Naturally occurring torsades de pointes and QT interval prolongation in a domestic cat.

A 10-year-old male American Shorthair cat was presented after a witnessed syncopal event. A Holter monitor demonstrated a long QT interval and revealed a rhythm characteristic of torsades de pointes (TdP) coincident with a bout of syncope. On subsequent Holter monitor recordings, sotalol did not prolong the QT interval further and did not reduce the severity of the underlying ventricular tachyarrhythmias, but no TdP was identified. When another syncopal event occurred, sotalol was discontinued, and oral amiodarone and magnesium were started. This resulted in improvement in the ventricular tachyarrhythmia. No syncopal events occurred in the ensuing 3 months, but the cat died of an unrelated disease shortly after. This is the first report of naturally occurring torsades de pointes in a domestic cat.

Assisted reproduction mediated resurrection of a feline model for Chediak-Higashi syndrome caused by a large duplication in LYST.

Chediak-Higashi Syndrome (CHS) is a well-characterized, autosomal recessively inherited lysosomal disease caused by mutations in lysosomal trafficking regulator (LYST). The feline model for CHS was originally maintained for ~20 years. However, the colonies were disbanded and the CHS cat model was lost to the research community before the causative mutation was identified. To resurrect the cat model, semen was collected and cryopreserved from a lone, fertile,  CHS carrier male. Using cryopreserved semen, laparoscopic oviductal artificial insemination was performed on three queens, two queens produced 11 viable kittens. To identify the causative mutation, a fibroblast cell line, derived from an affected cat from the original colony, was whole genome sequenced. Visual inspection of the sequence data identified a candidate causal variant as a ~20 kb tandem duplication within LYST, spanning exons 30 through to 38 (NM_001290242.1:c.8347-2422_9548 + 1749dup). PCR genotyping of the produced offspring demonstrated three individuals inherited the mutant allele from the CHS carrier male. This study demonstrated the successful use of cryopreservation and assisted reproduction to maintain and resurrect biomedical models and has defined the variant causing Chediak-Higashi syndrome in the domestic cat.

Echocardiographic Features of Giant Right Atrial Diverticulum in a Dog.

A 12-year-old spayed female miniature Poodle presented for coughing, respiratory distress, and anorexia. After thoracentesis for pleural effusion, radiography revealed an enlarged cardiac silhouette with a bulge in the area of the body of the right atrium. Echocardiography revealed an anechoic chamber-like cavity lateral to the right atrium that communicated with the right atrium through a 13 mm defect in the right atrial free wall. Contrast echocardiography and color flow Doppler were used to prove that the cavity communicated with the right atrium. The cavity was diagnosed as a giant right atrial diverticulum.

Naturally Occurring Biventricular Noncompaction in an Adult Domestic Cat.

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non-human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth-eaten appearance to the inner wall of the mid- to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial-lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.

Balloon Valvuloplasty of Tricuspid Stenosis: A Retrospective Study of 5 Labrador Retriever Dogs.

BACKGROUND: There are limited reports of severe tricuspid valve stenosis in dogs and limited data regarding treatment and outcome. OBJECTIVE: To evaluate clinical signs, echocardiographic features, and outcome of balloon valvuloplasty (BV) in dogs with severe tricuspid valve stenosis (TVS) in which BV was attempted. ANIMALS: Five client-owned dogs with severe TVS. METHODS: Records were retrospectively reviewed and data collected regarding signalment, clinical signs, diagnostic findings, procedures, and outcome. RESULTS: All dogs were Labrador Retrievers. Presenting complaints included episodic weakness/syncope (4/5), abdominal distension (4/5), lethargy (2/5), and exercise intolerance (2/5). The median and range of measurements before BV were as follows: TV mean velocity 1.5 m/s (range 1.4-1.7 m/s); velocity-time integral (VTI) 79.8 cm (42.4-99.1 cm); and TV maximum velocity 2.9 m/s (2.3-3.2 m/s). Measurements (available for 3 of 5 dogs) after BV were as follows: TV mean velocity 1.15 m/s (0.9-1.4 m/s); VTI 44.95 cm (41.4-54.8 cm); and TV maximum velocity 1.15 m/s (1.9-2.3 m/s). The procedure was attempted in all dogs and completed in 4/5 dogs. The largest balloon diameter ranged from 15 mm to 25 mm, and length ranged from 4 cm to 5 cm. Right atrial pressure decreased in 4/5 dogs. All but 1 dog had clinical improvement after BV, but recurrence of clinical signs occurred (2/5). Tricuspid regurgitation worsened in 1 dog culminating in right heart failure and euthanasia. CONCLUSIONS AND CLINICAL IMPORTANCE: BV can be an effective treatment; however, clinical signs can recur. Right heart failure due to worsened TR is a potential complication in dogs with pre-existing moderate-to-severe TR.

