A survey of the use of ultrasound by small animal veterinary clinicians.

This study aimed to determine the current use of ultrasound amongst small animal veterinarians. A total of 1216 small animal veterinary practitioners responded to an electronic survey that was administered through the Veterinary Information Network to all its members. Descriptive statistics were generated; limited inferential statistics were performed to examine specific relationships. Eighty-four percent of respondents had access to an ultrasound unit, and 86% of respondents reported using their unit multiple times per week. The most common uses were assistance with cystocentesis (93%) and abdominocentesis (71%), pregnancy diagnosis (69%), limited abdominal evaluation (63%), to aid in thoracocentesis (59%), and limited thoracic evaluation (52%). Eighty-nine percent of respondents received some formal training in ultrasound, most commonly from continuing education courses. Most respondents (52%) reported receiving ≤25 h of training. Additionally, 88% of respondents believed it was either extremely or very important for there to be ultrasound training for veterinary students prior to graduation. Based on this survey, most small animal practitioners commonly use ultrasound for limited examinations, being most confident in the sonographic evaluation and centesis of the bladder and for the detection and centesis of effusion in a body cavity. With most respondents having ≤25 h of training in ultrasound, typically obtained in postgraduate courses, an expansion in standardized basic ultrasound training within the veterinary curriculum may be warranted.

Use of whole genome analysis to identify shared genomic variants across breeds in canine mitral valve disease.

Familial mitral valve prolapse in human beings has been associated with several genetic variants; however, in most cases, a known variant has not been identified. Dogs also have a naturally occurring form of familial mitral valve disease (MMVD) with similarities to the human disease. A shared genetic background and clinical phenotype of this disease in some dog breeds has indicated that the disease may share a common genetic cause. We evaluated DNA from 50 affected dogs from five different dog breeds in a whole genome sequencing approach to identify shared variants across and within breeds that could be associated with MMVD. No single causative genetic mutation was found from the 50 dogs with MMVD. Ten variants were identified in 37/50 dogs around and within the MED13L gene. These variants were no longer associated with MMVD when evaluated with a larger cohort including both affected and unaffected dogs. No high/moderate impact variants were identified in 10/10 miniature poodles, one was identified in 10/10 Yorkshire Terriers and 10/10 dachshunds, respectively, 14 were identified in 10/10 Miniature schnauzers, and 19 in 10/10 CKCS. Only one of these could be associated with the cardiac valve (Chr12:36801705, COL12A1; CKCS) but when evaluated in an additional 100 affected CKCS the variant was only identified in 84/100 affected dogs, perhaps indicating genetic heterogeneity in this disease. Our findings indicate that development of MMVD in the dog may be related to a combination of genetic and environmental factors that impact specific molecular pathways rather than a single shared genetic variant across or within breeds.

A missense variant in the titin gene in Doberman pinscher dogs with familial dilated cardiomyopathy and sudden cardiac death.

The dog provides a large animal model of familial dilated cardiomyopathy for the study of important aspects of this common familial cardiovascular disease. We have previously demonstrated a form of canine dilated cardiomyopathy in the Doberman pinscher breed that is inherited as an autosomal dominant trait and is associated with a splice site variant in the pyruvate dehydrogenase kinase 4 (PDK4) gene, however, genetic heterogeneity exists in this species as well and not all affected dogs have the PDK4 variant. Whole genome sequencing of a family of Doberman pinchers with dilated cardiomyopathy and sudden cardiac death without the PDK4 variant was performed. A pathologic missense variant in the titin gene located in an immunoglobulin-like domain in the I-band spanning region of the molecule was identified and was highly associated with the disease (p < 0.0001). We demonstrate here the identification of a variant in the titin gene highly associated with the disease in this spontaneous canine model of dilated cardiomyopathy. This large animal model of familial dilated cardiomyopathy shares many similarities with the human disease including mode of inheritance, clinical presentation, genetic heterogeneity and a pathologic variant in the titin gene. The dog is an excellent model to improve our understanding of the genotypic phenotypic relationships, penetrance, expression and the pathophysiology of variants in the titin gene.

