Neutrophil-to-lymphocyte ratio is increased in dogs with acute congestive heart failure secondary to myxomatous mitral valve disease compared to both dogs with heart murmurs and healthy controls.

OBJECTIVE: To retrospectively evaluate neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) as a biomarker for severity and short-term outcomes of congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD) in dogs. ANIMALS: 47 dogs with CHF secondary to MMVD, 47 dogs with presumptive preclinical MMVD, and 47 control dogs. METHODS: Medical record data (signalment, physical examination findings, medical treatments instituted, American College of Veterinary Internal Medicine MMVD stage, length of hospitalization, outcome, and hospital re-presentation due to CHF) from March 2012 through March 2022 for each dog were collected. Statistical analyses were performed with Mann-Whitney, Spearman correlation, and Fisher exact tests. RESULTS: NLR (but not PLR) was significantly higher in dogs with CHF secondary to MMVD (6.41) compared to presumptive preclinical MMVD dogs (4.66; P < .001) and control dogs (3.95; P < .001). Dogs with higher NLR and PLR received significantly higher cumulative dosages of loop-diuretic therapy during hospitalization (ρ = 0.3, P = .04; and ρ = 0.4, P = .02, respectively). There was a positive association between NLR and duration of oxygen supplementation within the CHF group (ρ = 0.4; P = .01). CLINICAL RELEVANCE: The increased diuretic dose and time receiving oxygen supplementation may represent increased disease severity for which NLR (and to a lesser extent PLR) may serve as a readily available marker. The data presented provide information regarding some of the systemic inflammatory changes seen in CHF secondary to MMVD in dogs. Future research should include prospective, longitudinal studies to provide insight into the long-term prognostic value of NLR and PLR in dogs with CHF.

Myxomatous mitral valve disease in Miniature Schnauzers and Yorkshire Terriers: 134 cases (2007-2016).

OBJECTIVE: To characterize features of myxomatous mitral valve disease (MMVD) in Miniature Schnauzers and Yorkshire Terriers. ANIMALS: 69 Miniature Schnauzers and 65 Yorkshire Terriers, each with MMVD. PROCEDURES: Medical record data for each dog were collected; the study period was January 2007 through December 2016. If available, radiographic data were evaluated, and a vertebral heart scale score was assigned for each dog. Statistical analysis was performed with Student t and Fisher exact tests. RESULTS: Compared with Yorkshire Terriers, the prevalence of MMVD was significantly higher in Miniature Schnauzers and affected dogs were significantly younger at the time of diagnosis. Miniature Schnauzers were significantly more likely to have mitral valve prolapse and syncope, compared with Yorkshire Terriers. Yorkshire Terriers were significantly more likely to have coughing and have had previous or current treatment with cardiac medications, compared with Miniature Schnauzers. There was no statistical difference between breeds with regard to abnormally high vertebral heart scale scores or radiographic evidence of congestive heart failure. CONCLUSIONS AND CLINICAL RELEVANCE: With regard to MMVD, features of the disease among Miniature Schnauzers and Yorkshire Terriers were similar, but there were also a few discernable differences between these 2 breeds and from historical findings for dogs with MMVD of other breeds. Clinical signs at the time of diagnosis differed between the 2 breeds, which may have reflected concurrent breed-specific conditions (sick sinus syndrome or airway disease [eg, tracheal collapse]). Future work should include prospective studies to provide additional information regarding the natural progression of MMVD in these dog breeds.

A novel career development course for animal science students pursuing veterinary college admissions.

A one-credit hour, elective, professional development course was created at North Carolina State University to introduce pre-veterinary track students to the admissions process and the breadth of the veterinary profession. The course was designed to facilitate career exploration while building self-efficacy through vicarious learning, interacting with speakers in various veterinary subfields, and addressing misperceptions about veterinary admissions. To evaluate the student learning objectives and improve upon the current practices of the course, data from two pretest and posttest course surveys for 235 course participants between Spring 2014 and 2017 were analyzed. The results of the study showed that students experienced significant gains in self-appraisal (Cohen's d ranged 1.88 to 2.53), gathering occupational information (Cohen's d ranged 1.59 to 2.53), goal selection (Cohen's d ranged 2.14 to 2.53), and planning and problem-solving (Cohen's d ranged 1.88 to 2.77) as well as experienced a decrease in five misperceptions about veterinary admissions. This novel course is presented as a prospective course for other universities.

A deleterious mutation in the ALMS1 gene in a naturally occurring model of hypertrophic cardiomyopathy in the Sphynx cat.

