Hypertrophic cardiomyopathy in a dog: a systematic diagnostic approach.

A seven-year-old female neutered Parson Russel terrier was referred for syncopal episodes. An electrocardiogram revealed paroxysmal atrial flutter followed by periods of sinus arrest, suggesting sick sinus syndrome. Echocardiography showed severe biventricular wall thickening (hypertrophic cardiomyopathy (HCM) phenotype) with no signs of fixed or dynamic left ventricular outflow tract obstruction. Blood pressure, abdominal ultrasound, serum total thyroxin and thyroid-stimulating hormone, and insulin-like growth factor-1 were all within normal limits. Cardiac troponin I was elevated (1.7 ng/mL, ref<0.07). Serological tests for common infectious diseases were negative. A 24-h Holter confirmed that the syncopal episodes were associated with asystolic pauses (sinus arrest after runs of atrial flutter) ranging between 8.5 and 9.6 s. Right ventricular endomyocardial biopsies (EMB) were performed at the time of pacemaker implantation to assess for storage or infiltrative diseases that mimic HCM in people. Histological analysis of the EMB revealed plurifocal inflammatory infiltrates with macrophages and lymphocytes (CD3+ > 7/mm2) associated with myocyte necrosis, but no evidence of myocyte vacuolisation or infiltrative myocardial disorders. These findings were compatible with myocardial ischaemic injury or acute lymphocytic myocarditis. Molecular analysis of canine cardiotropic viruses were negative. The dog developed refractory congestive heart failure and was euthanised 16 months later. Cardiac post-mortem examination revealed cardiomyocyte hypertrophy and disarray with diffuse interstitial and patchy replacement fibrosis, and small vessel disease, confirming HCM. We described a systemic diagnostic approach to an HCM phenotype in a dog, where a diagnosis of HCM was reached by excluding HCM phenocopies.

Fluctuation of Clinical Signs With Near-Syncopal Episodes in a Dog With Gliomatosis Cerebri: A Diagnostic Challenge.

A 2-year-old Bull Mastiff cross Boxer neutered male dog was evaluated because of 2-month history of non-progressive right head tilt and mild vestibular ataxia. MRI of the brain revealed a faint T2W, FLAIR, DWI and ADC heterogenous hyperintense and T1W isointense intra-axial lesion with indistinct margins at the level of the pons and medulla oblongata. The lesion did not show any susceptibility artefact on T2* GRE images or contrast enhancement and CSF analysis was normal. Analysis of the spectra from MRS of the thalamus not promptly available at the time of the MRI study revealed a decreased level of NAA, as seen in people with gliomatosis cerebri. The dog represented 3 weeks later and, on this occasion, displayed left-sided head tilt, left-sided postural reaction deficits and near-syncopal episodes associated with state of confusion. Repeated MRI revealed a larger non-enhancing intra-axial lesion with a more hyperintense signal than previously described. CSF was normal and PCR of CSF for infectious diseases was negative. Thoracic and abdominal computed tomography did not reveal any primary or metastatic process. Immunosuppressive treatment was attempted and the dog remained stable over 5 days, then developed generalized tonic-clonic seizures which led to status epilepticus and death. Histopathology supported the diagnosis of gliomatosis cerebri. Gliomatosis cerebri remains difficult to diagnose ante-mortem, due to the broad age of onset and the variable duration and wide range of clinical signs. The mismatch between MRI findings and clinical presentation, the fluctuating clinical signs with near-syncopal episodes associated with a state of confusion, the presence of an infiltrative brain disease as depicted on MR imaging and a normal CSF analysis, should prompt the clinician to consider possible diagnosis of a widespread infiltrative neoplasm. Although, MRS may help narrow the differential diagnosis in favor of a neoplastic lesion, the overall prognosis remains poor.

Primary cardiac tumor presenting as left ventricular outflow tract obstruction and complex arrhythmia.

An adult female mixed breed dog presented for recurrent collapsing episodes over several weeks. Holter evaluation revealed periods of sinus arrest and echocardiography identified a soft tissue mass with subsequent severe dynamic obstruction of the left ventricular outflow tract. The patient was euthanized five days after presentation for severe dyspnea. Necropsy revealed an irregular mass circumferentially lining the left ventricular outflow tract as well as multiple myocardial metastases. The final diagnosis was an undifferentiated pleomorphic endocardial sarcoma.