Angiotensin-converting enzyme activity in Cavalier King Charles Spaniels with an ACE gene polymorphism and myxomatous mitral valve disease.

OBJECTIVES: Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog. It is particularly common in the Cavalier King Charles Spaniel (CKCS) breed and affected dogs are frequently managed with angiotensin-converting enzyme inhibitors (ACE-I). We have previously identified a canine ACE gene polymorphism associated with a decrease in angiotensin-converting enzyme (ACE) activity. The aim of this study was to evaluate for the prevalence of the ACE polymorphism in CKCS with mitral valve disease and to determine whether the presence of the polymorphism is associated with alterations in ACE activity at different stages of cardiac disease. METHODS: Seventy-three dogs with a diagnosis of mitral valve disease were evaluated and a blood sample was drawn for ACE polymorphism genotyping and ACE activity measurement. RESULTS: Forty-three dogs were homozygous for the ACE polymorphism; five were heterozygous and 25 were homozygous wild type. The mean age and the median severity of disease were not different for dogs with the polymorphism and dogs with the wild-type sequence. The median baseline ACE activity was significantly lower for the ACE polymorphism (27.0 U/l) than the wild-type sequence dogs (31.0 U/l) (P=0.02). Dogs with more severe disease and the ACE polymorphism had significantly lower levels of ACE activity than dogs with the wild-type sequence (P=0.03). CONCLUSION: The CKCS appears to have a high prevalence of the ACE variant. Dogs with the ACE variant had lower levels of ACE activity even in more advanced mitral valve disease than dogs without the variant. The clinical significance of this finding and its impact on the need for ACE-I in dogs with the polymorphism and heart disease deserves further study.

Intracoronary allogeneic cardiosphere-derived stem cells are safe for use in dogs with dilated cardiomyopathy.

Cardiosphere-derived cells (CDCs) have been shown to reduce scar size and increase viable myocardium in human patients with mild/moderate myocardial infarction. Studies in rodent models suggest that CDC therapy may confer therapeutic benefits in patients with non-ischaemic dilated cardiomyopathy (DCM). We sought to determine the safety and efficacy of allogeneic CDC in a large animal (canine) model of spontaneous DCM. Canine CDCs (cCDCs) were grown from a donor dog heart. Similar to human CDCs, cCDCs express CD105 and are slightly positive for c-kit and CD90. Thirty million of allogeneic cCDCs was infused into the coronary vessels of Doberman pinscher dogs with spontaneous DCM. Adverse events were closely monitored, and cardiac functions were measured by echocardiography. No adverse events occurred during and after cell infusion. Histology on dog hearts (after natural death) revealed no sign of immune rejection from the transplanted cells.

The Role of Point-of-Care Ultrasound in Managing Cardiac Emergencies.

Point-of-care ultrasound (POCUS) is a useful imaging tool for the diagnosis and monitoring of cardiac emergencies. Unlike complete echocardiography, POCUS is a time-sensitive examination involving a subset of targeted thoracic ultrasound views to identify abnormalities of the heart, lungs, pleural space, and caudal vena cava. When integrated with other clinical information, POCUS can be helpful in the diagnosis of left-sided and right-sided congestive heart failure, pericardial effusion and tamponade, and severe pulmonary hypertension and can help clinicians monitor resolution or recurrence of these conditions.

Evaluation of Renin-Angiotensin-Aldosterone System Components and Enzymes in Systemically Hypertensive Cats Receiving Amlodipine.

