Effect of cilobradine in cats with a first episode of congestive heart failure due to primary cardiomyopathy.

INTRODUCTION: Heart rate (HR) is often elevated in cats with cardiomyopathies (CMPs). Pharmacologic modulation of HR may reduce cardiac morbidity and mortality. OBJECTIVES: To investigate the effects of cilobradine vs. placebo, regarding time to cardiac mortality or morbidity in cats with first episode of congestive heart failure (CHF) due to primary CMP. ANIMALS: Three hundred and sixty-seven client-owned cats with primary CMP that had presented with a first episode of CHF at 50 centers in Europe. Per-protocol population comprised 193 cats (n = 89 cilobradine, n = 104 placebo). An interim analysis for futility was planned. METHODS: Prospective, randomized, placebo-controlled, double-blinded, multicenter clinical trial. Primary outcome variable was the time to a composite of cardiac mortality or cardiac morbidity. RESULTS: Median time to primary outcome was 84 days (95% confidence interval [CI]: 63-219 days) in the cilobradine group (CG) and 203 days in the placebo group (95% CI: 145-377 days) with observed hazard ratio of 1.44, indicating a higher hazard for the CG (P = 0.057). Mean HR was 28 beats per minute (bpm) lower at Day 7 (P < 0.0001) and remained 29 bpm lower at Day 360 (P = 0.026) in the CG than that in the placebo group. Although the number of adverse events did not differ, there were more serious adverse events in the CG. CONCLUSIONS: Heart rate reduction by cilobradine in cats with a first episode of CHF due to primary CMP did not reduce cardiac mortality and morbidity.

Epidemiological, clinical, and echocardiographic features, and outcome of dogs with Ebstein's anomaly: 32 cases (2002-2016).

INTRODUCTION/OBJECTIVES: Ebstein's anomaly (EA) is a congenital heart disease characterized by apical displacement of the tricuspid valve leaflets in the right ventricle. The objective of this retrospective study was to investigate the signalment, clinical features, echocardiographic findings, and outcome of dogs with EA. ANIMALS, MATERIALS AND METHODS: Medical records of 40 dogs with EA were reviewed. Echocardiographic variables used to assess EA severity in human pediatrics were also evaluated (e.g. displacement index, Celermajer index, Carpentier class, and apex-mitral annulus:apex-tricuspid annulus distance ratio). RESULTS: Labrador retriever was the most commonly recruited breed (24 of the 40 dogs, 60%). Eight of the 40 dogs with EA had hemodynamically compromising concurrent heart (n = 7) or respiratory diseases (n = 1). A right apical systolic heart murmur (median grade = 5/6) was detected in the remaining 32 dogs, without any other clinical sign related to EA in 19 of the 32 dogs (59%). Median (interquartile range) values of the displacement index and Celermajer index were 17.4 mm/m2 (12.0-21.9) and 100% (50-130), respectively. Median time to all-cause death was 74 months, and 72% dogs (95% confidence interval, 50-86%) had not succumbed to cardiac death (CD) 160 months after diagnosis. Univariate analyses showed that the time from diagnosis to CD was associated with the presence of clinical signs, ascites, severe right atrial dilation, palpable thrill, and a Celermajer index ≥100%. DISCUSSION: Right atrial enlargement is significantly associated with decreased survival time of dogs with EA although most may live for years and may not die from CD. CONCLUSIONS: These results support medium to long-term survival for most dogs with EA.

Longitudinal Analysis of Quality of Life, Clinical, Radiographic, Echocardiographic, and Laboratory Variables in Dogs with Preclinical Myxomatous Mitral Valve Disease Receiving Pimobendan or Placebo: The EPIC Study.

BACKGROUND: Changes in clinical variables associated with the administration of pimobendan to dogs with preclinical myxomatous mitral valve disease (MMVD) and cardiomegaly have not been described. OBJECTIVES: To investigate the effect of pimobendan on clinical variables and the relationship between a change in heart size and the time to congestive heart failure (CHF) or cardiac-related death (CRD) in dogs with MMVD and cardiomegaly. To determine whether pimobendan-treated dogs differ from dogs receiving placebo at onset of CHF. ANIMALS: Three hundred and fifty-four dogs with MMVD and cardiomegaly. MATERIALS AND METHODS: Prospective, blinded study with dogs randomized (ratio 1:1) to pimobendan (0.4-0.6 mg/kg/d) or placebo. Clinical, laboratory, and heart-size variables in both groups were measured and compared at different time points (day 35 and onset of CHF) and over the study duration. Relationships between short-term changes in echocardiographic variables and time to CHF or CRD were explored. RESULTS: At day 35, heart size had reduced in the pimobendan group: median change in (Δ) LVIDDN -0.06 (IQR: -0.15 to +0.02), P < 0.0001, and LA:Ao -0.08 (IQR: -0.23 to +0.03), P < 0.0001. Reduction in heart size was associated with increased time to CHF or CRD. Hazard ratio for a 0.1 increase in ΔLVIDDN was 1.26, P = 0.0003. Hazard ratio for a 0.1 increase in ΔLA:Ao was 1.14, P = 0.0002. At onset of CHF, groups were similar. CONCLUSIONS AND CLINICAL IMPORTANCE: Pimobendan treatment reduces heart size. Reduced heart size is associated with improved outcome. At the onset of CHF, dogs treated with pimobendan were indistinguishable from those receiving placebo.

