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Dobutamine is a positive inotropic agent often used in treatment of cardiogenic shock. Although there are well-documented adverse effects, dobutamine-induced myoclonus is a rarely reported phenomenon. Our case offers a direct and temporally related description of myoclonus, with onset observed within hours of dobutamine initiation and complete resolution within minutes of discontinuation.

Wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM) is more prevalent than appreciated in the elderly. We present the case of an 88-year-old woman who underwent heart transplantation for ischemic cardiomyopathy and then presented 21 years later with new onset atrial flutter, found on endomyocardial biopsy to have new ATTRwt-CM. (Level of Difficulty: Advanced.)

Chediak-Higashi Syndrome (CHS) is a well-characterized, autosomal recessively inherited lysosomal disease caused by mutations in lysosomal trafficking regulator (LYST). The feline model for CHS was originally maintained for ~20 years. However, the colonies were disbanded and the CHS cat model was lost to the research community before the causative mutation was identified. To resurrect the cat model, semen was collected and cryopreserved from a lone, fertile,  CHS carrier male. Using cryopreserved semen, laparoscopic oviductal artificial insemination was performed on three queens, two queens produced 11 viable kittens. To identify the causative mutation, a fibroblast cell line, derived from an affected cat from the original colony, was whole genome sequenced. Visual inspection of the sequence data identified a candidate causal variant as a ~20 kb tandem duplication within LYST, spanning exons 30 through to 38 (NM_001290242.1:c.8347-2422_9548 + 1749dup). PCR genotyping of the produced offspring demonstrated three individuals inherited the mutant allele from the CHS carrier male. This study demonstrated the successful use of cryopreservation and assisted reproduction to maintain and resurrect biomedical models and has defined the variant causing Chediak-Higashi syndrome in the domestic cat.

We present 3 heart transplant recipients who developed hypertrophic cardiomyopathy years after transplantation. In all 3 cases, the diagnosis was initially made based on echocardiography and confirmed using cardiac magnetic resonance imaging. (Level of Difficulty: Advanced.)

A 12-year-old spayed female miniature Poodle presented for coughing, respiratory distress, and anorexia. After thoracentesis for pleural effusion, radiography revealed an enlarged cardiac silhouette with a bulge in the area of the body of the right atrium. Echocardiography revealed an anechoic chamber-like cavity lateral to the right atrium that communicated with the right atrium through a 13 mm defect in the right atrial free wall. Contrast echocardiography and color flow Doppler were used to prove that the cavity communicated with the right atrium. The cavity was diagnosed as a giant right atrial diverticulum.

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non-human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth-eaten appearance to the inner wall of the mid- to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial-lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.

BackgroundThere are limited reports of severe tricuspid valve stenosis in dogs and limited data regarding treatment and outcome.ObjectiveTo evaluate clinical signs, echocardiographic features, and outcome of balloon valvuloplasty (BV) in dogs with severe tricuspid valve stenosis (TVS) in which BV was attempted.AnimalsFive client-owned dogs with severe TVS.MethodsRecords were retrospectively reviewed and data collected regarding signalment, clinical signs, diagnostic findings, procedures, and outcome.ResultsAll dogs were Labrador Retrievers. Presenting complaints included episodic weakness/syncope (4/5), abdominal distension (4/5), lethargy (2/5), and exercise intolerance (2/5). The median and range of measurements before BV were as follows: TV mean velocity 1.5 m/s (range 1.4-1.7 m/s); velocity-time integral (VTI) 79.8 cm (42.4-99.1 cm); and TV maximum velocity 2.9 m/s (2.3-3.2 m/s). Measurements (available for 3 of 5 dogs) after BV were as follows: TV mean velocity 1.15 m/s (0.9-1.4 m/s); VTI 44.95 cm (41.4-54.8 cm); and TV maximum velocity 1.15 m/s (1.9-2.3 m/s). The procedure was attempted in all dogs and completed in 4/5 dogs. The largest balloon diameter ranged from 15 mm to 25 mm, and length ranged from 4 cm to 5 cm. Right atrial pressure decreased in 4/5 dogs. All but 1 dog had clinical improvement after BV, but recurrence of clinical signs occurred (2/5). Tricuspid regurgitation worsened in 1 dog culminating in right heart failure and euthanasia.Conclusions and clinical importanceBV can be an effective treatment; however, clinical signs can recur. Right heart failure due to worsened TR is a potential complication in dogs with pre-existing moderate-to-severe TR.

