Background: Asymptomatic Doberman Pinschers with dilated cardiomyopathy (DCM) often die suddenly owing to ventricular tachycardia that degenerates into ventricular fibrillation. A safe and effective antiarrhythmic drug treatment is needed. This will require a large, well-controlled, prospective study.Hypothesis: Amiodarone toxicity is common in Dobermans with occult DCM and ventricular tachyarrhythmias refractory to antiarrhythmia therapy. Infrequent monitoring of hepatic function is inadequate. Frequent monitoring may be useful to determine dogs in which the dosage should be decreased or the drug withdrawn.Methods: Medical records from the University of Georgia and Cornell University were searched for Doberman Pinschers diagnosed with preclinical DCM that received amiodarone for severe ventricular arrhythmias refractory to other antiarrhythmic agents. Echocardiographic data, Holter recording data, hepatic enzyme serum activity, and serum amiodarone concentrations were recorded. The presence of clinical signs of toxicity was recorded. Serum amiodarone concentrations were obtained in some dogs.Results: Reversible toxicity was identified in 10 of 22 (45%) dogs. Conclusion and Clinical Importance: Adverse effects from amiodarone were common and were, in part, dosage related. Patients should be monitored for signs of toxicity and liver enzyme activity should be measured at least monthly.

Background: Syncope is a recognized problem in Boxers and often is the result of rapid ventricular tachycardia (VT). Affected dogs may have echocardiographic evidence of dilated cardiomyopathy, but frequently have normal echocardiograms. Although VT is probably the most common cause of syncope in Boxers, neurocardiogenic bradycardia can also occur.Objective: We describe 7 Boxers with comorbid VT and neurocardiogenic bradycardia, wherein the syncope was secondary to bradycardia rather than VT.Animals: Seven Boxers were selected from a larger population of Boxers with Holter-documented VT because these dogs had documented bradycardia at the time of syncope.Methods: Retrospective study.Results: Although all dogs had Holter-documented VT, the etiology of the syncopal episodes was consistent with neurocardiogenic bradycardia.Clinical Importance: Neurocardiogenic bradycardia or VT can occur as isolated problems in Boxers. In some Boxers, VT and potential or manifest neurocardiogenic bradycardia coexist. The administration of a b-blocker or sotalol to such dogs can aggravate or precipitate neurocardiogenic bradycardia-related syncope.

Background: Calcium channel blocking drugs, usually nifedipine and less often amlodipine, have been reported to cause gingival hyperplasia (GH) in humans. Hypothesis: Amlodipine, a dihydropyridine calcium channel blocking drug, can cause GH when administered chronically to older small dogs with degenerative valvular disease. Animals Studied: From January 2004 to May 2008, 82 client‐owned dogs with degenerative valvular disease and left atrial dilatation were treated with amlodipine in combination with spironolactone and enalapril and followed for >6 months. Methods: Retrospective study. A chronological observation of GH in 2 dogs treated with amlodipine in 2004 and 2006 prompted the study. Patient histories and medical records of each dog treated with amlodipine for degenerative valvular disease from January 2004 to May 2008 were reviewed. Results: GH was observed by clients and the authors in 7 of 82 (8.5%) dogs. Histologic confirmation of the diagnosis was made in 2 dogs. The minimum duration of treatment before diagnosis of GH was 5 months. GH began to resolve within 2 weeks of discontinuing amlodipine and resolution was complete within 6 months. Amlodipine administration was reinstituted in 1 dog in which GH had resolved, and GH reoccurred within 4 months. Conclusion and Clinical Importance: Long‐term administration of amlodipine to dogs with degenerative valvular disease may cause GH in a small percentage of patients. GH resolves quickly after withdrawal of amlodipine treatment.

A 4-year-old Ragdoll cat presented for dyspnea secondary to chylous pleural effusion to the University of Georgia Veterinary Teaching Hospital. Physical examination, complete blood count, serum chemistries, urinalysis, thoracic radiographs, abdominal radiographs, and thoracic fluid cytology and culture failed to identify an etiology for the chylous effusion. The patient tested negative for feline leukemia virus, feline immunodeficiency virus and heartworm disease. Respiration phasic influences on early diastolic trans-mitral, trans-tricuspid and pulmonary vein blood flow velocities during Doppler echocardiography were consistent with constrictive pericarditis. The cat underwent subtotal pericardectomy. The patient recovered without complication and is overtly healthy without radiographic or echocardiographic abnormalities 6-months post-surgery. Constrictive pericarditis should be considered in cats with idiopathic pleural effusion, with or without ascites, in which standard echocardiographic assessment is not suggestive of structural heart disease. If constrictive pericarditis is present, the Doppler characteristics outlined here may allow for this diagnosis to be made. Pericardectomy may be highly rewarding, although the specific etiology of the constrictive pericarditis may remain unknown.

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