: affected, 0.51 ± 0.04; control, 3.81 ± 0.22; P < 0.0001). Calstabin2 deficiency in diseased dog hearts was associated with a significantly increased open probability of single RyR2 channels indicating intracellular Ca²⁺ leak. PCR-based sequencing of the promoter, exonic and splice site regions of the canine calstabin2 gene did not identify any causative mutations.ConclusionsCalstabin2 deficiency is a potential mechanism of Ca²⁺ leak-induced ventricular arrhythmias and heart disease in Boxer dogs with ARVC.     

Arrhythmogenic right ventricular cardiomyopathy in dogs

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited myocardial disease seen in dogs, cats, and humans. A common entity in Boxers and the related English bulldog, the disease is characterized by fatty or fibrofatty replacement of the myocardium, ventricular arrhythmias, and the potential for syncope or sudden death. In some individuals, concomitant left ventricular involvement results in systolic dysfunction and a progression to congestive heart failure. The clinical and pathological characteristics of ARVC share many similarities in dogs and humans, and Boxers serve as an important spontaneous model of the disease.Although multiple mechanisms have been implicated in the pathogenesis of ARVC, the disease is ultimately considered to be a disorder of the desmosome. Multiple causal genetic mutations have been identified in people, and over 50% of affected humans have an identifiable mutation in desmosomal proteins. To date, only a single genetic mutation has been associated with ARVC in Boxer dogs. Other as-yet-undiscovered genetic mutations and epigenetic modifiers of the disease are likely. Treatment of ARVC in dogs is focused on controlling ventricular arrhythmias and associated clinical signs. This article will review the pathophysiology, clinical diagnosis, treatment, and prognosis of ARVC in the dog.     

Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

Background: Ventricular arrhythmias (VA) and sudden death are inherited in German Shepherd Dogs (GSDs).
Objectives: To estimate the genetic parameters (heritabilities and correlations) of 3 traits of VA (single premature ventricular complexes (PVCs), 2 consecutive PVCs (couplets), and 3 or more consecutive PVCs—ventricular tachycardia [VT]).
Animals: Three hundred and ninety-eight GSDs.
Methods: Prospective, observational, case control study. Dogs were phenotyped by 24-hour ambulatory ECG from 6 to 45 weeks of age. Edited ECG records included the number of incidents of (1) single PVCs, (2) couplets, and (3) VT.
Results: A data set of 1,239 Holter records from 398 GSDs was used to estimate genetic variables. Phenotypic correlations for affectedness (binarily coded 0/1) of the 3 traits ranged from 0.55 to 0.74, whereas correlations for severity (continuous values of 24-hour VA counts) ranged from 0.26 to 0.39. Estimates of genetic correlation among the severity traits were 0.06 to 0.27. Estimated heritabilities were 0.54, 0.54, and 0.46 for affectedness and 0.33, 0.69, and 0.69 for severity of PVCs, couplets, and VT, respectively. Month and year of birth and age at ECG recording had significant effects on all 3 traits. Season of ECG recording had a significant effect on the number of single PVCs, but not couplets or incidents of VT. Age of onset differed, with single PVCs appearing an average of 4 days earlier than couplets and VT.
Conclusion: These results imply a strong genetic component for this disease but suggest that differences in the 3 traits should be taken into consideration in studies to identify the underlying genes.     

Genetic and Environmental Risk Indicators in Canine Non-Hodgkin's Lymphomas: Breed Associations and Geographic Distribution of 608 Cases Diagnosed throughout France over 1 Year