© 2016 American College of Veterinary Internal Medicine. Background: The prevalence and prognostic importance of atrial fibrillation (AF) on survival in nonsmall breed dogs with myxomatous mitral valvular disease (MMVD) and congestive heart failure (CHF) remain unknown. Aim: To identify the prevalence of AF in nonsmall breed dogs with CHF because of MMVD and to characterize the impact of AF on survival outcome. Animal: Sixty-four client-owned dogs (>15 kg) with MMVD and CHF. Methods: Retrospective review of medical records for dogs weighing >15 kg with MMVD treated for CHF. Results: Thirty-three dogs presented with AF or developed AF during follow-up examinations, and 31 dogs were free of AF until cardiac-related death. For dogs with AF, median survival time (MST) was 142 days (range: 9-478) while dogs without AF lived 234 days (range: 13-879 days). AF increased risk of cardiac-related death (HR = 2.544; 95% CI = 1.41-4.59; P =.0019) when compared to dogs without AF. MST was significantly prolonged for dogs with AF whose rates were adequately controlled (

BackgroundCats with hypertrophic cardiomyopathy (HCM) are at risk for development of systemic thromboembolic disease. However, the relationship between platelet activation state and cardiovascular parameters associated with HCM is not well described.ObjectivesTo characterize platelet activation by flow cytometric evaluation of platelet P-selectin and semiquantitative Western blot analysis of soluble platelet-endothelial cell adhesion molecule-1 (sPECAM-1).AnimalsEight normal healthy cats (controls) owned by staff and students of the School of Veterinary Medicine and 36 cats from the UC Davis Feline HCM Research Laboratory were studied.MethodsPlatelet-rich plasma (PRP) was used for all flow cytometry studies. Platelet surface CD41 and P-selectin expression were evaluated before and after ADP stimulation. sPECAM-1 expression was evaluated by Western blot analysis of platelet-poor plasma that had been stabilized with aprotinin. Standard echocardiographic studies were performed.ResultsResting platelets from cats with severe HCM had increased P-selectin expression compared to controls, and expressed higher surface density of P-selectin reflected by their increased mean fluorescence intensities (MFI). Stimulation with ADP also resulted in significantly increased P-selectin MFI of platelets from cats with severe HCM. Increased P-selectin expression and MFI correlated with the presence of a heart murmur and end-systolic cavity obliteration (ESCO). sPECAM-1 expression from cats with moderate and severe HCM was significantly increased above those of control cats.Conclusions and clinical importanceP-selectin and sPECAM expression may be useful biomarkers indicating increased platelet activation in cats with HCM.

Over the last decades, beta-blockers have been a key component of heart failure therapy. However, currently there is no method to identify patients who will benefit from beta-blocking therapy versus those who will be unresponsive or worsen. Furthermore, there is an unmet need to better understand molecular mechanisms through which heart failure therapies, such as beta-blockers, improve cardiac function, in order to design novel targeted therapies. Solving these issues is an important step towards personalized medicine. Here, we present a comprehensive transcriptomic analysis of molecular pathways that are affected by beta-blocking agents and a transcriptomic biomarker to predict therapy response.

Milrinone, a positive inotropic drug with vasodilating properties, was administered at doses of 0.5 to 1 mg/kg orally twice daily to 29 dogs with moderate to severe congestive heart failure (CHF). Significant echocardiographic improvement in ventricular systolic function was observed after 3 days of administration of milrinone and at the patients' last echocardiographic observation (day 21 in 25 subjects, day 7 in 2 subjects, and day 3 in 2 subjects). Echocardiographic shortening fraction at the initial measurement had a median increase of 6.14% (P less than 0.001), and for the last observation a 2.83% increase (P less than 0.005). Most patients also showed improvement in their clinical signs as assessed by the veterinarian (72%) and by owner's evaluation (81%). No consistent problem or adverse reaction to milrinone was observed, except for a small number of clinically manageable ventricular dysrhythmias. Milrinone appears in this trial to be effective for the treatment of advanced CHF in dogs.

