The development of high throughput SNP genotyping technologies has improved the genetic dissection of simple and complex traits in many species including cats. The properties of feline 62,897 SNPs Illumina Infinium iSelect DNA array are described using a dataset of over 2,000 feline samples, the most extensive to date, representing 41 cat breeds, a random bred population, and four wild felid species. Accuracy and efficiency of the array’s genotypes and its utility in performing population-based analyses were evaluated. Average marker distance across the array was 37,741 Kb, and across the dataset, only 1% (625) of the markers exhibited poor genotyping and only 0.35% (221) showed Mendelian errors. Marker polymorphism varied across cat breeds and the average minor allele frequency (MAF) of all markers across domestic cats was 0.21. Population structure analysis confirmed a Western to Eastern structural continuum of cat breeds. Genome-wide linkage disequilibrium ranged from 50–1,500 Kb for domestic cats and 750 Kb for European wildcats (Felis silvestris silvestris). Array use in trait association mapping was investigated under different modes of inheritance, selection and population sizes. The efficient array design and cat genotype dataset continues to advance the understanding of cat breeds and will support monogenic health studies across feline breeds and populations.

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The purposes of this study were to evaluate families of Boxers with ventricular arrhythmias to determine whether this disorder is a familial trait and, if so, to determine the mode of inheritance. Eighty-two Boxers were evaluated by physical examination, electrocardiogram, echocardiogram, and 24-hour ambulatory electrocardiogram. Dogs were considered affected if at least 50 premature ventricular complexes (PVCs) were observed during a 24-hour period. All dogs were at least 6 years of age at evaluation. Complete cardiovascular examinations were performed on dogs from 6 extended families. The 2 most complete pedigrees were used to determine the pattern of inheritance. The number of PVCs observed during a 24-hour period in affected dogs ranged from 112 to 4,894 (mean +/- SD, median; 1,309 +/- 2,609, 1,017). The number of PVCs observed during a 24-hour period in the unaffected dogs ranged from 0 to 16 (7 +/- 10, 12). Pedigree evaluation was performed to determine pattern of inheritance. An autosomal dominant pattern was determined to be most likely because a sex predisposition was not observed, affected individuals were observed in every generation, and 2 affected individuals produced unaffected offspring. We conclude that familial ventricular arrhythmias is inherited as an autosomal dominant trait in some Boxers.

Nineteen of 28 (67%) Greyhounds enrolled in the Blood Donor Program at The Veterinary Teaching Hospital, The Ohio State University (Columbus, OH), had a left basilar systolic murmur. Ten Greyhounds with murmurs and 9 without murmurs were evaluated to gain knowledge about the pathogenesis of this murmur. Echocardiograms were performed without sedation by means of a GE Vivid 7 Echocardiographic System with a continuous ECG; systolic arterial blood pressure (SABP) was measured with an Ultrasonic Doppler Flow detector model 811-B. The mean peak aortic velocity in the Greyhounds with murmurs (2.15 m/s; range, 1.8-2.2 m/s) was significantly higher than in the Greyhounds without murmurs (1.89 m/s; range, 1.6-2.0 m/s) (P < .001); there were no significant differences between groups for aortic valve or annulus diameter, fractional shortening, pulmonic velocity, SABP, hematocrit, serum protein concentration, or red blood cell counts. In this study, Greyhounds with soft, left basilar systolic murmurs had mildly (but significantly) higher mean peak aortic velocities than similar dogs without murmurs. In the dogs with murmurs (and higher velocities), we could not identify structural abnormalities, such as valvular lesions or other congenital defects. There was no inverse correlation between the systolic murmur and the higher hematocrit and red blood cell counts observed in this breed. This 1-2/6 basilar systolic murmur is common in Greyhounds, and it does not appear to be of any clinical consequence.