Background: The etiology of non-Hodgkin's lymphomas (NHL) is multifactorial. Environmental and genetic factors are frequently incriminated both in humans and dogs.
Objectives: Our purpose was to study the geographic distribution of canine NHL (CNHL) in France and to evaluate genetic and environmental influences.
Animals: Six hundred and eight cases of CNHL, diagnosed throughout France over 1 year, were collected from 7 Veterinary Histopathologic Laboratories.
Methods: Retrospective study. Breeds affected by lymphomas were compared with the national population and associations between breed and immunophenotype were studied. The distribution of CNHL and canine T-cell NHL per 100,000 dogs per department was compared with the distribution of waste incinerators, polluted sites, and radioactive waste.
Results: The breeds significantly overrepresented among lymphoma cases were Boxer, Setter, and Cocker Spaniel ( P < .001). There was a significant association between Boxer and T-cell NHL ( P < .001), and between German Shepherd and Rottweiler and B-cell NHL ( P < .01). The geographic distribution of CNHL and canine T-cell NHL indicated significant heterogeneity. Significant association between distributions of CNHL and waste incinerators (ρ= 0.25, P < .05), polluted sites (ρ= 0.36, P < .001), and radioactive waste (ρ= 0.51, P < .001) was found.
Conclusions and Clinical Importance: Influence of genetics in the development of CNHL was supported by the existence of an association between breed and immunophenotype. Waste incinerators, polluted sites, and radioactive waste could just be considered as risk indicators of CNHL, but not as risk factors. Case-control studies around critical sites are necessary to confirm the implication of those environmental factors in the development of CNHL.     

Echocardiographic assessment of right ventricular systolic function in Boxers with arrhythmogenic right ventricular cardiomyopathy

Objectives

To determine whether there are differences in measures of longitudinal right ventricular (RV) systolic function among Boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC) compared with healthy control Boxer dogs. To explore relationships between markers of RV systolic function and age, body weight, gender, arrhythmia frequency, and markers of left ventricular (LV) systolic function in Boxer dogs.

Evaluation of serum cardiac troponin I concentration in Boxers with arrhythmogenic right ventricular cardiomyopathy

OBJECTIVE: To evaluate serum cardiac troponin I (cTnI) concentrations in Boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC), unaffected (control) Boxers, and control non-Boxers. ANIMALS: 10 Boxers with a clinical diagnosis of ARVC defined by > or = 1,000 ventricular premature complexes (VPCs)/24 h on an ambulatory ECG, 10 control Boxers assessed as normal by the presence of < 5 VPCs/24h, and 10 control non-Boxers. PROCEDURES: Serum was extracted from a blood sample from each dog. Analysis of serum cTnI concentrations was performed. RESULTS: Mean +/- SD serum cTnI concentration was 0.142 +/- 0.05 ng/mL for Boxers with ARVC, 0.079 +/- 0.03 ng/mL for control Boxers, and 0.023 +/- 0.01 ng/mL for control non-Boxers. A significant difference in serum cTnI concentrations was observed among the 3 groups. In the combined Boxer population (ie, Boxers with ARVC and control Boxers), a significant correlation was found between serum cTnI concentration and number of VPCs/24 h (r = 0.78) and between serum cTnI concentration and grade of ventricular arrhythmia (r = 0.77). CONCLUSIONS AND CLINICAL RELEVANCE: Compared with clinically normal dogs, Boxers with ARVC had a significant increase in serum cTnI concentration. For Boxers, correlations were found between serum cTnI concentration and number of VPCs/24 h and between concentration and the grade of arrhythmia. Because of the overlap in serum cTnI concentrations in control Boxers and Boxers with ARVC, future studies should evaluate the correlation of serum cTnI concentration with severity of disease in terms of degree of myocardial fibrofatty changes.     

Familial Ventricular Arrhythmias in Boxers

The purposes of this study were to evaluate families of Boxers with ventricular arrhythmias to determine whether this disorder is a familial trait and, if so, to determine the mode of inheritance. Eighty-two Boxers were evaluated by physical examination, electrocardiogram, echocardiogram, and 24-hour ambulatory electrocardiogram. Dogs were considered affected if at least 50 premature ventricular complexes (PVCs) were observed during a 24-hour period. All dogs were at least 6 years of age at evaluation. Complete cardiovascular examinations were performed on dogs from 6 extended families. The 2 most complete pedigrees were used to determine the pattern of inheritance. The number of PVCs observed during a 24-hour period in affected dogs ranged from 112 to 4,894 (mean +/- SD, median; 1,309 +/- 2,609, 1,017). The number of PVCs observed during a 24-hour period in the unaffected dogs ranged from 0 to 16 (7 +/- 10, 12). Pedigree evaluation was performed to determine pattern of inheritance. An autosomal dominant pattern was determined to be most likely because a sex predisposition was not observed, affected individuals were observed in every generation, and 2 affected individuals produced unaffected offspring. We conclude that familial ventricular arrhythmias is inherited as an autosomal dominant trait in some Boxers.     