Assessing the pathogenicity of a disease-associated genetic variant in animals accurately is vital, both on a population and individual scale. At the population level, breeding decisions based on invalid DNA tests can lead to the incorrect inclusion or exclusion of animals and compromise the long-term health of a population, and at the level of the individual animal, lead to incorrect treatment and even life-ending decisions. Criteria to determine pathogenicity are not standardized, i.e., no guidelines for animal variants are available. Here, we aimed to develop and validate guidelines to be used by the community for Mendelian disorders in domestic animals to classify variants in categories based on standardized criteria. These so-called animal variant classification guidelines (AVCG) were based on those developed for humans by The American College of Medical Genetics and Genomics (ACMG). In a direct comparison, 83% of the pathogenic variants were correctly classified with ACMG, while this increased to 92% with AVCG. We described methods to develop datasets for benchmarking the criteria and identified the most optimal in silico variant effect predictor tools. As the reproducibility was high, we classified 72 known disease-associated variants in cats and 40 other disease-associated variants in eight additional species., Competing Interests: HA is an employee of Wisdom Panel Mars Petcare Science & Diagnostics, a company that offers canine and feline DNA testing as a commercial service. CDdC is an employee of Antagene, a DNA testing and genetic analysis company for dogs, cats, horses, and wildlife. The following authors interact (= discuss genetic tests, variants that have or will be published, …) on a regular basis with commercial companies: BJGB (Van Haeringen laboratorium, Laboklin, Wisdom Panel Mars Petcare Science & Diagnostics, Antagene), MA (Antagene, Wisdom Panel Mars Petcare Science & Diagnostics, Felome, Genindexe), JJH (Embark), ML (Vetogene, Genefast), however, there are no fees involved. None of the authors have received speaking fees from commercial genetic testing companies. None of the authors have performed paid consultant services for commercial genetic testing companies., (Copyright © 2024 Boeykens, Abitbol, Anderson, Casselman, de Citres, Hayward, Häggström, Kittleson, Lepri, Ljungvall, Longeri, Lyons, Ohlsson, Peelman, Smets, Vezzosi, van Steenbeek and Broeckx.)

Introduction: The correct labeling of a genetic variant as pathogenic is important as breeding decisions based on incorrect DNA tests can lead to the unwarranted exclusion of animals, potentially compromising the long-term health of a population. In human medicine, the American college of Medical Genetics (ACMG) guidelines provide a framework for variant classification. This study aims to apply these guidelines to six genetic variants associated with hypertrophic cardiomyopathy (HCM) in certain cat breeds and to propose a modified criterion for variant classification., Methods: Genetic samples were sourced from five cat breeds: Maine Coon, Sphynx, Ragdoll, Devon Rex, and British Short- and Longhair. Allele frequencies were determined, and in the subset with phenotypes available, odds ratios to determine the association with HCM were calculated. In silico evaluation followed with joint evidence and data from other publications assisting in the classification of each variant., Results: Two variants, MYBPC3:c.91G > C [A31P] and MYBPC3:c.2453C > T [R818W], were designated as pathogenic. One variant, MYH7:c.5647G > A [E1883K], was found likely pathogenic, while the remaining three were labeled as variants of unknown significance., Discussion: Routine genetic testing is advised solely for the MYBPC3:c.91G > C [A31P] in the Maine Coon and MYBPC3:c.2453C > T [R818W] in the Ragdoll breed. The human ACMG guidelines serve as a suitable foundational tool to ascertain which variants to include; however, refining them for application in veterinary medicine might be beneficial., Competing Interests: HA and SD are current and former employees of Wisdom Panel Mars Petcare Science & Diagnostics that offers canine and feline DNA testing as a commercial service. CC is a current employee of Antagene, a DNA testing and genetic analysis company for dogs, cats, horses, and wildlife. MT is employed by Genefast srl. LL has historically received funding from various commercial testing laboratories to support variant discovery but has no involvement with these HCM variants. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Boeykens, Abitbol, Anderson, Dargar, Ferrari, Fox, Hayward, Häggström, Davison, Kittleson, van Steenbeek, Ljungvall, Lyons, Longeri, Ohlsson, Peelman, Dufaure de Citres, Smets, Turba and Broeckx.)