BACKGROUND: Chronic renin-angiotensin-aldosterone system (RAAS) activation is harmful. Amlodipine activates RAAS in humans and dogs, but contradictory data exist for systemically hypertensive (SHT) cats. HYPOTHESIS: Cats with SHT and chronic kidney disease treated with amlodipine (SHT/CKD-A) are RAAS activated. ANIMALS: Client-owned cats: unmedicated normotensive (NT) cats (n = 9); SHT/CKD-A cats (n = 5) with median systolic blood pressure of 170 mmHg (vs. 195 mmHg, pre-treatment), chronic kidney disease, and receiving no RAAS-suppressive therapy. METHODS: Serum was frozen (-80 °C) until RAAS analysis via equilibrium analysis. The RAAS variables (reported as median (minimum-maximum)) were compared between groups, using Mann-Whitney U test. RESULTS: Angiotensin 1, angiotensin 1,7, angiotensin III, and angiotensin 1,5, and angiotensin-converting enzyme (ACE)-2 activity were higher in SHT/CKD-A cats compared to NT cats, while ACE activity was lower in SHT/CKD-A cats compared to NT cats (p < 0.05 all). A marker for alternative RAAS influence (ALT-S) was significantly higher (69; 58-73 pmol/pmol) in SHT/CKD-A cats compared to NT cats (35; 14-63 pmol/pmol; p = 0.001). Aldosterone concentrations were significantly higher (393; 137-564 pmol/L) in SHT/CKD-A cats compared to NT cats (129; 28-206 pmol/L; p = 0.007). CONCLUSION AND CLINICAL IMPORTANCE: Circulating RAAS is activated in systemically hypertensive cats receiving amlodipine. Although this study did not parse out the individual contributions of SHT, chronic kidney disease, and amlodipine, the findings suggest that the use of concurrent RAAS-suppressant therapy, specifically aldosterone antagonism, in amlodipine-treated SHT cats with chronic kidney disease might be indicated.

Pharmacokinetics of pimobendan after oral administration to dogs with myxomatous mitral valve disease.

BACKGROUND: Pimobendan is an important therapy for dogs with myxomatous mitral valve disease (MMVD). The pharmacokinetics are reported in healthy dogs but not in dogs with heart disease. HYPOTHESIS/OBJECTIVES: To determine if dog characteristics such as age, breed, body condition score, ACVIM stage of heart disease or biochemical laboratory value alter the pharmacokinetics of orally administered pimobendan and its metabolite in a cohort of dogs with naturally occurring MMVD. ANIMALS: Fifty-seven client-owned dogs with MMVD ACVIM Stage B2, C, or D and administered pimobendan to steady state blood concentrations. METHODS: Prospective, observational study. Samples were collected using a sparse-sampling protocol at specific intervals after administration of pimobendan. Plasma pimobendan and the active metabolite (O-desmethyl-pimobendan, ODMP) concentrations were determined via high-pressure liquid chromatography and fluorescence detection. Data was analyzed via a population pharmacokinetic approach and nonlinear mixed effects modeling (NLME). Numerous covariates were examined in the NLME model. RESULTS: The absorption and elimination half-lives (t1/2 ) were approximately 1.4 and 1 hour for pimobendan and 1.4 and 1.3 hours for ODMP, respectively. Pharmacokinetic parameters were highly variable, especially the values for pimobendan absorption and elimination rate, and absorption rate of ODMP with coefficients of variation of 147.84%, 64.51% and 64.49%, respectively. No covariate evaluated was a significant source of variability. CONCLUSIONS AND CLINICAL IMPORTANCE: The pharmacokinetic parameters were highly variable among this group of dogs with MMVD. The variability was not associated with the dog's age, body weight or condition score, stage of heart disease, dose, serum creatinine, or alkaline phosphatase.

Delayed-release rapamycin halts progression of left ventricular hypertrophy in subclinical feline hypertrophic cardiomyopathy: results of the RAPACAT trial.