Assessment of plasma brain natriuretic peptide concentration in Boxers with arrhythmogenic right ventricular cardiomyopathy

OBJECTIVE: To determine whether Boxers with a clinical diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) have increased plasma concentrations of brain natriuretic peptide (BNP), compared with concentrations in clinically normal dogs. ANIMALS: 13 Boxers with ARVC, 9 clinically normal Boxers, 10 clinically normal non-Boxer dogs, and 5 hound dogs with systolic dysfunction. PROCEDURE: All Boxers were evaluated via 24-hour ambulatory electrocardiography and echocardiography; the number of ventricular premature contractions (VPCs) per 24 hours was assessed. Hound dogs with cardiac pacing-induced systolic dysfunction (positive control dogs) and clinically normal non-Boxer dogs (negative control dogs) were evaluated echocardiographically. Three milliliters of blood was collected from each dog for measurement of plasma BNP concentration by use of a radioimmunoassay. RESULTS: Mean +/- SD plasma BNP concentration for the ARVC-affected Boxers, clinically normal Boxers, negative control dogs, and positive control dogs was 11.0 +/- 4.6 pg/mL, 7.9 +/- 3.2 pg/mL, 11.5 +/- 4.9 pg/mL, and 100.8 +/- 56.8 pg/mL, respectively. Compared with findings in the positive control group, plasma BNP concentration in each of the other 3 groups was significantly different. There was no significant difference in BNP concentration between the 2 groups of Boxers. A significant correlation between plasma BNP concentration and number of VPCs per 24 hours in the ARVC-affected Boxers was not identified. CONCLUSIONS AND CLINICAL RELEVANCE: A significant difference in BNP concentration between Boxers with ARVC and clinically normal Boxers was not identified. Results suggest that BNP concentration may not be an indicator of ARVC in Boxers.     

Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers

OBJECTIVE: To evaluate the effect of 4 antiarrhythmic treatment protocols on number of ventricular premature complexes (VPC), severity of arrhythmia, heart rate (HR), and number of syncopal episodes in Boxers with ventricular tachyarrhythmias. DESIGN: Randomized controlled clinical trial. ANIMALS: 49 Boxers. PROCEDURE: Dogs with > 500 VPC/24 h via 24-hour ambulatory ECG (AECG) were treated with atenolol (n = 11), procainamide (11), sotalol (16), or mexiletine and atenolol (11) for 21 to 28 days. Results of pre- and posttreatment AECG were compared with regard to number of VPC/24 h; maximum, mean, and minimum HR; severity of arrhythmia; and occurrence of syncope. RESULTS: Significant differences between pre- and posttreatment number of VPC, severity of arrhythmia, HR variables, or occurrence of syncope were not observed in dogs treated with atenolol or procainamide. Significant reductions in number of VPC, severity of arrythmia, and maximum and mean HR were observed in dogs treated with mexiletine-atenolol or sotalol; occurrence of syncope was not significantly different between these 2 treatment groups. CONCLUSIONS AND CLINICAL RELEVANCE: Treatment with sotalol or mexiletine-atenolol was well tolerated and efficacious. Treatment with procainamide or atenolol was not effective.     

The efficacy and safety of external biphasic defibrillation in toy breed dogs

Objective: To evaluate the efficacy and safety of biphasic (BP) defibrillation in toy breed dogs (<5 kg of body weight).
Design: Prospective, clinical experimental study.
Setting: Veterinary teaching hospital.
Animals: Five dogs (pilot study) and 10 dogs (comparison study of biphasic versus monophasic defibrillation).
Measurements and main results: The efficacy of defibrillation was compared by estimating E80 (80% probability of successful defibrillation) after biphasic (BP) and monophasic (MP) defibrillations. The E80 for BP defibrillation was 7.24±1.33 J (2.24±0.41 J/kg) and 10.24±1.34 J (3.18±0.12 J/kg) for MP defibrillation. BP waveform required 30% less shock energy for a successful defibrillation. In order to compare the safety of defibrillation, we evaluated changes in cardiac biomarkers, electrocardiogram, echocardiographical left ventricular index, and aortic pressure during and after BP and MP defibrillation. All dogs treated by either BP or MP defibrillation survived. Pulseless electrical activity occurred in 2 of 5 dogs during MP defibrillation. The levels of cardiac biomarkers were elevated and sustained for longer periods in the MP defibrillation group. Electrocardiographic changes (e.g., QT prolongation, the time to return to an isoelectric ST segment after shocks) were more severe and longer in the MP defibrillation group. In addition, overall left ventricular cardiac performance was severely depressed in the MP group compared with the BP group.
Conclusion: Our findings suggest that BP defibrillation is more effective and safer than MP defibrillation. We determined the acceptable shock energy to be 2–4 J/kg for toy breed dogs.     