Practical Relevance: Although feline hypertrophic cardiomyopathy (HCM) occurs more commonly, dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), left ventricular noncompaction (LVNC) and cardiomyopathy - nonspecific phenotype (NCM; formerly unclassified cardiomyopathy) are all recognized in domestic cats., Patient Group: Any adult domestic cat, of either sex and of any breed, can be affected., Diagnostics: The non-HCM cardiomyopathies are rarely suspected in subclinically affected cats, so most are first identified when a cat presents with signs of heart failure or systemic thromboembolic disease. The definitive clinical confirmatory test for these other feline cardiomyopathies is echocardiography., Key Findings: 'Cardiomyopathy - nonspecific phenotype' is a catch-all term that groups hearts with myocardial changes that either do not meet the criteria for any one type of cardiomyopathy (HCM, RCM, DCM, ARVC, LVNC) or meet the echocardiography criteria for more than one type. RCM is characterized by diastolic dysfunction due to fibrosis that results in a restrictive transmitral flow pattern on Doppler echocardiography and usually marked left or biatrial enlargement. DCM is characterized by decreased myocardial contractility and is rare in cats. When it occurs, it is seldom due to taurine deficiency. However, since taurine-deficient DCM is usually reversible, a diet history should be obtained, whole blood and plasma taurine levels should be measured and taurine should be supplemented in the diet if the diet is not commercially manufactured. ARVC should be suspected in adult cats with severe right heart enlargement and right heart failure (ascites and/or pleural effusion), especially if arrhythmia is present. Feline LVNC is rare; its significance continues to be explored. Treatment of the consequences of these cardiomyopathies (management of heart failure, thromboprophylaxis, treatment of systemic arterial thromboembolism) is the same as for HCM., Conclusions: While these other cardiomyopathies are less prevalent than HCM in cats, their clinical and radiographic presentation is often indistinguishable from HCM. Echocardiography is usually the only ante-mortem method to determine which type of cardiomyopathy is present. However, since treatment and prognosis are often similar for the feline cardiomyopathies, distinguishing among the cardiomyopathies is often not essential for determining appropriate therapy., Areas of Uncertainty: The feline cardiomyopathies do not always fit into one distinct category. Interrelationships among cardiomyopathies in cats may exist and understanding these relationships in the future might provide critical insights regarding treatment and prognosis.

Practical Relevance: The feline cardiomyopathies are the most prevalent type of heart disease in adult domestic cats. Several forms have been identified (see Parts 2 and 3), with hypertrophic cardiomyopathy (HCM) being the most common. Clinically the cardiomyopathies are often indistinguishable. Cats with subclinical cardiomyopathy may or may not have characteristic physical examination findings (eg, heart murmur, gallop sound), or radiographic cardiomegaly. Cats with severe disease may develop signs of heart failure (eg, dyspnea, tachypnea) or systemic arterial thromboembolism (ATE; eg, pain and paralysis). Sudden death is possible. Treatment usually does not alter the progression from subclinical to clinical disease and often the treatment approach, once clinical signs are apparent, is the same regardless of the type of cardiomyopathy. However, differentiating cardiomyopathy from normal variation may be important prognostically., Patient Group: Domestic cats of any age from 3 months upward, of either sex and of any breed, can be affected. Mixed-breed cats are most commonly affected but certain breeds are disproportionately prone to developing HCM., Diagnostics: Subclinical feline cardiomyopathies may be suspected based on physical examination findings, thoracic radiographs and cardiac biomarker results but often the disease is clinically silent. The definitive clinical confirmatory test is echocardiography. Left heart failure (pulmonary edema and/or pleural effusion) is most commonly diagnosed radiographically, but point-of-care ultrasound and amino terminal pro-B-type natriuretic peptide (NT-proBNP) biomarker testing can also be useful, especially when the stress of taking radiographs is best avoided., Key Findings: Knowledge of pathophysiological mechanisms helps the practitioner identify the feline cardiomyopathies and understand how these diseases progress and how they manifest clinically (heart failure, ATE). Existing diagnostic tests have strengths and limitations, and being aware of these can help a practitioner deliver optimal recommendations regarding referral., Conclusions: Several types of feline cardiomyopathies exist in both subclinical (mild to severe disease) and clinical (severe disease) phases. Heart failure and ATE are the most common clinical manifestations of severe cardiomyopathy and are therapeutic targets regardless of the type of cardiomyopathy. The long-term prognosis is often guarded or poor once overt clinical manifestations are present., Areas of Uncertainty: Some cats with presumed cardiomyopathy do not have echocardiographic features that fit the classic cardiomyopathies (cardiomyopathy - nonspecific phenotype). Although no definitive treatment is usually available, understanding how cardiomyopathies evolve remains worthy of investigation.

