Cardiomyopathy in a Harris hawk (Parabuteo unicinctus).

CASE DESCRIPTION An adult sexually intact female Harris hawk (Parabuteo unicinctus) housed at a wildlife hospital was evaluated because of acute collapse during an educational exhibition. CLINICAL FINDINGS Physical examination and hematologic analysis revealed no abnormalities; radiography revealed findings consistent with a previous tibiotarsal fracture. Coelioscopy with histologic examination and fungal culture of lung and air sac samples revealed anthracosis but no fungal infection. The hawk was discharged and temporarily removed from the education program; 1 month later, upon reintroduction into the program, it collapsed again. Physical examination and hematologic findings were similar to those after the first episode. Transcoelomic and transesophageal echocardiography and CT angiocardiography findings were consistent with cardiomyopathy. TREATMENT AND OUTCOME Initial cardiac treatment included furosemide (0.5 mg/kg [0.23 mg/lb], PO, q 24 h) and pimobendan (10 mg/kg [4.5 mg/lb], PO, q 12 h). After 10 days of treatment, peak and trough plasma concentrations of pimobendan were measured at 25, 196 and 715.97 ng/mL, respectively; the dosage was decreased to 0.25 mg/kg (0.11 mg/lb), PO, every 12 hours. No overt signs of toxicosis were detected. A sample was collected to reevaluate plasma pimobendan concentration after 30 days of treatment; results were not obtained prior to the patient's death but revealed a peak concentration of 16.8 ng/mL, with an undetectable trough concentration. The hawk was found dead 6 months after initial evaluation. Necropsy revealed cardiomegaly, but histologic examination did not reveal an inciting cause of cardiac dysfunction. CLINICAL RELEVANCE Cardiac disease in raptors may be underreported. Transcoelomic and transesophageal echocardiography and CT angiography provided useful information for the diagnosis of cardiac disease in the hawk of this report.

Evaluation of shock waveform configuration on the defibrillation capacity of implantable cardioverter defibrillators in dogs.

BACKGROUND: Implantable cardioverter defibrillators (ICD) are programmed to detect ventricular arrhythmias and terminate them by delivering an electrical shock. A defibrillation threshold (DFT) at least 10 J below the maximum device output is recommended for successful therapy. Shock waveform configuration is a programmable parameter used to achieve a low DFT. It is hypothesized that a fixed-pulse configuration results in lower defibrillation energy requirements than a fixed-tilt configuration. ANIMALS: 10 mongrel dogs. MATERIALS AND METHODS: ICD generator and transvenous lead were surgically implanted. Defibrillation threshold was determined using a protocol guided by the upper limit of vulnerability. Fixed-pulse and fixed-tilt (50%/50%) waveform configurations were tested in a random order. Plasma cardiac troponin I (cTnI) was measured for signs of myocardial injury. RESULTS: The experiment was completed in 9 dogs. Overall mean DFT value was 424 ± 88 V (9.2 ± 3.9 J). Mean differences among voltage, energy and impedance at the DFT for fixed-pulse (422 ± 97 V, 9.1 ± 4.2 J, 62.6 ± 13.8 Ω) and fixed-tilt (426 ± 83 V, 9.3 ± 3.8 J, 62.8 ± 18.5 Ω) configurations were not statistically significant (All P > 0.21). Cardiac TnI concentration changed from 0.03 ng/mL (95% CI: 0.02-0.04) at baseline to 0.11 ng/mL (95 CI: 0.08-0.16) after DFT was obtained with the first waveform configuration and 0.19 ng/mL (95% CI: 0.13-0.28) at the end of the study period. There were no significant changes in heart rate, end-tidal CO2 and blood pressure over time (all P > 0.09). CONCLUSION: The tested ICD device and lead placement reliably produced acceptable DFT values, based on a 10-J safety margin below the maximum device output. A benefit of fixed-pulse configuration could not be demonstrated over the standard fixed-tilt waveform. Signs of acute myocardial damage from repeated high-voltage shocks and episodes of ventricular fibrillation seemed of limited clinical significance.

Effect of torsemide and furosemide on clinical, laboratory, radiographic and quality of life variables in dogs with heart failure secondary to mitral valve disease.