OBJECTIVE: Feline hypertrophic cardiomyopathy (HCM) remains a disease with little therapeutic advancement. Rapamycin modulates the mTOR pathway, preventing and reversing cardiac hypertrophy in rodent disease models. Its use in human renal allograft patients is associated with reduced cardiac wall thickness. We sought to evaluate the effects of once-weekly delayed-release (DR) rapamycin over 6 months on echocardiographic, biochemical, and biomarker responses in cats with subclinical, nonobstructive HCM. ANIMALS: 43 client-owned cats with subclinical HCM. METHODS: Cats enrolled in this double-blinded, multicentered, randomized, and placebo-controlled clinical trial were allocated to low- or high-dose DR rapamycin or placebo. Cats underwent physical examination, quality-of-life assessment, blood pressure, hematology, biochemistry, total T4, urinalysis, N-terminal pro-B-type natriuretic peptide, and cardiac troponin I at baseline and days 60, 120, and 180. Fructosamine was analyzed at screening and day 180. Echocardiograms were performed at all time points excluding day 120. Outcome variables were compared using a repeated measures ANCOVA. RESULTS: No demographic, echocardiographic, or clinicopathologic values were significantly different between study groups at baseline, confirming successful randomization. At day 180, the primary study outcome variable, maximum LV myocardial wall thickness at any location, was significantly lower in the low-dose DR rapamycin group compared to placebo (P = .01). Oral DR rapamycin was well tolerated with no significant differences in adverse events between groups. CLINICAL RELEVANCE: Results demonstrate that DR rapamycin was well tolerated and may prevent or delay progressive LV hypertrophy in cats with subclinical HCM. Additional studies are warranted to confirm and further characterize these results.

Bilateral lysis of aortic saddle thrombus with early tissue plasminogen activator (BLASTT): a prospective, randomized, placebo-controlled study in feline acute aortic thromboembolism.

OBJECTIVES: The aim of this study was to investigate the impact of tissue plasminogen activator (TPA) on the treatment of feline aortic thromboembolism (FATE). METHODS: Cats diagnosed with FATE involving ⩾2 limbs were enrolled in a prospective, multicenter, double-blinded, randomized, placebo-controlled study within 6 h of an event. Diagnosis was made by clinical findings and one confirmatory criterion. Cats received placebo or TPA (1 mg/kg/h with the first 10% by bolus). All cats received pain control and thromboprophylaxis. The primary outcome was a change from baseline in a published limb score at 48 h. Secondary outcomes included 48 h survival, survival to discharge and complication proportions. Statistical analyses included pattern-mixture models, logistic regression and Fisher's exact, Student's t- and Mann-Whitney-Wilcoxon tests. RESULTS: Based on a power analysis, 40 cats were enrolled; however, only 20 survived to 48 h (TPA, n = 12; placebo, n = 8 [P = 0.34]). There was a statistically significant improvement in limb scores compared with baseline for both groups (P <0.001). Limb score at 48 h was 1 point lower (better) in the TPA group (P = 0.19). Thrombolysis had no statistically significant effect on 48 h survival (P = 0.22). Lower affected limb lactate was associated with better 48 h survival (odds ratio 1.53, 95% confidence interval 1.08-2.17; P = 0.02). The survival to discharge rates were 45% (TPA) and 30% (placebo; P = 0.51). Complications in the TPA and placebo groups included acute kidney injury (22% and 19%, respectively; P = 1.00) and/or reperfusion injuries (33% and 19%, respectively; P = 0.45). CONCLUSIONS AND RELEVANCE: Survival and complication rates of acute FATE were not different with or without thrombolysis. High in-hospital mortality decreased the statistical power to detect a statistically significant difference between treatments with regard to our primary outcome.

Clinical progression of X-linked muscular dystrophy in two German Shorthaired Pointers.

CASE DESCRIPTION: 2 full-sibling male German Shorthaired Pointer (GSHP) puppies (dogs 1 and 2) with X-linked muscular dystrophy and deletion of the dystrophin gene (gene symbol, DMD) each had poor growth, skeletal muscle atrophy, pelvic limb weakness, episodic collapse, and episodes of coughing. CLINICAL FINDINGS: Initial examination revealed stunted growth, brachygnathism, trismus, and diffuse neuromuscular signs in each puppy; clinical signs were more severe in dog 2 than in dog 1. Immunohistochemical analysis revealed a lack of dystrophin protein in both dogs. During the next 3 years, each dog developed hyperinflation of the lungs, hypertrophy of the cervical musculature, and hypertrophy of the lateral head of the triceps brachii muscle. TREATMENT AND OUTCOME: Monitoring and supportive care were provided at follow-up visits during an approximately 7-year period. No other specific treatment was provided. Neuromuscular signs in both dogs remained stable after 3 years of age, with dog 2 consistently more severely affected than dog 1. The dogs had multiple episodes of aspiration pneumonia; dogs 1 and 2 were euthanatized at 84 and 93 months of age, respectively. CLINICAL RELEVANCE: The clinical course of disease in these dogs was monitored for a longer period than has been monitored in previous reports of dystrophin-deficient dogs. The clinical progression of muscular dystrophy in the 2 GSHPs was compared with that for other breeds and species with dystrophin-deficient conditions, and the potential basis for the phenotypic variation observed between these littermates, along with potential therapeutic ramifications for dogs and humans, was evaluated.