Practical Relevance: Hypertrophic cardiomyopathy (HCM) is the most common form of feline cardiomyopathy observed clinically and may affect up to approximately 15% of the domestic cat population, primarily as a subclinical disease. Fortunately, severe HCM, leading to heart failure or arterial thromboembolism (ATE), only occurs in a small proportion of these cats., Patient Group: Domestic cats of any age from 3 months upward, of either sex and of any breed, can be affected. A higher prevalence in male and domestic shorthair cats has been reported., Diagnostics: Subclinical feline HCM may or may not produce a heart murmur or gallop sound. Substantial left atrial enlargement can often be identified radiographically in cats with severe HCM. Biomarkers should not be relied on solely to diagnose the disease. While severe feline HCM can usually be diagnosed via echocardiography alone, feline HCM with mild to moderate left ventricular (LV) wall thickening is a diagnosis of exclusion, which means there is no definitive test for HCM in these cats and so other disorders that can cause mild to moderate LV wall thickening (eg, hyperthyroidism, systemic hypertension, acromegaly, dehydration) need to be ruled out., Key Findings: While a genetic cause of HCM has been identified in two breeds and is suspected in another, for most cats the cause is unknown. Systolic anterior motion of the mitral valve (SAM) is the most common cause of dynamic left ventricular outflow tract obstruction (DLVOTO) and, in turn, the most common cause of a heart murmur with feline HCM. While severe DLVOTO is probably clinically significant and so should be treated, lesser degrees probably are not. Furthermore, since SAM can likely be induced in most cats with HCM, the distinction between HCM without obstruction and HCM with obstruction (HOCM) is of limited importance in cats. Diastolic dysfunction, and its consequences of abnormally increased atrial pressure leading to signs of heart failure, and sluggish atrial blood flow leading to ATE, is the primary abnormality that causes clinical signs and death in affected cats. Treatment (eg, loop diuretics) is aimed at controlling heart failure. Preventive treatment (eg, antithrombotic drugs) is aimed at reducing the risk of complications (eg, ATE)., Conclusions: Most cats with HCM show no overt clinical signs and live a normal or near-normal life despite this disease. However, a substantial minority of cats develop overt clinical signs referable to heart failure or ATE that require treatment. For most cats with clinical signs caused by HCM, the long-term prognosis is poor to grave despite therapy., Areas of Uncertainty: Genetic mutations (variants) that cause HCM have been identified in a few breeds, but, despite valiant efforts, the cause of HCM in the vast majority of cats remains unknown. No treatment currently exists that reverses or even slows the cardiomyopathic process in HCM, again despite valiant efforts. The search goes on.