OBJECTIVES: Diuretic therapy reduces preload and relieves congestion secondary to cardiac dysfunction. Torsemide (torasemide) is a loop diuretic with longer duration of action, decreased susceptibility to diuretic resistance, and adjunctive aldosterone antagonist properties compared with furosemide. We hypothesized that torsemide would be well tolerated and no less effective than furosemide at diuresis, control of clinical signs, and maintenance of quality of life (QOL) in dogs with congestive heart failure (CHF). ANIMALS, MATERIALS AND METHODS: Seven client-owned dogs with stable CHF receiving twice daily oral furosemide and adjunctive medications. Utilizing a double-blinded, randomized, crossover design, dogs were administered either oral furosemide at their current dose or an equivalent oral dose of torsemide (1/10 of the daily furosemide dose divided into twice daily dosing) on day 0. Crossover occurred at day 7 and the study ended on day 14. Clinical, laboratory, radiographic, and QOL variables were evaluated on days 0, 7 and 14. RESULTS: No dogs developed recurrent CHF during the study. Mean furosemide dose on day 0 was 5.13 mg/kg/day (range 2.8-9.6). Following torsemide treatment, creatinine (P = 0.020), urea nitrogen (P = 0.013), phosphorus (P = 0.032), albumin (P = 0.019), carbon dioxide (P = 0.015) and anion gap (P = 0.005) were significantly increased, and urine specific gravity (P = 0.004) and chloride (P = 0.021) were significantly decreased compared with furosemide dosing. No differences in QOL were found. CONCLUSIONS: Results indicate that torsemide is equivalent to furosemide at controlling clinical signs of CHF in dogs and is likely to achieve greater diuresis vs. furosemide. Larger clinical trials evaluating torsemide as a first or second-line loop diuretic for congestive heart failure in dogs are warranted.

Prediction of first onset of congestive heart failure in dogs with degenerative mitral valve disease: the PREDICT cohort study.

OBJECTIVE: To identify risk factors for first-onset congestive heart failure (CHF) in dogs with degenerative mitral valve disease (DMVD). ANIMALS: Eighty-two dogs with and without CHF secondary to DMVD were retrospectively assigned to a derivation cohort. Sixty-five dogs with asymptomatic DMVD were recruited into a prospective validation cohort. METHODS: Variables associated with risk of CHF in dogs were identified in a derivation cohort and used to construct a predictive model, which was then prospectively tested through longitudinal examination of a validation cohort. RESULTS: Logistic regression analysis of the derivation cohort yielded a predictive model that included the left atrial to aortic root dimension ratio (LA:Ao) and plasma concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP). When this model was prospectively applied to the validation cohort, it correctly predicted first-onset of CHF in 69.2% of cases. Analysis of the validation cohort revealed that plasma NT-proBNP concentration and indexed left ventricular end-diastolic diameter (LVIDd:Ao) were independent risk factors for development of first-onset CHF in dogs with DMVD (NT-proBNP ≥ 1500 pmol/L, odds ratio (OR), 5.76, 95% confidence interval (CI), 1.37-24.28, P = 0.017; LVIDd:Ao ≥ 3, OR, 6.11, 95% CI, 1.09-34.05, P = 0.039). CONCLUSIONS: Measures of left heart size and plasma NT-proBNP concentration independently estimate risk of first-onset of CHF in dogs with DMVD. These parameters can contribute to the management of dogs with DMVD.

Use of the loop diuretic torsemide in three dogs with advanced heart failure.

Diuretics are a mainstay of therapy in dogs with heart failure. In dogs with advanced heart failure, moderate to high doses of loop diuretics such as furosemide are used with diminishing effects as profound activation of neuroendocrine systems promote signs of congestive heart failure. The loop diuretic torsemide has several characteristics that make it suitable for treatment of advanced heart failure including longer half-life, increased potency of diuretic action, and anti-aldosterone effects. This case report details the administration of torsemide in 3 dogs with advanced heart failure and apparent furosemide resistance.

Cardiac troponin-I concentrations in dogs with bradyarrhythmias before and after artificial pacing.