Evaluation of spontaneous variability in the frequency of ventricular arrhythmias in Boxers with arrhythmogenic right ventricular cardiomyopathy

OBJECTIVE: To evaluate spontaneous variability in the frequency of ventricular arrhythmias and assess the influence of day of ECG recording and day of week on arrhythmia frequency in Boxers affected with arrhythmogenic right ventricular cardiomyopathy (ARVC). DESIGN: Prospective study. ANIMALS: 10 Boxers with ARVC with prior ambulatory ECG recordings that included > or = 500 ventricular premature complexes/24 h. PROCEDURE: Consecutive 24-hour ambulatory ECG recordings were obtained during a 7-day period in each dog. The number of ventricular premature complexes and grade of the arrhythmia were obtained from each recording. For each dog, the number of ventricular premature complexes for each recording was evaluated to identify any differences relative to the day of recording (recording 1 to 7) and day of the week (Monday through Sunday). RESULTS: Spontaneous variability accounted for as much as 80% of the change in frequency of ventricular premature complexes in dogs with frequent arrhythmias; this value was almost 100% in dogs with less frequent arrhythmias. Grade of arrhythmia was less variable but was also inversely related to frequency of arrhythmia. No significant differences in frequency values were identified among days of recording or among days of the week. CONCLUSIONS AND CLINICAL RELEVANCE: Changes of < or = 80% in the frequency of ventricular arrhythmias may be within the limit of spontaneous variability in dogs with ARVC. This degree of variability should be considered in evaluations of ambulatory ECG recordings, particularly in the assessment of the efficacy of antiarrhythmic drugs.     

Echocardiographic ratio indices in overtly healthy Boxer dogs screened for heart disease

BACKGROUND: Boxer dogs are routinely screened by echocardiography to exclude congenital and acquired heart disease. Individuals of a given breed may span a large range of body sizes, potentially invalidating linear regression of M-mode measurements against body weight. Echocardiographic ratio indices (ERIs) provide a novel method of characterizing echocardiographic differences between Boxers and other dog breeds. HYPOTHESIS: ERIs obtained from overtly healthy Boxer dogs presented for cardiac screening will be different from ERIs established for normal non-Boxer dogs, and those differences will be unrelated to aortic velocity or systolic blood pressure. ANIMALS: Eighty-one Boxers with no outward clinical signs of heart disease were studied. METHODS: All dogs were examined by 2-dimensional, M-mode, and Doppler echocardiography. M-mode measurements were used to perform ERI calculations, and the indices in Boxers were compared between Boxers with varying severity of arrhythmia and those of normal non-Boxer dogs. RESULTS: Differences in weight-based ERIs, which reflect increased thickness of the left ventricular free wall (LVW) and interventricular septum (IVS) and smaller aortic size, were found in overtly healthy Boxer dogs compared with normal non-Boxer dogs. ERIs of left atrial and LV cavity size in overtly healthy Boxers were not significantly different from those of non-Boxer dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: Boxer dogs may have an increased relative thickness of the LVW and IVS that is independent of aortic size, aortic velocity, or arterial blood pressure, and this morphology should be taken into consideration when screening Boxers by echocardiography.     

Coagulation effects of low molecular weight heparin compared with heparin in dogs considered to be at risk for clinically significant venous thrombosis