To evaluate the psychometric properties of the Spanish version of the "FETCH-Q™", 228 dogs with cardiovascular diseases were included. After forward and back translation of the original questionnaire, nonexperts, ethologists and veterinary colleagues evaluated the content's validity through feedback. For criteria validity, the total score was correlated with the heart disease/failure class. For construct validity, the overall quality of life of the dog and the results obtained in each question was correlated. The reliability of the questionnaire was assessed using the Cronbach's alpha coefficient. To evaluate the test-retest validity the intra-class correlation coefficient and Wilcoxon signed-rank test were used. A good agreement with the original questionnaire was evident. For construct validity, the questionnaire obtained r > 0.09 to < 0.82. The criterion validity was appropriate and the correlation was rho = 0.82, with an effect size of 0.55 (P < 0.05). Cronbach's alpha coefficient was (α = 0.89). The test-retest assessment revealed adequate repeatability (correlation coefficient = 0.87; P < .001). There was no difference in the owner responses to the questionnaire at baseline and 2 weeks later in dogs with stable cardiac disease (P > .05). This study supports the validity of psychometric properties of the Spanish version of the functional evaluation of cardiac health questionnaire "FETCHSV2-Q™" to assess Health-related Quality of Life in dogs with cardiovascular disease in clinical settings and research., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Cardiomyopathies are a heterogeneous group of myocardial disorders of mostly unknown etiology, and they occur commonly in cats. In some cats, they are well-tolerated and are associated with normal life expectancy, but in other cats they can result in congestive heart failure, arterial thromboembolism or sudden death. Cardiomyopathy classification in cats can be challenging, and in this consensus statement we outline a classification system based on cardiac structure and function (phenotype). We also introduce a staging system for cardiomyopathy that includes subdivision of cats with subclinical cardiomyopathy into those at low risk of life-threatening complications and those at higher risk. Based on the available literature, we offer recommendations for the approach to diagnosis and staging of cardiomyopathies, as well as for management at each stage., (© 2020 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Mutations in MYBPC3, the gene encoding cardiac myosin binding protein C (cMyBP-C), are a major cause of hypertrophic cardiomyopathy (HCM). While most mutations encode premature stop codons, missense mutations causing single amino acid substitutions are also common. Here we investigated effects of a single proline for alanine substitution at amino acid 31 (A31P) in the C0 domain of cMyBP-C, which was identified as a natural cause of HCM in cats. Results using recombinant proteins showed that the mutation disrupted C0 structure, altered sensitivity to trypsin digestion, and reduced recognition by an antibody that preferentially recognizes N-terminal domains of cMyBP-C. Western blots detecting A31P cMyBP-C in myocardium of cats heterozygous for the mutation showed a reduced amount of A31P mutant protein relative to wild-type cMyBP-C, but the total amount of cMyBP-C was not different in myocardium from cats with or without the A31P mutation indicating altered rates of synthesis/degradation of A31P cMyBP-C. Also, the mutant A31P cMyBP-C was properly localized in cardiac sarcomeres. These results indicate that reduced protein expression (haploinsufficiency) cannot account for effects of the A31P cMyBP-C mutation and instead suggest that the A31P mutation causes HCM through a poison polypeptide mechanism that disrupts cMyBP-C or myocyte function., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Mutations in genes that encode for muscle sarcomeric proteins have been identified in humans and two breeds of domestic cats with hypertrophic cardiomyopathy (HCM). This article reviews the history, genetics, and pathogenesis of HCM in the two species in order to give veterinarians a perspective on the genetics of HCM. Hypertrophic cardiomyopathy in people is a genetic disease that has been called a disease of the sarcomere because the preponderance of mutations identified that cause HCM are in genes that encode for sarcomeric proteins (Maron and Maron, 2013). Sarcomeres are the basic contractile units of muscle and thus sarcomeric proteins are responsible for the strength, speed, and extent of muscle contraction. In people with HCM, the two most common genes affected by HCM mutations are the myosin heavy chain gene (MYH7), the gene that encodes for the motor protein β-myosin heavy chain (the sarcomeric protein that splits ATP to generate force), and the cardiac myosin binding protein-C gene (MYBPC3), a gene that encodes for the closely related structural and regulatory protein, cardiac myosin binding protein-C (cMyBP-C). To date, the two mutations linked to HCM in domestic cats (one each in Maine Coon and Ragdoll breeds) also occur in MYBPC3 (Meurs et al., 2005, 2007). This is a review of the genetics of HCM in both humans and domestic cats that focuses on the aspects of human genetics that are germane to veterinarians and on all aspects of feline HCM genetics., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background: Myocardial disease in the Boxer dog is characterized by 1 of 2 clinical presentations, dilated cardiomyopathy (DCM) characterized by ventricular systolic dysfunction, dilatation and tachyarrhythmias, and arrhythmogenic right ventricular cardiomyopathy (ARVC) characterized by ventricular tachyarrhythmias, syncope, and sudden death. Boxer ARVC has been associated with a deletion in the striatin gene in some families., Hypothesis/objectives: We hypothesized that both presentations represent a single disease, and the development of DCM in the Boxer is associated with the striatin deletion., Animals: Thirty-three adult Boxer dogs with DCM, 29 adult Boxer dogs with the striatin deletion and ARVC, and 16 Boxers without cardiac disease., Methods: DNA samples were evaluated for the striatin deletion. Association of the deletion with the DCM phenotype was tested by a Fisher's exact test. T-tests were used to evaluate potential differences between the positive heterozygous and positive homozygous groups with DCM with regard to age, LVIDD, LVIDS, and FS%., Results: Thirty of 33 dogs with DCM were positive for the striatin deletion. The striatin mutation and the homozygous genotype were strongly associated with the DCM phenotype (P < .001 and P = .005). There was no statistical difference between the heterozygous and homozygous groups with regard to age and echocardiographic measurements., Conclusions and Clinical Importance: This study demonstrates an association between DCM in the Boxer dog and the striatin mutation, particularly with the homozygous genotype. The observation that 3/33 dogs developed DCM and lacked the striatin mutation suggests that there is at least 1 other cause of DCM in the Boxer dog., (Copyright © 2013 by the American College of Veterinary Internal Medicine.)