Arrhythmogenic right ventricular cardiomyopathy in Boxer dogs: the diagnosis as a link to the human disease.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disease with an increased risk for ventricular arrhythmias. The condition, which occurs in Boxer dogs, shares phenotypic features with the human disease arrhythmogenic cardiomyopathy (ACM) suggesting its potential as a natural animal model. However, there are currently no universally accepted clinical criteria to diagnose ARVC in Boxer dogs. We aimed to identify diagnostic criteria for ARVC in Boxer dogs defining a more uniform and consistent phenotype. METHODS AND RESULTS: Clinical records from 264 Boxer dogs from a referral veterinary hospital were retrospectively analysed. ARVC was initially diagnosed according to the number of ventricular premature complexes (VPCs) in the 24-hour-Holter-ECG in the absence of another obvious cause. Dogs diagnosed this way had more VPCs, polymorphic VPCs, couplets, triplets, VTs and R-on-T-phenomenon and syncope, decreased right ventricular function and dilatation in comparison to a control group of all other Boxer dogs seen by the Cardiology Service over the same period. Presence of couplets and R-on-T-phenomenon on a 24h-ECG were identified as independent predictors of the diagnosis. A diagnosis based on ≥100 VPCs in 24 hours, presence of couplets and R-on-T phenomenon on a 24h-ECG was able to select Boxer dogs with a phenotype most similar to human ACM. CONCLUSION: We suggest the diagnosis of ARVC in Boxer dogs requires two out of the three following criteria: presence of ≥ 100 VPCs, presence of couplets or R-on-T-phenomenon on a 24 h-ECG. This results in a uniform phenotype similar to that described in human ACM and may result in the adoption of the term ACM for this analogous condition in Boxer dogs.

Holter monitoring of small breed dogs with advanced myxomatous mitral valve disease with and without a history of syncope.

BACKGROUND: Syncope is a transient loss of consciousness occasionally occurring in dogs with advanced myxomatous mitral valve disease (MMVD). OBJECTIVE: (1) To study ECG changes during syncopal episodes in dogs with advanced MMVD and (2) to compare the occurrence of arrhythmias and changes in heart rate variability (HRV) between dogs with advanced MMVD with and without a history of syncope. ANIMALS: Forty-three privately owned dogs (<15 kg) with advanced MMVD: 21 with and 22 without a history of syncope. METHODS: Prospective study with dogs recruited for an evaluation including history, physical examination, echocardiography, and arrhythmia and HRV analysis performed on 24-hour Holter recordings. RESULTS: A syncopal episode was observed during Holter monitoring in 4 dogs: 3 dogs had sinus rhythm and 1 dog had sinus arrest followed by escape rhythm. An arrhythmia variable representing sinus arrhythmia was significantly lower in dogs with a history of syncope than in those without (P = .008). Eight of 26 HRV variables were significantly different between dogs with and without a history of syncope. CONCLUSIONS AND CLINICAL IMPORTANCE: Compared with dogs without a history of syncope, dogs with advanced MMVD and a history of syncope did not have a higher occurrence of arrhythmias, but had less sinus arrhythmia, and had changes in HRV variables representing decreased overall HRV, decreased parasympathetic, and increased sympathetic modulation of heart rate.

Syncope associated with swallowing in two British Bulldogs with unilateral carotid body tumours.

Carotid body tumours were diagnosed in two British Bulldogs that each had a history of syncopal episodes induced by eating, drinking or pulling on the leash. In both dogs, a cervical mass was identified using computed tomography (CT) or magnetic resonance imaging, with carotid body tumour (CBT) being the histopathological diagnosis. A heart base mass was also identified in one dog by both CT and echocardiography. Swallowing syncope has been reported in the human literature in association with cervical mass lesions, but this is the first report in dogs. The present cases emphasise the value of advanced imaging of the head and neck in dogs presenting with clinical signs of syncope associated with swallowing and the importance of careful manipulation of the neck in patients with CBTs.

Recurrent syncope associated with paroxysmal supraventricular tachycardia in a Devon Rex cat diagnosed by implantable loop recorder.

A 9-year-old male neutered Devon Rex cat was presented for continued investigations following a 7-year history of recurrent syncope. Previous diagnostic tests, including 24h (Holter) electrocardiographic monitoring, had failed to identify the aetiology of such episodes, and former empirical treatment with atenolol had not provided satisfactory control of the clinical signs. A conclusive diagnosis was eventually achieved using an implantable loop recorder (Reveal), which identified paroxysmal supraventricular tachycardia (SVT) associated with a syncopal episode. Treatment with oral sotalol was instituted and, 18 months after initiation of anti-arrhythmic therapy, no further syncopal episodes have been observed by the cat's owners.

Defaecation syncope and pulmonary thromboembolism in a cat.

A 7-year-old male neutered domestic shorthair cat was referred for worsening gastrointestinal and haematologic abnormalities. Physical status deteriorated further despite intravenous crystalloids, blood transfusion and nutritional support. Cardiorespiratory signs developed and the cat died suddenly while straining to defaecate. Diffuse thrombosis, pulmonary thromboembolism, metastatic pancreatic carcinoma and histologic evidence of cardiomyopathy were present at necropsy. This is the first reported case of feline pulmonary thromboembolism associated with defaecation syncope. Predisposing factors for thrombotic disease in this case and aspects of human defaecation syncope are discussed. The risk of clot dislodgement by the Valsalva manoeuvre in patients with a thrombotic tendency is highlighted.