Objective – Compare the effects of 3 anticoagulation protocols on anti-factor Xa activity (AXa).
Design – Prospective, randomized, double-blind study.
Setting – University veterinary teaching hospital.
Animals – Eighteen dogs considered to be at risk for venous thrombosis.
Interventions – Each dog was randomly assigned to 1 of the following 3 groups ( n =6/group) and was treated for 24 hours: low-dose heparin (LDH), high-dose heparin (HDH), and dalteparin (DP). Dogs in the LDH group received a constant rate infusion (CRI) of unfractionated heparin (UFH) at 300 U/kg/d, the HDH group received a bolus of 100 U/kg of UFH IV, then a CRI of 900 U/kg/day, and the DP group received 100 U/kg DP SC at 0, 12, and 24 hours.
Measurements and Main Results – A total of 54 samples for activated partial thromboplastin time (aPTT) and AXa assays were collected at 0, 4, and 28 hours. Six samples had an AXa >0.1 U/mL, 5 of those were from the HDH group at hour 4. Two samples from the HDH group at hour 4 had a prolonged aPTT (93 and 200 seconds) and the highest AXa (0.6 and 1.0 U/mL, respectively). Four additional dogs in the HDH group did not complete the study due to hemorrhage; none of the dogs completing the study showed signs of hemorrhage.
Conclusions: Neither DP nor LDH increased AXa to values considered therapeutic in humans (0.5–1 and 0.35–0.75 U/mL, respectively), and both protocols appear to be inadequate to increase AXa in dogs with clinical illness. HDH increased AXa to this range in 2 of 6 dogs, but had unpredictable effects on aPTT and resulted in hemorrhage in some dogs.     

Assessment of heart rate variability in Boxers with arrhythmogenic right ventricular cardiomyopathy

OBJECTIVE: To assess heart rate variability (HRV) in Boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC), assess the ability of HRV analysis to identify differences in Boxers on the basis of severity of their arrhythmia, and evaluate the use of HRV to determine whether persistently high sympathetic tone is present in these dogs. DESIGN: Prospective study. ANIMALS: 24 Boxers with ARVC and 10 clinically normal non-Boxer dogs. PROCEDURE: Boxers were categorized as dogs with congestive heart failure (CHF), dogs with < or = 2 ventricular premature complexes (VPCs)/24 h (designated unaffected), or dogs with > 1,000 VPCs/24 h (designated affected). Ambulatory electrocardiography (24 hours) was performed in each dog. Recordings were analyzed for HRV variables at a commercial laboratory; differences in HRV variables among groups were compared with 1-way ANOVA. RESULTS: Compared with control non-Boxer dogs and Boxers without CHF (affected and unaffected Boxers), HRV was reduced in Boxers with CHF. No differences in HRV variables were detected between affected and unaffected Boxers. Inconsistent differences were identified between the control dogs and Boxers without CHF that had various degrees of arrhythmias. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that persistently high sympathetic tone is not a consistent feature of ARVC. Differences in some HRV variables between Boxers without CHF and control dogs suggest that Boxers may have different autonomic control of heart rate, compared with that of clinically normal non-Boxer dogs. The usefulness of HRV analysis appears limited to Boxers with ARVC that have systolic dysfunction and CHF.     

Serum Acute Phase Protein Concentrations in Dogs with Autoimmune Hemolytic Anemia

Background: Serial monitoring of acute phase protein (APP) concentrations in canine autoimmune hemolytic anemia (AIHA) has not been reported.
Hypotheses: Acute canine AIHA is accompanied by an acute phase response (APR) characterized by increased C-reactive protein (CRP) and α1-acid glycoprotein (AAG) concentrations and decreased albumin concentrations.
Animals: Twenty-seven dogs with AIHA and 11 control dogs.
Methods: Prospective, cohort study. CRP, AAG, and albumin concentrations, white blood cell (WBC) count, and packed cell volume (PCV) were determined at admission (day 1), every 48 hours until death or discharge, and on days 30, 90, 180, and 365.
Results: Compared with controls, CRP and AAG concentrations were increased and albumin concentration was decreased in dogs with AIHA (days 1–7; P < .002) and normalized with disease stabilization (days 9–365; P > .05). APP concentrations on day 1 were not predictive of survival, duration of hospitalization, or number of blood transfusions ( P = .153–.940). PCV correlated with APP concentrations over time (CRP r =−.600, AAG r =−.665, albumin r = .533; P < .0001) as did WBC count (CRP r = .253, AAG r = .486, albumin r =−.246; P < .006). Day 1 CRP concentration was lower for dogs that received corticosteroids before referral (115.3 μg/mL) compared with dogs that did not (191.2 μg/mL; P = .02).
Conclusions: An APR occurs in canine AIHA. Initial APP concentrations are not predictive of acute survival, correlate with hematologic markers of remission, and normalize rapidly with disease stabilization.