BACKGROUND: Familial hypertrophic cardiomyopathy is a common inherited cardiovascular disorder in people. Many causal mutations have been identified, but about 40% of cases do not have a known causative mutation. Mutations in the ALMS1 gene are associated with the development of Alstrom syndrome, a multisystem familial disease that can include cardiomyopathy (dilated, restrictive). Hypertrophic cardiomyopathy has not been described. The ALMS1 gene is a large gene that encodes for a ubiquitously expressed protein. The function of the protein is not well understood although it is believed to be associated with energy metabolism and homeostasis, cell differentiation and cell cycle control. The ALMS1 protein has also been shown to be involved in the regulation of cell cycle proliferation in perinatal cardiomyocytes. Although cardiomyocyte cell division and replication in mammals generally declines soon after birth, inhibition of ALMS1 expression in mice lead to increased cardiomyocyte proliferation, and deficiency of Alstrom protein has been suggested to impair post-natal cardiomyocyte cell cycle arrest. Here we describe the association of familial hypertrophic cardiomyopathy in Sphynx cats with a novel ALMS1 mutation. RESULTS: A G/C variant was identified in exon 12 (human exon 13) of the ALMS1 gene in affected cats and was positively associated with the presence of hypertrophic cardiomyopathy in the feline population (p < 0.0001). The variant was predicted to change a highly conserved nonpolar Glycine to a positively charged Arginine. This was predicted to be a deleterious change by three in silico programs. Protein prediction programs indicated that the variant changed the protein structure in this region from a coil to a helix. Light microscopy findings included myofiber disarray with interstitial fibrosis with significantly more nuclear proliferative activity in the affected cats than controls (p < 0.0001). CONCLUSION: This study demonstrates a novel form of cardiomyopathy associated with ALMS1 in the cat. Familial hypertrophic cardiomyopathy is a disease of genetic heterogeneity; many of the known causative genes encoding for sarcomeric proteins. Our findings suggest that variants in genes involved with cardiac development and cell regulation, like the ALMS1 gene, may deserve further consideration for association with familial hypertrophic cardiomyopathy.

Visual representations of canine cardiac arrhythmias with Lorenz (Poincaré) plots.

OBJECTIVE: To characterize the patterns associated with Lorenz plots (LPs) or Poincaré plots derived from the Holter recordings of dogs with various cardiac rhythms. ANIMALS: 77 dogs with 24-hour Holter recordings. PROCEDURES: A 1-hour period from the Holter recordings from each of 20 dogs without arrhythmias and from each of 57 dogs with arrhythmias (10 each with supraventricular premature complexes, complex supraventricular ectopy, ventricular premature complexes, complex ventricular ectopy, and atrial fibrillation, and 7 with high-grade second-degree atrioventricular block) were used to generate the LPs. Patterns depicted in the LPs were described. RESULTS: Arrhythmia-free Holter recordings yielded LPs with a Y-shaped pattern and variable silent zones. Recordings with single premature complexes yielded LPs with double side and triple side lobes. Complex ectopy was denoted by dots clustered in the lower left corner of the LPs. The LPs of recordings with atrial fibrillation had fan patterns consistent with a nonlinear relationship between atrial electrical impulses and atrioventricular nodal conduction. The recordings with atrioventricular block yielded LPs with island patterns consistent with variable atrioventricular nodal conduction. CONCLUSIONS AND CLINICAL RELEVANCE: Distinct LP patterns were identified for common cardiac rhythms of dogs, supportive of nonrandom mechanisms as the cause of most rhythms. Visual interpretation of an LP generated from a Holter recording may aid in determining the arrhythmia type and understanding the arrhythmia's mechanism in dogs and other species.

A mutation in MTM1 causes X-Linked myotubular myopathy in Boykin spaniels.

The purpose of this study was to report the findings of clinical and genetic evaluation of a 3-month old male Boykin spaniel (the proband) that presented with progressive weakness. The puppy underwent a physical and neurological examination, serum biochemistry and complete blood cell count, electrophysiological testing, muscle biopsy and whole genome sequencing. Clinical evaluation revealed generalized neuromuscular weakness with tetraparesis and difficulty holding the head up and a dropped jaw. There was diffuse spontaneous activity on electromyography, most severe in the cervical musculature. Nerve conduction studies were normal, the findings were interpreted as consistent with a myopathy. Skeletal muscle was grossly abnormal on biopsy and there were necklace fibers and abnormal triad structure localization on histopathology, consistent with myotubular myopathy. Whole genome sequencing revealed a premature stop codon in exon 13 of MTM1 (ChrX: 118,903,496 C > T, c.1467C>T, p.Arg512X). The puppy was humanely euthanized at 5 months of age. The puppy's dam was heterozygous for the variant, and 3 male puppies from a subsequent litter all of which died by 2 weeks of age were hemizygous for the variant. This naturally occurring mutation in Boykin spaniels causes a severe form of X-linked myotubular myopathy, comparable to the human counterpart.