Atrial cardiomyopathy in an adult Labrador retriever dog.

INTRODUCTION: A 7-year-old castrated male Labrador retriever was examined for a 10-day history of weakness and syncope. Physical examination revealed bradycardia and a grade III/VI left apical systolic heart murmur. Electrocardiography demonstrated bradycardia, absence of P waves and an atrio-ventricular nodal escape rhythm. Echocardiography revealed marked biatrial enlargement. Thoracic radiographs showed no evidence of pulmonary edema. Routine plasma biochemistry and electrolytes, basal serum cortisol, total thyroxin concentration, and complete blood count were within normal limits. Serum cardiac troponin I concentration was moderately increased. Serological examinations for antibodies against vector-borne diseases were negative. A pacemaker was implanted one month after the initial presentation due to worsening of the dog's clinical condition despite medical treatment. The dog remained asymptomatic for 18 months but was then re-presented with a gastric dilatation volvulus and subsequently euthanized. Necropsy and histology of the heart yielded a diagnosis of atrial cardiomyopathy.

Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study-A Randomized Clinical Trial.

BACKGROUND: Pimobendan is effective in treatment of dogs with congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD). Its effect on dogs before the onset of CHF is unknown. HYPOTHESIS/OBJECTIVES: Administration of pimobendan (0.4-0.6 mg/kg/d in divided doses) to dogs with increased heart size secondary to preclinical MMVD, not receiving other cardiovascular medications, will delay the onset of signs of CHF, cardiac-related death, or euthanasia. ANIMALS: 360 client-owned dogs with MMVD with left atrial-to-aortic ratio ≥1.6, normalized left ventricular internal diameter in diastole ≥1.7, and vertebral heart sum >10.5. METHODS: Prospective, randomized, placebo-controlled, blinded, multicenter clinical trial. Primary outcome variable was time to a composite of the onset of CHF, cardiac-related death, or euthanasia. RESULTS: Median time to primary endpoint was 1228 days (95% CI: 856-NA) in the pimobendan group and 766 days (95% CI: 667-875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47-0.87) compared with the placebo group. The benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952-NA) in the pimobendan group and 902 days (95% CI: 747-1061) in the placebo group) (P = .012). CONCLUSIONS AND CLINICAL IMPORTANCE: Administration of pimobendan to dogs with MMVD and echocardiographic and radiographic evidence of cardiomegaly results in prolongation of preclinical period and is safe and well tolerated. Prolongation of preclinical period by approximately 15 months represents substantial clinical benefit.

Extraction of urethral calculi by transabdominal cystoscopy and urethroscopy in nine dogs.

OBJECTIVES: To describe a minimally invasive technique for treating urethral obstructions in male dogs and to review the postoperative results. METHODS: All dogs (n=9) had urethral obstruction due to calculi. Obstructions were verified by radiographic and ultrasonographic examinations. Dogs with impaired kidney function were not included in the study. A 5-mm diameter trocar and cannula were placed in the ventral midline, 2 cm cranial to the umbilicus, allowing placement of a 10-mm diameter cannula under visual guidance, adjacent to the apex of the bladder. The bladder was then partially exteriorised and sutured to the skin. A 5-mm diameter cystoscopy sheath was introduced into the bladder lumen and advanced into the urethra. Continuous retrograde flushing was used to dislodge the calculi from the site of obstruction and collect them upstream. RESULTS: The nine dogs were followed up for a minimum of 6 months. No major postoperative complications were identified. One dog exhibited transient macroscopic haematuria (for 3 weeks postoperatively). All urethral calculi were removed in the nine dogs. No recurrence was found during the follow-up period. CLINICAL SIGNIFICANCE: A minimally invasive approach is used to treat urethral obstructions resulting from calculi in the male dogs.

Patent ductus arteriosus in a family of Chihuahuas.

This report describes a patent ductus arteriosus (PDA) in four puppies from the same family of Chihuahuas, bred from the same mother and from two different litters. Identification of this congenital anomaly relies on clinical examination, radiography and ultrasonography. Three of these puppies were female, and had a type-1 PDA. A conventional surgical ligation was performed on one of them, whilst the others underwent no treatment. One puppy was male, and presented with a type-4 PDA, requiring euthanasia. Post-mortem examination and histopathological examination of the PDA allowed characterisation of the histological anomalies, which were identical to those described in other breeds. The mother and the two stud dogs were not affected. Even though the mode of transmission has not been fully identified, it is evident that this PDA is hereditary in nature. To the authors' knowledge this is the first description of this congenital cardiopathy in a family of this breed, and in a significant number of first-generation individuals.