Left atrial tear is an infrequent sequela of severe mitral regurgitation due to myxomatous mitral valve degeneration. Interatrial septal tear due to mitral regurgitation causing a left-to-right shunt is uncommon. Right to left shunting secondary to acute interatrial septal tear is very rarely reported in the human literature, and has not been reported in the veterinary literature in a dog. This case describes the clinical, radiographic, echocardiographic, gross pathologic, and histopathologic features of a dog presented in acute respiratory distress secondary to acute onset right to left shunting through the interatrial septum. This was later documented to be due to a tear in the septum secondary to tricuspid regurgitation and pulmonary hypertension. The presence of an acquired right to left shunting atrial septal defect is of clinical and prognostic significance, and should be considered in cases of acute respiratory distress., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Objective: To determine the prevalence of heart murmurs in chinchillas (Chinchilla lanigera) and determine whether heart murmurs were associated with cardiac disease., Design: Retrospective multi-institutional case series., Animals: 260 chinchillas., Procedures: Medical records of all chinchilla patients evaluated at the Tufts University Foster Hospital for Small Animals between 2001 and 2009, the University of California-Davis William R. Pritchard Veterinary Medical Teaching Hospital between 1996 and 2009, and the University of Wisconsin Veterinary Medical Teaching Hospital between 1998 and 2009 were reviewed., Results: Prevalence of heart murmurs was 23% (59/260). Of 15 chinchillas with heart murmurs that underwent echocardiography, 8 had echocardiographic abnormalities, including dynamic right ventricular outflow tract obstruction, mitral regurgitation, hypertrophy of the left ventricle, tricuspid regurgitation, and hypovolemia. Echocardiographic abnormalities were approximately 29 times as likely (OR, 28.7) to be present in chinchillas with a murmur of grade 3 or higher than in chinchillas without a murmur., Conclusions and Clinical Relevance: Results suggested that heart murmurs are common in chinchillas and that chinchillas with heart murmurs often have echocardiographic abnormalities, with valvular disease being the most common. On the basis of these results, we believe that echocardiography should be recommended for chinchillas with heart murmurs, especially older chinchillas with murmurs of grade 3 or higher. Further prospective studies are needed to accurately evaluate the prevalence of cardiac disease in chinchillas with heart murmurs.

Objective: To determine cardiopulmonary effects of incremental doses of dopamine and phenylephrine during isoflurane-induced hypotension in cats with hypertrophic cardiomyopathy (HCM)., Animals: 6 adult cats with severe naturally occurring HCM., Procedures: Each cat was anesthetized twice (once for dopamine treatment and once for phenylephrine treatment; treatment order was randomized). Hypotension was induced by increasing isoflurane concentration. Cardiopulmonary data, including measurement of plasma concentration of cardiac troponin I (cTnI), were obtained before anesthesia, 20 minutes after onset of hypotension, and 20 minutes after each incremental infusion of dopamine (2.5, 5, and 10 μg/kg/min) or phenylephrine (0.25, 0.5, and 1 μg/kg/min)., Results: Mean ± SD end-tidal isoflurane concentration for dopamine and phenylephrine was 2.44 ± 0.05% and 2.48 ± 0.04%, respectively. Cardiac index and tissue oxygen delivery were significantly increased after administration of dopamine, compared with results after administration of phenylephrine. Systemic vascular resistance index was significantly increased after administration of phenylephrine, compared with results after administration of dopamine. Oxygen consumption remained unchanged for both treatments. Systemic and pulmonary arterial blood pressures were increased after administration of both dopamine and phenylephrine. Acid-base status and blood lactate concentration did not change and were not different between treatments. The cTnI concentration increased during anesthesia and infusion of dopamine and phenylephrine but did not differ significantly between treatments., Conclusions and Clinical Relevance: Dopamine and phenylephrine induced dose-dependent increases in systemic and pulmonary blood pressure, but only dopamine resulted in increased cardiac output. Hypotension and infusions of dopamine and phenylephrine caused significant increases in cTnI concentrations.