Background: Soft, variable ejection murmurs are common in Boxers and are associated with increased left ventricular outflow tract (LVOT) ejection velocities. Whether these murmurs are physiologic or indicate mild aortic stenosis is controversial. Ejection velocity is impacted by LVOT area and ventricular stroke volume (SV), suggesting that these variables are pertinent to murmur development.Hypothesis: Boxers with ejection murmurs have a smaller LVOT and equivalent SV indices, compared with values in dogs without murmurs.Animals: Three age-and weight-matched groups of dogs-15 Boxers with soft ejection murmurs (group I); 15 Boxers without murmurs (group II); and 15 nonBoxer dogs without murmurs (group III)-were studied.Methods: All dogs underwent 2-dimensional and Doppler echocardiographic examinations. The LVOT size at multiple levels; LVOT ejection velocity, stroke distance, and SV index; and right ventricular SV index were determined and compared by analysis of variance.Results: Indexed LVOT areas in Boxer groups were not different, but were significantly smaller than those of non-Boxer dogs. Ejection velocities and stroke distances were significantly different across all groups, with group I having the highest and group III having the lowest values. Doppler SV indices (ml/m 2 ) for group-I versus group-II Boxers were 70616(SD) versus 62612 for the LVOT (P 5 .27) and 58612 versus 4869 for the right ventricle (P 5 .14).Conclusions and clinical importance: These data suggest that a relatively smaller LVOT in Boxers predisposes them to increased ejection velocity and development of murmurs. The contribution of SV to the genesis of these often labile murmurs requires additional study.

Background: The Doberman Pinscher is one of the most common breeds of dogs to develop dilated cardiomyopathy (DCM), a primary heart muscle disorder characterized by myocardial dysfunction, cardiac arrhythmias, and congestive heart failure. In the Doberman Pinscher, the disease is typically adult onset, and a familial etiology has been suggested. Hypothesis: DCM in the Doberman Pinscher, is a familial disease linked to a specific genetic marker. Animals: The study comprised an extended family of Doberman Pinschers with a history of DCM. Methods: Participating dogs were prospectively evaluated over an 8-year period. Phenotype of participating dogs was determined by annual echocardiography and ambulatory electrocardiography, and the pedigree was evaluated to determine a specific mode of inheritance. Three hundred seventy-two microsatellite markers were selected and genotyped to cover the 38 autosomal chromosomes. Phenotyping, genotyping, and pedigree information was entered into a database, and parametric, 2-point analysis was performed. Markers were considered to be linked to the development of DCM if the logarithm of odds LOD score was $3.0. Results: An autosomal dominant mode of inheritance was defined by the appearance of the disease in multiple generations, equal gender representation (P 5 .973) and male-to-male transmission. A maximum LOD score of 1.31 was obtained for 1 marker on chromosome 20, a score not high enough to be associated with DCM. Conclusion: DCM in the Doberman Pinscher is a familial disease inherited as an autosomal dominant trait. The causative gene(s) responsible for this condition remain unresolved. Association studies by means of array technology may provide new insights into gene identification.

Right ventricular (RV) dysfunction is a cause of exercise intolerance, hypotension, syncope, and heart failure in dogs with cardiac and respiratory disorders. The study objective was to determine Doppler-derived reference values that reflect global RV function in healthy dogs. We measured systolic time intervals and an RV index of myocardial performance (IMP) in 45 healthy dogs between 8 months and 8 years of age. Pulsed-wave Doppler recordings of mitral, tricuspid, aortic, and pulmonic were acquired. Pre-ejection period (PEP), ejection time (ET), PEP/ET, and IMP were determined for both ventricles by separate cardiac cycles. Compared to the mean left ventricular (LV) IMP (0.410; 95% confidence intervals [CI] 0.378-0.442), mean RV IMP (0.250; 95% CI 0.222-0.278) was significantly smaller, and mean ET for the RV (187 millisecond [ms]; 95% CI 182-192) was significantly longer than the LV (173 ms; 95% CI 168-179). A clinically relevant correlation was not found among RV IMP and body weight, heart rate, RV ET, RV PEP, or RV PEP/ET. Calculation of LV IMP with 2 separate sample volumes yielded smaller values than from a single sample volume, with a difference in means of 0.040. We conclude that the RV IMP is relatively independent of body weight and heart rate within the ranges studied and is consistently lower than values derived from the LV in healthy dogs. This study provides additional reference values for RV function in dogs and may be useful for identification of RV dysfunction in dogs.

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