Focused Canine Cardiac Ultrasound.

Focused cardiac ultrasound (FCU) is a useful point-of-care imaging tool to assess cardiovascular status in symptomatic dogs in the acute care setting. Unlike complete echocardiography, FCU is a time-sensitive examination involving a subset of targeted ultrasound views to identify severe cardiac abnormalities and is performed as part of an integrated thoracic ultrasound including interrogation of the pleural space and lungs. When integrated with other clinical information, FCU can be helpful in the diagnosis of left-sided and right-sided congestive heart failure, pericardial effusion and tamponade, and severe pulmonary hypertension, and can provide estimates of fluid responsiveness in hypotensive dogs.

Comparison of curvilinear-array (microconvex) and phased-array transducers for ultrasonography of the lungs in dogs.

OBJECTIVES: To compare the use of curvilinear-array (microconvex) and phased-array transducers for ultrasonographic examination of the lungs in dogs. ANIMALS: 13 client-owned dogs with left-sided congestive heart failure. PROCEDURES: In a prospective methods comparison study, 24 ultrasonographic examinations of the lungs (4 sites/hemithorax) were performed with both curvilinear-array and phased-array transducers at 3 clinical time points. Two observers independently assessed the number of B lines (scored per site and in total), number of sites strongly positive for B lines (ie, those with > 3 B lines/site), and image quality (scored on a 5-point scale). Analyses included assessment of interobserver agreement with κ analysis, comparison of quality scores between transducers with mixed-effects modeling, and investigation of agreement and bias for B-line data and quality scores between transducers with Passing-Bablok regression. RESULTS: Interobserver agreement for total B-line scores and number of strong-positive sites was excellent (κ > 0.80) for both transducers. There was no evidence of analytic bias for the number of B lines or strong-positive sites between transducers. Interobserver agreement for image quality scores was moderate (κ, 0.498 and 0.517 for the curvilinear-array and phased-array transducers, respectively). Both observers consistently assigned higher-quality scores to curvilinear-array images than to phased-array images. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated both curvilinear-array (microconvex) and phased-array transducers can be used by experienced sonographers to obtain diagnostic ultrasonographic images of the lungs in dogs with acute or resolving left-sided congestive heart failure and suggested the former transducer may be preferred, particularly to aid identification of anatomic landmarks for orientation.

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.

Focused ultrasound of the caudal vena cava in dogs with cavitary effusions or congestive heart failure: A prospective, observational study.

INTRODUCTION: Ultrasonographic indices of the inferior vena cava are useful for predicting right heart filling pressures in people. OBJECTIVES: To determine whether ultrasonographic indices of caudal vena cava (CVC) differ between dogs with right-sided CHF (R-CHF), left-sided CHF (L-CHF), and noncardiac causes of cavitary effusion (NC). MATERIALS AND METHODS: 113 dogs diagnosed with R-CHF (n = 51), L-CHF (30), or NC effusion (32) were enrolled. Seventeen of the R-CHF dogs had pericardial effusion and tamponade. Focused ultrasound was performed prospectively to obtain 2-dimensional and M-mode subxiphoid measures of CVC maximal and minimal size (CVCmax and CVCmin), CVCmax indexed to aortic dimension (CVC:Ao), and CVC collapsibility index (CVC-CI). Variables were compared between study groups using Kruskal-Wallis and Dunn's-Bonferroni testing, and receiver operating characteristics curves were used to assess sensitivity and specificity. RESULTS: All sonographic CVC indices were significantly different between R-CHF and NC dogs (P < 0.001). Variables demonstrating the highest diagnostic accuracy for discriminating R-CHF versus NC were CVC-CI <33% in 2D (91% sensitive and 96% specific) and presence of hepatic venous distension (84% sensitive and 90% specific). L-CHF dogs had higher CVC:Ao and lower CVC-CI compared to NC dogs (P = 0.016 and P = 0.043 in 2D, respectively) but increased CVC-CI compared to the R-CHF group (P < 0.001). CONCLUSIONS: Ultrasonographic indices of CVC size and collapsibility differed between dogs with R-CHF compared to NC causes of cavitary effusions. Dogs with L-CHF have CVC measurements intermediate between R-CHF and NC dogs.