Atrial Fibrillation as a Prognostic Indicator in Medium to Large-Sized Dogs with Myxomatous Mitral Valvular Degeneration and Congestive Heart Failure.

BACKGROUND: The prevalence and prognostic importance of atrial fibrillation (AF) on survival in nonsmall breed dogs with myxomatous mitral valvular disease (MMVD) and congestive heart failure (CHF) remain unknown. AIM: To identify the prevalence of AF in nonsmall breed dogs with CHF because of MMVD and to characterize the impact of AF on survival outcome. ANIMAL: Sixty-four client-owned dogs (>15 kg) with MMVD and CHF. METHODS: Retrospective review of medical records for dogs weighing >15 kg with MMVD treated for CHF. RESULTS: Thirty-three dogs presented with AF or developed AF during follow-up examinations, and 31 dogs were free of AF until cardiac-related death. For dogs with AF, median survival time (MST) was 142 days (range: 9-478) while dogs without AF lived 234 days (range: 13-879 days). AF increased risk of cardiac-related death (HR = 2.544; 95% CI = 1.41-4.59; P = .0019) when compared to dogs without AF. MST was significantly prolonged for dogs with AF whose rates were adequately controlled (<160 bpm; 171 days; n = 13) when compared to dogs that failed to respond to negative chronotropic agents (61 days; n = 20; P = .032). The administration of combination treatment (diltiazem and digoxin) significantly decreased median HR to 144 bpm (range: 84-218 bpm) in dogs with AF and significantly prolonged MST (diltiazem+digoxin: 130 days versus diltiazem: 35 days, P = .0241) when compared to diltiazem alone. CONCLUSIONS AND CLINICAL IMPORTANCE: Inadequately controlled AF is associated with a higher rate of mortality. Optimization of therapeutic strategies for the rate control of AF remains determined.

Platelet activation in cats with hypertrophic cardiomyopathy.

BACKGROUND: Cats with hypertrophic cardiomyopathy (HCM) are at risk for development of systemic thromboembolic disease. However, the relationship between platelet activation state and cardiovascular parameters associated with HCM is not well described. OBJECTIVES: To characterize platelet activation by flow cytometric evaluation of platelet P-selectin and semiquantitative Western blot analysis of soluble platelet-endothelial cell adhesion molecule-1 (sPECAM-1). ANIMALS: Eight normal healthy cats (controls) owned by staff and students of the School of Veterinary Medicine and 36 cats from the UC Davis Feline HCM Research Laboratory were studied. METHODS: Platelet-rich plasma (PRP) was used for all flow cytometry studies. Platelet surface CD41 and P-selectin expression were evaluated before and after ADP stimulation. sPECAM-1 expression was evaluated by Western blot analysis of platelet-poor plasma that had been stabilized with aprotinin. Standard echocardiographic studies were performed. RESULTS: Resting platelets from cats with severe HCM had increased P-selectin expression compared to controls, and expressed higher surface density of P-selectin reflected by their increased mean fluorescence intensities (MFI). Stimulation with ADP also resulted in significantly increased P-selectin MFI of platelets from cats with severe HCM. Increased P-selectin expression and MFI correlated with the presence of a heart murmur and end-systolic cavity obliteration (ESCO). sPECAM-1 expression from cats with moderate and severe HCM was significantly increased above those of control cats. CONCLUSIONS AND CLINICAL IMPORTANCE: P-selectin and sPECAM expression may be useful biomarkers indicating increased platelet activation in cats with HCM.

Association of dilated cardiomyopathy with the striatin mutation genotype in boxer dogs.