OBJECTIVES: To quantify cardiac troponin-I (cTnI) concentration in dogs with symptomatic bradyarrhythmias before and after artificial pacing and to correlate cTnI concentration with diagnosis, echocardiographic parameters, serology, and outcome. ANIMALS, MATERIALS AND METHODS: Medical records from the University of Pennsylvania from 2006 to 2009 were reviewed, and 14 dogs with cTnI assay results before and after pacemaker were identified. The ECG diagnosis included complete atrioventricular block (AVB), sick sinus syndrome, 2nd degree AVB, and atrial standstill. Serology, presence of premature beats, echocardiographic measurements, and pacing modality were recorded. RESULTS: Mean cTnI concentration was elevated both pre- and post-pacing, and was significantly higher pre-pacing vs. post-pacing. Post-pacing cTnI concentration in 9 of 14 dogs (64%) remained above the reference range. Four dogs yielded high serum titers for Bartonella spp. Four dogs with markedly increased cTnI concentration had progressive left ventricular enlargement and myocardial failure as compared to pre-pacing examination. CONCLUSIONS: Elevated cTnI concentration suggests that cardiac injury persists after artificial pacing in dogs with bradyarrhythmias. Myocarditis secondary to Bartonella spp. or other causes may be an important cause of AVB in dogs. Prospective studies investigating the correlation of cTnI to potential etiology and development of post-pacing LV dysfunction and outcome are needed.

Assessment of serum N-terminal pro-B-type natriuretic peptide concentration for differentiation of congestive heart failure from primary respiratory tract disease as the cause of respiratory signs in dogs.

OBJECTIVE: To determine whether serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration is useful in discriminating between cardiac and noncardiac (ie, primary respiratory tract disease) causes of respiratory signs (ie, coughing, stertor, stridor, excessive panting, increased respiratory effort, tachypnea, or overt respiratory distress) in dogs. DESIGN: Multicenter cross-sectional study. ANIMALS: P 115 dogs with respiratory signs. PROCEDURES: Dogs with respiratory signs were solicited for study. Physical examination, thoracic radiography, and echocardiography were used to determine whether respiratory signs were the result of cardiac (ie, congestive heart failure) or noncardiac (ie, primary respiratory tract disease) causes. Serum samples for NT-proBNP assay were obtained at time of admission for each dog. Receiver-operating characteristic curves were constructed to determine the ability of serum NT-proBNP concentration to discriminate between cardiac and noncardiac causes of respiratory signs. RESULTS: Serum NT-proBNP concentration was significantly higher in dogs with cardiac versus noncardiac causes of respiratory signs. In dogs with primary respiratory tract disease, serum NT-proBNP concentration was significantly higher in those with concurrent pulmonary hypertension than in those without. A serum NT-proBNP cutoff concentration > 1,158 pmol/L discriminated between dogs with congestive heart failure and dogs with primary respiratory tract disease with a sensitivity of 85.5% and a specificity of 81.3%. CONCLUSIONS AND CLINICAL RELEVANCE: Measuring serum NT-proBNP concentration in dogs with respiratory signs helps to differentiate between congestive heart failure and primary respiratory tract disease as an underlying cause.

Weekly variability of plasma and serum NT-proBNP measurements in normal dogs.

OBJECTIVES: To determine the weekly variability of serum and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations in healthy dogs. ANIMALS, MATERIALS AND METHODS: Fifty-three normal dogs were examined prospectively. Serum (n=25) or plasma (n=28) samples were obtained for NT-proBNP assay at one week interval for 3 consecutive weeks. RESULTS: Median serum or plasma NT-proBNP concentration did not change over 3 consecutive weeks. Twenty-two of 53 dogs (42%) had at least one NT-proBNP value >500 pmol/L, including 14 dogs with at least one serum NT-proBNP concentration >500 pmol/L and 8 dogs with at least one plasma NT-proBNP concentration >500 pmol/L during the 3-week sampling period. The difference between the maximum and minimum NT-proBNP value obtained over the 3-week sampling period was <100 pmol/L in 40% of dogs, between 100 and 200 pmol/L in 40% of dogs, and >200 pmol/L in 20% of dogs. Of the 19 dogs with a value >500 pmol/L on either week 1 or 2, 11 dogs (58%) had a subsequent NT-proBNP value <500 pmol/L on either week 2 or 3. CONCLUSIONS: There is a high degree of variability in weekly serum and plasma NT-proBNP values in healthy dogs. Individual variability should be considered when interpreting NT-proBNP results in dogs.