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.

Utility of point-of-care lung ultrasound for monitoring cardiogenic pulmonary edema in dogs.

BACKGROUND: Point-of-care lung ultrasound (LUS) is an effective tool to diagnose left-sided congestive heart failure (L-CHF) in dogs via detection of ultrasound artifacts (B-lines) caused by increased lung water. HYPOTHESIS/OBJECTIVES: To determine whether LUS can be used to monitor resolution of cardiogenic pulmonary edema in dogs, and to compare LUS to other indicators of L-CHF control. ANIMALS: Twenty-five client-owned dogs hospitalized for treatment of first-onset L-CHF. METHODS: Protocolized LUS, thoracic radiographs (TXR), and plasma N-terminal pro-B-type natriuretic peptide were performed at hospital admission, hospital discharge, and recheck examinations. Lung ultrasound findings were compared between timepoints and to other clinical measures of L-CHF. RESULTS: From time of hospital admission to discharge (mean 19.6 hours), median number of LUS sites strongly positive for B-lines (>3 B-lines per site) decreased from 5 (range, 1-8) to 1 (range, 0-5; P < .001), and median total B-line score decreased from 37 (range, 6-74) to 5 (range, 0-32; P = .002). Lung ultrasound indices remained improved at first recheck (P < .001). Number of strong positive sites correlated positively with respiratory rate (r = 0.52, P = .008) and TXR edema score (r = 0.51, P = .009) at hospital admission. Patterns of edema resolution differed between LUS and TXR, with cranial quadrants showing more significant reduction in B-lines compared to TXR edema score (80% vs 29% reduction, respectively; P = .003). CONCLUSIONS AND CLINICAL IMPORTANCE: Lung ultrasound could be a useful tool for monitoring resolution of pulmonary edema in dogs with L-CHF.

Retrospective evaluation of the safety and tolerability of pimobendan in cats with obstructive vs nonobstructive cardiomyopathy.

BACKGROUND: Pimobendan is frequently used off-label for treatments of cats with congestive heart failure (CHF). Concern exists regarding the safety of pimobendan in cats with outflow tract obstruction (OTO). OBJECTIVES: In cats treated with pimobendan, incidence of adverse effects will not differ between cats with OTO vs cats with nonobstructive cardiomyopathy. ANIMALS: Two-hundred sixty cats with CHF (57 with OTO, 203 with nonobstructive disease). METHODS: Retrospective medical record review. Groups were compared using 2-sample t-tests, Wilcoxon rank-sum tests, and Fisher exact tests. RESULTS: Compared to cats with nonobstructive cardiomyopathy, cats with OTO were younger (8.9 [interquartile range (IQR) 6.6] vs 10.8 [6.3] years, P = .0036), more likely to have a heart murmur (51/57 [90%] vs 76/203 [37.8%] cats, P < .0001), more likely to manifest CHF as pulmonary edema (53/57 [83%] vs 144/203 [70.9%] cats, P = .0004), and less likely to have pleural effusion (19/57 [33%] vs 122/203 [60.1%] cats, P = .0005). Adverse effects suspected to be related to pimobendan administration occurred in 12/260 cats (4.6%), including 11/203 cats (5.4%) with nonobstructive cardiomyopathy and 1/57 cat (2%) with OTO (P = .7). Pimobendan was discontinued due to adverse effects in 4/260 cats (1.5%), 3 with nonobstructive disease and 1 with OTO (P = 1.0). Acute adverse hemodynamic effects after pimobendan administration were not detected in any cats. CONCLUSIONS AND CLINICAL IMPORTANCE: Pimobendan is well tolerated in cats with cardiomyopathy and CHF, regardless of the presence of OTO.