BACKGROUND: Myocardial disease in the Boxer dog is characterized by 1 of 2 clinical presentations, dilated cardiomyopathy (DCM) characterized by ventricular systolic dysfunction, dilatation and tachyarrhythmias, and arrhythmogenic right ventricular cardiomyopathy (ARVC) characterized by ventricular tachyarrhythmias, syncope, and sudden death. Boxer ARVC has been associated with a deletion in the striatin gene in some families. HYPOTHESIS/OBJECTIVES: We hypothesized that both presentations represent a single disease, and the development of DCM in the Boxer is associated with the striatin deletion. ANIMALS: Thirty-three adult Boxer dogs with DCM, 29 adult Boxer dogs with the striatin deletion and ARVC, and 16 Boxers without cardiac disease. METHODS: DNA samples were evaluated for the striatin deletion. Association of the deletion with the DCM phenotype was tested by a Fisher's exact test. T-tests were used to evaluate potential differences between the positive heterozygous and positive homozygous groups with DCM with regard to age, LVIDD, LVIDS, and FS%. RESULTS: Thirty of 33 dogs with DCM were positive for the striatin deletion. The striatin mutation and the homozygous genotype were strongly associated with the DCM phenotype (P < .001 and P = .005). There was no statistical difference between the heterozygous and homozygous groups with regard to age and echocardiographic measurements. CONCLUSIONS AND CLINICAL IMPORTANCE: This study demonstrates an association between DCM in the Boxer dog and the striatin mutation, particularly with the homozygous genotype. The observation that 3/33 dogs developed DCM and lacked the striatin mutation suggests that there is at least 1 other cause of DCM in the Boxer dog.

Bronchomalacia in dogs with myxomatous mitral valve degeneration.

BACKGROUND: Cough in the geriatric small breed dog with myxomatous mitral valve degeneration (MMVD), a large left atrium, and absence of heart failure often is attributed to compression of the left mainstem bronchus by the left atrium. Studies investigating this syndrome are lacking in dogs. HYPOTHESIS: Airway collapse is independent of left atrial enlargement. ANIMALS: A total of 16 dogs presenting with chronic cough in the absence of congestive heart failure. Group 1 dogs (n = 10) had moderate-to-severe left atrial enlargement based on an echocardiographically calculated left atrial:aortic surface area [LA:Ao(a)] > 6. Group 2 dogs (n = 6) had no to mild left atrial enlargement [LA:Ao(a) ≤ 6]. METHODS: Dogs were prospectively evaluated. CBC, biochemistry, urinalysis, cervical and thoracic radiographs, fluoroscopy, echocardiography, and bronchoscopy were performed. Bronchoscopic abnormalities were compared between groups using Fisher's Exact Test. P < .05 was considered significant. RESULTS: Fluoroscopy identified airway collapse in both groups. Bronchoscopic evidence of airway collapse >50% was observed in multiple bronchi with no difference between groups. All dogs had inflammation on airway cytology with respiratory infection in 1 dog in group 2. Left atrial size was interpreted radiographically as enlarged in 9 of 10 group 1 dog and in 2 of 6 group 2 dogs. VHS was above normal in both groups of dogs regardless of echocardiographic evidence of cardiomegaly. CONCLUSIONS: Results failed to identify an association between left atrial enlargement and airway collapse in dogs with MMVD, but did suggest that airway inflammation is common in dogs with airway collapse.

Occlusion devices and approaches in canine patent ductus arteriosus: comparison of outcomes.

BACKGROUND: A comparison of transvascular occlusion methods for closing patent ductus arteriosus (PDA) in dogs has not been done. OBJECTIVES: To determine if clinically important differences exist between the approaches and devices currently used. ANIMALS: A total of 112 client-owned dogs with left-to-right shunting PDA. METHODS: Retrospective study. Records from dogs that underwent attempted transvascular PDA occlusion from January 2006 to December 2009 were examined. Dogs were placed into 4 groups: Group 1: Amplatz Canine Duct Occluder (ACDO) (transarterial) - 36 dogs; Group 2: Gianturco or MReye Flipper Detachable Embolization (Flipper) coil (transarterial) - 38 dogs; Group 3: Amplatzer Vascular Plug (AVP) (transarterial) - 23 dogs; Group 4: Flipper coil (transvenous) - 15 dogs. RESULTS: The overall success rate of the procedures was high (92%) with comparable success rates among groups (87-97%). There were significantly fewer complications (P < .0001) in dogs receiving an ACDO than in the remaining groups (3% for ACDO versus 26-33% for the other groups). Fluoroscopy time for the transvenous method was significantly longer (median, 13 minutes) than for the other groups (median, 6 minutes) (P < .0001). Severity of residual flow 24 hours postprocedure was significantly less in the ACDO group than in the remaining groups (P = .0001-.05). CONCLUSIONS: The ACDO appears superior in ease of use, complication rate, and completeness of occlusion. The remaining limiting factor with this device is patient size. Until a smaller ACDO device is marketed, coils remain the only choice for interventional closure in very small dogs.

The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study.

BACKGROUND: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long-term prognosis, and in monitoring the response to therapy in humans. HYPOTHESIS: Circulating concentrations of the biomarkers N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure. ANIMALS: Six Maine Coon or Maine Coon cross cats with severe HCM. METHODS: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT-proBNP and cTnI were assayed before and on the last day of drug administration. RESULTS: There was no statistically significant change in NT-proBNP (median before, 394 pmol/L; range, 71-1,500 pmol/L; median after, 439 pmol/L; range, 24-1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10-0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09-1.0 ng/mL; P = .69) after administration of atenolol. CONCLUSIONS: Atenolol administration did not decrease NT-proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings.

