Presumed congenital Gerbode defect in an American Domestic Shorthair cat.

A five-month-old, intact female Domestic Shorthair cat presented to the Kansas State Veterinary Health Center for evaluation of a murmur and exercise intolerance. Physical exam revealed a grade V/VI right, parasternal, holosystolic murmur. On echocardiogram, there was an abnormality in the membranous interventricular septum and tricuspid valve, allowing blood to shunt from the left ventricle to the right atrium. This lesion is consistent with an infravalvular Gerbode defect. The Gerbode defect is a rare, left ventricle-to-right atrial shunt that can be congenital or acquired, and in cats, has only been reported once. At the time of submission, the patient is alive and is maintaining a good quality of life.

Epicardial pacemaker implantation and outcome in eight pet ferrets (Mustela putorius furo).

INTRODUCTION/OBJECTIVES: Minimal information exists regarding epicardial pacemaker (EP) implantation in pet ferrets (Mustela putorius furo). The objectives were to describe the indications, surgical technique, and outcome of EP implantation in ferrets for the treatment of advanced atrioventricular block (AVB). ANIMALS, MATERIALS, AND METHODS: Eight client-owned ferrets presenting to five veterinary referral centers. Signalment, physical exam findings, diagnostic tests, anesthesia protocols, surgical implantation techniques, postoperative treatment plans, and EP interrogations were reviewed. Intra- and postoperative, minor and major, and EP-related complications were established. Descriptive statistics were performed to report complication rates. Survival analyses were performed. RESULTS: All ferrets had advanced AVB: 3/8 had high-grade second-degree and 5/8 had third-degree. The primary clinical signs were collapse and weakness. Seven EP were implanted via a transdiaphragmatic approach and one via a left intercostal thoracotomy. Intraoperative complications occurred in 2/8 ferrets, both major. One ferret with severe comorbidities died during general anesthesia. Postoperative pacemaker-related complications were minor: inappropriate sinus beat sensing in 2/8 and occasional muscle fasciculations in 1/8. Two ferrets were alive at the time of manuscript submission, at 10 and 21 months postoperatively. The overall median survival time was 24 months. CONCLUSIONS: Implantation of EP was performed successfully in most ferrets for treatment of advanced AVB and was well tolerated. Ferrets with advanced AVB may experience resolution of clinical signs associated with their cardiac disease following EP implantation. Additional studies are warranted to investigate the effects of epicardial pacing on survival times in this species.

Pharmacokinetic evaluation of a sustained-release compounded procainamide preparation after 24-h (acute) administration in normal dogs.

INTRODUCTION: The objective of the present study was to evaluate the pharmacokinetics of a compounded sustained-release procainamide formulation in normal dogs. ANIMALS: Six healthy, purpose-bred mixed-breed dogs participated in the study. METHODS: In phase I, two dogs were administered oral procainamide (30 mg/kg), and plasma was obtained to determine plasma concentration ranges and duration. In phase II, six dogs were administered procainamide (30 mg/kg by mouth every 12 hours) to determine the pharmacokinetics of sustained-release procainamide. Serum procainamide concentration was determined using an immunochemistry assay. RESULTS: No adverse clinical effects were noted in any of the dogs studied. The average maximum serum concentration, average serum concentration, and average minimum serum concentration were 10.17, 7.13, and 3.07 µg/mL, respectively. The average time over a 12-h period during which procainamide concentration exceeded 12 µg/mL was 2.35 h, was between 4 and 12 µg/mL was 7.19 h, and was less than 4 µg/mL was 2.46 h. The average times at maximum concentration and minimum concentration were 18.67 and 12.25 h, respectively. CONCLUSIONS: Administration of sustained-release procainamide twice daily achieved targeted plasma concentrations in most dogs. Evaluation of serum trough concentrations should be considered owing to interanimal variability to confirm that serum concentrations are within the reported therapeutic range for an individual patient.