Background: Cough in the geriatric small breed dog with myxomatous mitral valve degeneration (MMVD), a large left atrium, and absence of heart failure often is attributed to compression of the left mainstem bronchus by the left atrium. Studies investigating this syndrome are lacking in dogs., Hypothesis: Airway collapse is independent of left atrial enlargement., Animals: A total of 16 dogs presenting with chronic cough in the absence of congestive heart failure. Group 1 dogs (n = 10) had moderate-to-severe left atrial enlargement based on an echocardiographically calculated left atrial:aortic surface area [LA:Ao(a)] > 6. Group 2 dogs (n = 6) had no to mild left atrial enlargement [LA:Ao(a) ≤ 6]., Methods: Dogs were prospectively evaluated. CBC, biochemistry, urinalysis, cervical and thoracic radiographs, fluoroscopy, echocardiography, and bronchoscopy were performed. Bronchoscopic abnormalities were compared between groups using Fisher's Exact Test. P < .05 was considered significant., Results: Fluoroscopy identified airway collapse in both groups. Bronchoscopic evidence of airway collapse >50% was observed in multiple bronchi with no difference between groups. All dogs had inflammation on airway cytology with respiratory infection in 1 dog in group 2. Left atrial size was interpreted radiographically as enlarged in 9 of 10 group 1 dog and in 2 of 6 group 2 dogs. VHS was above normal in both groups of dogs regardless of echocardiographic evidence of cardiomegaly., Conclusions: Results failed to identify an association between left atrial enlargement and airway collapse in dogs with MMVD, but did suggest that airway inflammation is common in dogs with airway collapse., (Copyright © 2012 by the American College of Veterinary Internal Medicine.)

Background: A comparison of transvascular occlusion methods for closing patent ductus arteriosus (PDA) in dogs has not been done., Objectives: To determine if clinically important differences exist between the approaches and devices currently used., Animals: A total of 112 client-owned dogs with left-to-right shunting PDA., Methods: Retrospective study. Records from dogs that underwent attempted transvascular PDA occlusion from January 2006 to December 2009 were examined. Dogs were placed into 4 groups: Group 1: Amplatz Canine Duct Occluder (ACDO) (transarterial) - 36 dogs; Group 2: Gianturco or MReye Flipper Detachable Embolization (Flipper) coil (transarterial) - 38 dogs; Group 3: Amplatzer Vascular Plug (AVP) (transarterial) - 23 dogs; Group 4: Flipper coil (transvenous) - 15 dogs., Results: The overall success rate of the procedures was high (92%) with comparable success rates among groups (87-97%). There were significantly fewer complications (P < .0001) in dogs receiving an ACDO than in the remaining groups (3% for ACDO versus 26-33% for the other groups). Fluoroscopy time for the transvenous method was significantly longer (median, 13 minutes) than for the other groups (median, 6 minutes) (P < .0001). Severity of residual flow 24 hours postprocedure was significantly less in the ACDO group than in the remaining groups (P = .0001-.05)., Conclusions: The ACDO appears superior in ease of use, complication rate, and completeness of occlusion. The remaining limiting factor with this device is patient size. Until a smaller ACDO device is marketed, coils remain the only choice for interventional closure in very small dogs., (Copyright © 2011 by the American College of Veterinary Internal Medicine.)

Background: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long-term prognosis, and in monitoring the response to therapy in humans., Hypothesis: Circulating concentrations of the biomarkers N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure., Animals: Six Maine Coon or Maine Coon cross cats with severe HCM., Methods: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT-proBNP and cTnI were assayed before and on the last day of drug administration., Results: There was no statistically significant change in NT-proBNP (median before, 394 pmol/L; range, 71-1,500 pmol/L; median after, 439 pmol/L; range, 24-1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10-0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09-1.0 ng/mL; P = .69) after administration of atenolol., Conclusions: Atenolol administration did not decrease NT-proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings., (Copyright © 2011 by the American College of Veterinary Internal Medicine.)

The purpose of this study was to evaluate the value of measuring plasma NT-proBNP concentration as a screening tool in cats with varying severity of subclinical hypertrophic cardiomyopathy (HCM). Plasma NT-proBNP concentration was measured in 35 cats that had previously been classified as normal, equivocal, moderate HCM or severe HCM via echocardiography. No cat had ever been in congestive heart failure. Cats with severe HCM had a significantly higher NT-proBNP concentration compared to the other groups (P<0.0003), however, the sensitivity of NT-proBNP for diagnosing cats with severe disease was only 44% (cutoff≤100pmol/l) to 55% (cutoff≤40pmol/l). There was no significant difference in NT-proBNP concentration between normal, equivocal and moderate categories (sensitivity for detecting moderate HCM was 0%). Based on the results of this study, NT-proBNP concentration is not considered adequate as a screening test for detecting mild to moderate HCM in Maine Coon cats and it appears that it may miss many cats with severe HCM., (Copyright © 2010 ISFM and AAFP. Published by Elsevier Ltd. All rights reserved.)