Congenital cardiac defects in neonatal foals: 18 cases (1992-2007).

BACKGROUND: Literature available regarding congenital cardiac defects in foals is limited to reports of individual cases or small case series. OBJECTIVE: To describe the clinical, echocardiographic, and necropsy findings and breed predilection of congenital cardiac defects in neonatal foals. ANIMALS: Eighteen foals < 15 days of age with 1 or more congenital cardiac defects. METHODS: Medical records of foals diagnosed with congenital cardiac defects at the William R. Pritchard Veterinary Medical Teaching Hospital were reviewed. Data collected included history, signalment, clinical signs, laboratory data, diagnostic and necropsy results, and outcome. RESULTS: Arabian foals represented 39% of cases with congenital cardiac defects and were significantly (P = .004) overrepresented (OR = 4.7 [CI: 1.8-12.4]) compared with the general hospital population. Ventricular septal defect (VSD) (14/18), tetralogy of Fallot (5/18), and tricuspid valve atresia (4/18) were the most common defects identified. A > or = 3/6 heart murmur (14/ 14) accompanied by tachycardia (14/17), tachypnea (17/17), and cyanosis of mucous membranes (7/16) were the most common clinical signs. Concurrent congenital defects were common (9/18). Two foals, both with VSD, survived for > or = 8 years after diagnosis and 1 was a successful performance horse. CONCLUSIONS AND CLINICAL RELEVANCE: Arabian horses appear to have a predisposition for cardiac defects. The presence of a loud murmur (> or = 3/6), cyanotic membranes, and tachycardia or tachypnea in a neonatal foal should warrant thorough evaluation of the heart for congenital defects. Foals with cardiac defects should be closely evaluated for concurrent congenital defects in other body systems.

Effect of spironolactone on diastolic function and left ventricular mass in Maine Coon cats with familial hypertrophic cardiomyopathy.

BACKGROUND: Myocardial fibrosis occurs in cats with hypertrophic cardiomyopathy (HCM), and is one factor that leads to diastolic dysfunction. Spironolactone (SPIR) reduces myocardial fibrosis in several models of HCM and in humans with cardiac disease. HYPOTHESIS: SPIR will improve diastolic function and reduce left ventricular (LV) mass in Maine Coon cats with HCM. METHODS: Maine Coon cats with familial HCM were included if there was concentric hypertrophy (> or =6 mm end diastolic wall thickness) and decreased early lateral mitral annular velocity (Em) or summated early and late mitral annular velocity (EAsum) measured by pulsed wave tissue Doppler imaging echocardiography. Cats were paired by Em-EAsum and randomized to receive 2 mg/kg SPIR (n = 13) or placebo (n = 13) PO q12 h for 4 months. Em-EAsum, systolic velocity, LV mass, and the ratio of left atrial to aortic diameter were measured at baseline, 2 months, and 4 months. Statistical analysis included 2-way repeated measures analysis of variance and the Student's t-test. RESULTS: Plasma aldosterone concentration increased in cats treated with SPIR (235 ng/mL, baseline; 935 ng/mL, 2 months; 1,077 ng/mL, 4 months; P < .001 at 2 and 4 months). No significant treatment effect was identified for early or early-late summated diastolic mitral annular velocity or any other variable except plasma aldosterone concentration. Severe facial ulcerative dermatitis developed in 4 of 13 cats treated with SPIR, requiring discontinuation of the drug. CONCLUSION: SPIR did not improve Em or EAsum of the lateral mitral annulus or alter LV mass over 4 months. One third of cats treated with SPIR developed severe ulcerative facial dermatitis.

The effect of hydration status on the echocardiographic measurements of normal cats.