Renin-angiotensin aldosterone profile before and after angiotensin-converting enzyme-inhibitor administration in dogs with angiotensin-converting enzyme gene polymorphism.

BACKGROUND: An angiotensin-converting enzyme (ACE) gene polymorphism occurs in dogs; however, functional importance is not well studied. HYPOTHESIS: We hypothesized that dogs with the polymorphism would show alternative renin-angiotensin aldosterone system (RAAS) pathway activation and classical RAAS pathway suppression before and after ACE-inhibitor administration, as compared to dogs without the polymorphism that would show this pattern only after ACE-inhibitor administration. ANIMALS: Twenty-one dogs with mitral valve disease that were genotyped for the ACE gene polymorphism. METHODS: This retrospective study utilized stored samples from 8 ACE gene polymorphism-negative (PN) dogs and 13 ACE gene polymorphism-positive (PP) dogs before and after enalapril administration. Equilibrium analysis was performed to evaluate serum RAAS metabolites and enzyme activities. Results were compared before and after enalapril, and between groups. RESULTS: The classical RAAS pathway was suppressed and the alternative RAAS pathway was enhanced for both genotypes after administration of enalapril, with no differences before enalapril administration. Aldosterone breakthrough occurred in both PN (38%) and PP (54%) dogs despite angiotensin II suppression. Aldosterone was significantly higher (P = .02) in ACE gene PP dogs (median, 92.17 pM; IQR, 21.85-184.70) compared to ACE gene PN dogs (median, 15.91 pM; IQR, <15.00-33.92) after enalapril. CONCLUSIONS AND CLINICAL IMPORTANCE: The ACE gene polymorphism did not alter baseline RAAS activity. Aldosterone breatkthrough in some dogs suggests nonangiotensin mediated aldosterone production that might be negatively influenced by genotype. These results support the use of aldosterone receptor antagonists with ACE-inhibitors when RAAS inhibition is indicated for dogs, especially those positive for the ACE gene polymorphism.

Lung ultrasonography findings in dogs with various underlying causes of cough.

OBJECTIVE: To characterize lung ultrasonography (LUS) findings in dogs with a primary clinical complaint of cough. ANIMALS: 100 client-owned coughing dogs. PROCEDURES: A standardized LUS examination was performed for all dogs to quantify the number of B lines and identify subpleural abnormalities at 4 sites on each hemithorax. The final clinical diagnosis (reference standard) was determined by medical record review, and sensitivity and specificity of LUS for the diagnosis of selected causes of cough was determined. RESULTS: Common underlying causes of cough included dynamic airway collapse (n = 37), cardiogenic pulmonary edema (CPE; 12), and bronchitis (10). Compared with dogs with other causes of cough, dogs with bacterial pneumonia (n = 7) were more likely to have subpleural shred signs, whereas dogs with pulmonary neoplasia (4) were more likely to have subpleural nodule signs. Dogs with CPE had higher total B-line scores and higher numbers of LUS sites strongly positive for B lines (> 3 B lines/site) than other dogs. The LUS criteria of total B-line score ≥ 10 and presence of ≥ 2 sites strongly positive for B lines were each 92% sensitive and 94% specific for CPE diagnosis. Notably, 18% (16/88) of dogs with noncardiac causes of cough had been treated previously with diuretics because of prior CPE misdiagnosis. CONCLUSIONS AND CLINICAL RELEVANCE: LUS profiles in dogs with cough differed by the underlying cause. In dogs with a clinical history of cough, this imaging modality could be diagnostically useful, particularly to help exclude the possibility of underlying CPE.