Twenty-four hour Holter monitoring in finishing cattle housed outdoors.

INTRODUCTION: Atrial premature complexes have been reported to be the most common arrhythmia in cattle and is suspected to be secondary to systemic disease, especially gastrointestinal disease. In order to properly identify pathologic arrhythmia in cattle, the normal rhythm and arrhythmia prevalence should be defined. The objective of this study was to determine the normal heart rate, rhythm, number of ventricular premature complexes (VPCs), and atrial premature complexes (APCs) in unrestrained Angus steers. ANIMALS: Twenty-seven client owned steers with unremarkable physical examinations and serum biochemical analyses were used. MATERIALS AND METHODS: Twenty-four hour Holter monitors, attached by a custom-made harness, were retrospectively evaluated. Three lead electrocardiographic registrations of good quality and normal sinus rhythm were obtained from all steers in the study. RESULTS: The mean heart rate was 66.8 bpm ± 16.4 bpm. Ventricular premature complexes were rare (noted in 14.8% of steers), and APCs were common (noted in 85% of the steers). Simple second degree AV block was observed in 18.5% of the steers. CONCLUSION: In summary, healthy steers have rare single VPCs, although it is possible for an individual animal to have apparent more frequent VPCs. Mean heart rate varies with a diurnal pattern similar to other species. Atrial premature complexes are the most prevalent abnormality observed in feedlot steers.

Congestive heart failure caused by transvenous pacemaker lead prolapse and associated right ventricular outflow tract obstruction in a dog.

A 16-year-old dog was presented for cough as well as increased respiratory rate and effort three years after implantation of a single-lead transvenous artificial pacemaker system. Thoracic radiographs and echocardiography disclosed prolapse of the pacemaker lead into the main pulmonary artery, causing severe pulmonary insufficiency and right-sided volume overload. Repositioning of the pacemaker lead led to improvement of pulmonary insufficiency and resolution of the dog's clinical signs and cavitary effusions. This case describes a late complication of pacemaker implantation that may be avoided by appropriate use of the manufacturer-provided anchoring sleeve and avoidance of excessive lead redundancy.

The influence of enalapril and spironolactone on electrolyte concentrations in Doberman pinschers with dilated cardiomyopathy.

The combination of an angiotensin-converting enzyme inhibitor (ACEI) with an aldosterone receptor antagonist can increase serum potassium and magnesium and lower serum sodium concentrations. The objective of this study was to retrospectively determine whether an ACEI and spironolactone can be co-administered to Doberman pinschers with occult dilated cardiomyopathy without serious adverse influences on serum electrolyte concentrations. Between 2001 and 2007, 26 client-owned Doberman pinschers were given enalapril, spironolactone, and carvedilol and followed for at least 6 months. Most dogs had been prescribed mexiletine for ventricular tachyarrhythmia suppression. Dogs were treated with pimobendan when congestive heart failure was imminent. Baseline and follow-up (3-10 visits) color-flow Doppler echocardiograms, serum urea nitrogen (SUN), creatinine, sodium, potassium, and magnesium concentration data were tabulated. Compared to baseline data, there were no significant changes in serum sodium or serum creatinine concentrations. Serum magnesium (P = 0.003), serum potassium (P = 0.0001), and SUN (P = 0.0001) concentrations increased significantly with time. Although the combination of ACEI and spironolactone was associated with significant increases in magnesium, potassium, and SUN concentrations, these changes were of no apparent clinical relevance. At the dosages used in this study, this combination of drugs appears safe.

Toxicity in Doberman Pinchers with ventricular arrhythmias treated with amiodarone (1996-2005).

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.

Gingival hyperplasia associated with the administration of amlodipine to dogs with degenerative valvular disease (2004-2008).

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.

Bradycardia-associated syncope in 7 Boxers with ventricular tachycardia (2002-2005).

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 beta-blocker or sotalol to such dogs can aggravate or precipitate neurocardiogenic bradycardia-related syncope.