BACKGROUND: Diagnosis of cardiomyopathy of cats is based on 2-dimensional (2D) echocardiography. However, circulating fluid volume largely determines diastolic cardiac chamber dimensions, and reduced diastolic volume in other species results in what has been called "pseudohypertrophy of the ventricular myocardium." HYPOTHESIS: Altered hydration produces changes on 2D echocardiography that may confound the diagnosis or severity assessment of cardiomyopathy of cats. ANIMALS: Ten normal colony-sourced mixed breed cats were included. METHODS: Cats were examined by echocardiography at baseline and at completion of 3 protocols (volume depletion and maintenance-rate and anesthetic-rate IV fluid administration) applied in randomized crossover design with a 6-7 day washout period. RESULTS: Volume depletion increased diastolic left ventricular interventricular septal (IVSd) and free wall diameter (4.5 +/- 0.4 to 5.8 +/- 0.6 mm; P < .001) with wall thickness exceeding 6 mm in 4 cats. Diastolic left ventricular internal diameter (LVIDd) decreased, and reduction in systolic left ventricular internal diameter (LVIDs) produced end-systolic cavity obliteration in 7 cats. Left-atrial-to-aortic-root ratio (LA: Ao, 1.4 +/- 0.2 to 1.2 +/- 0.1, P < .05) and left atrial area in diastole (LAAd) decreased with volume depletion. Maintenance-rate IV fluid administration increased LAAd and fractional shortening (FS%). Anesthetic-rate IV fluid administration increased LVIDd, FS%, LAAd, and LA:Ao ratios (to 1.7 +/- 0.1, P < .01), producing an LA: Ao ratio above normal limits in 6 cats. A systolic heart murmur developed with administration of fluid at maintenance (n = 1) and anesthetic rates (n = 6). CONCLUSIONS: Altered hydration status produces changes in the echocardiographic examination of normal cats that may lead to an erroneous diagnosis of cardiomyopathy or mask its presence. Hydration status should be considered during echocardiographic examination in cats.

Immediate and late outcomes of transarterial coil occlusion of patent ductus arteriosus in dogs.

Records from dogs (n = 125) that underwent attempted transarterial coil occlusion of patent ductus arteriosus (PDA) at the University of California, Davis, between 1998 and 2003, were reviewed, and a subset of these dogs (n = 31) in which the procedure was performed at least 12 months earlier were reexamined to determine long-term outcome. Coil implantation was achieved in 108 dogs (86%). Despite immediate complete ductal closure in only 34% of dogs, the procedure was hemodynamically successful as evidenced by a reduction in indexed left ventricular internal diameter in diastole (LVIDd; P < .0001), fractional shortening (P < .0001), and left atrial to aortic ratio (LA: Ao; P = .022) within 24 hours. Complete ductal closure was documented in 61% of dogs examined 12 to 63 months after coil occlusion. Long-standing residual ductal flow in the other 39% of dogs was not associated with increased indexed LVIDd or LA: Ao and was not hemodynamically relevant. Repeat intervention was deemed advisable in only 4 dogs with persistent (n = 1) or recurrent (n = 3) ductal flow. Complications included aberrant embolization (n = 27), death (n = 3), ductal reopening (n = 3), transient hemoglobinuria (n = 2), hemorrhage (n = 1), aberrant coil placement (n = 1), pulmonary hypertension (n = 1), and skin abscessation (n = 1). Serious infectious complications did not occur despite antibiotic administration to only 40% of these dogs. Transarterial coil occlusion was not possible in 14 dogs (11%) because of coil instability in the PDA and was associated with increased indexed minimum ductal diameter (P = .03), LVIDd (P = .0002), LVIDs (P = 0.001), and congestive left heart failure (P = .03) reflecting a relatively large shunt volume.

Aortic valve endocarditis in a dog due to Bartonella clarridgeiae.

We report the first documented case of endocarditis associated with Bartonella clarridgeiae in any species. B. clarridgeiae was identified as a possible etiological agent of human cat scratch disease. Infective vegetative valvular aortic endocarditis was diagnosed in a 2.5-year-old male neutered boxer. Historically, the dog had been diagnosed with a systolic murmur at 16 months of age and underwent balloon valvuloplasty for severe valvular aortic stenosis. Six months later, the dog was brought to a veterinary hospital with an acute third-degree atrioventricular block and was diagnosed with infective endocarditis. The dog died of cardiopulmonary arrest prior to pacemaker implantation. Necropsy confirmed severe aortic vegetative endocarditis. Blood culture grew a fastidious, gram-negative organism 8 days after being plated. Phenotypic and genotypic characterization of the isolate, including partial sequencing of the citrate synthase (gltA) and 16S rRNA genes indicated that this organism was B. clarridgeiae. DNA extraction from the deformed aortic valve and the healthy pulmonic valve revealed the presence of B. clarridgeiae DNA only from the diseased valve. No Borrelia burgdorferi or Ehrlichia sp. DNA could be identified. Using indirect immunofluorescence tests, the dog was seropositive for B. clarridgeiae and had antibodies against Ehrlichia phagocytophila but not against Ehrlichia canis, Ehrlichia ewingii, B. burgdorferi, or Coxiella burnetii.