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Background: The benefits of pimobendan in the treatment of congestive heart failure (CHF) in cats with hypertrophic cardiomyopathy (HCM) have not been evaluated prospectively. Hypothesis/objectives: To investigate the effects of pimobendan in cats with HCM and recent CHF and to identify possible endpoints for a pivotal study. We hypothesized that pimobendan would be well-tolerated and associated with improved outcome. Animals: Eighty-three cats with HCM and recently controlled CHF: 30 with and 53 without left ventricular outflow tract obstruction. Methods: Prospective randomized placebo-controlled double-blind multicenter nonpivotal field study. Cats received either pimobendan (0.30 mg/kg q12h, n = 43), placebo (n = 39), or no medication (n = 1) together with furosemide (

Background Whether anemic cats and dogs with increased left heart dimensions are at higher risk of transfusion‐associated circulatory overload, and the effect of blood transfusion on left heart dimensions in naturally occurring anemia is unknown. Hypothesis/objectives To evaluate the effect of blood transfusion on left heart dimensions in clinically relevant anemia. Animals Twenty dogs and 20 cats presenting to a university veterinary teaching hospital. Methods In this prospective observational study, anemic dogs and cats requiring blood transfusion were included. Packed cell volume (PCV), total solids, and echocardiography were performed before and within 24 hours of blood transfusion. Signalment, bodyweight, disease process, transfusion duration and volume, and prior treatments were recorded. Nonparametric statistics were reported as median [range]. Post hoc Bonferroni correction set significance at P

Graphical abstract, Highlights • IVSH may occur in dogs following surgical MVR. • The cause of IVSH in dogs undergoing MVR remains unknown. • Mortality attributable to IVSH in these four dogs was 50%.

Background N‐terminal pro B‐type natriuretic peptide (NT‐proBNP) and cardiac troponin‐I (cTnI) are biomarkers commonly evaluated in cats with suspected heart disease. Many cats with hypertrophic cardiomyopathy (HCM) have systolic anterior motion of the mitral valve (SAM), but its influence on circulating NT‐proBNP or cTnI concentrations is currently unknown. Hypothesis/Objectives Cats with HCM and SAM (HCMSAM+) have higher NT‐proBNP and cTnI concentrations than do cats with HCM but without SAM (HCMSAM−). Animals One hundred forty cats with HCM: 70 with SAM and 70 without SAM. Methods Retrospective case‐to‐case study. Cats were recruited if diagnosed with HCM by echocardiography and results were available for NT‐proBNP or cTnI concentrations or both. Cats with SAM were matched to those without SAM for clinical presentation, left atrial (LA) size and left ventricular (LV) fractional shortening. Results A total of 119 NT‐proBNP and 123 cTnI results were available. The HCMSAM+ cats had higher median concentrations than did HCMSAM− cats for NT‐proBNP (729 pmoL/L; interquartile range [IQR], 275‐1467 versus 65 pmoL/L; IQR, 25‐271; P

Background Cats with hypertrophic cardiomyopathy (HCM) have decreased left ventricular (LV) longitudinal deformation detected by mitral annular plane systolic excursion (MAPSE) and speckle tracking echocardiography. People with preclinical HCM have decreased systolic LV longitudinal and radial strain (S) and strain rate (SR), with preserved circumferential S and SR. Hypothesis/Objectives Cats with preclinical HCM have decreased systolic LV deformation compared to normal cats. Animals Seventy‐three client‐owned cats with (n = 37) and without (n = 36) preclinical HCM. Methods Retrospective echocardiographic study. Left and right ventricular longitudinal S and SR, LV radial and circumferential S and SR were calculated by STE. Left ventricular mass was also calculated. Correlation between STE variables and LV hypertrophy was determined and receiver‐operating characteristic (ROC) curves were plotted for prediction of HCM. Results Cats with HCM had smaller absolute longitudinal S (−14.8 ± 3.3% vs −19.7 ± 2.7%, P

Aortic thromboembolism (ATE) occurs in cats with cardiomyopathy and often results in euthanasia due to poor prognosis. However, the underlying predisposing mechanisms leading to left atrial (LA) thrombus formation are not fully characterised. von Willebrand Factor (vWF) is a marker of endothelium and shows increased expression following endothelial injury. In people with poor LA function and LA remodelling, vWF has been implicated in the development of LA thrombosis. In this study we have shown (1) the expression of endocardial vWF protein detected using immunohistofluorescence was elevated in cats with cardiomyopathy, LA enlargement (LAE) and clinical signs compared to cats with subclinical cardiomyopathy and control cats, (2) vWF was present at the periphery of microthrombi and macrothrombi within the LA where they come into contact with the LA endocardium and (3) vWF was integral to the structure of the macrothrombi retrieved from the atria. These results provide evidence for damage of the endocardial endothelium in the remodelled LA and support a role for endocardial vWF as a pro-thrombotic substrate potentially contributing to the development of ATE in cats with underlying cardiomyopathy and LAE. Results from this naturally occurring feline model may inform research into human thrombogenesis.

Comunicació presentada a 11th International Conference on Functional Imaging and Modeling of the Heart (FIMH 2021), celebrat del 21 al 25 de juny de 2021 de manera virtual. In humans, there is a well-established relationship between atrial fibrillation (AF), blood flow abnormalities and thrombus formation, even if there is no clear consensus on the role of left atrial appendage (LAA) morphologies. Cats can also suffer heart diseases, often leading to an enlargement of the left atrium that promotes stagnant blood flow, activating the clotting process and promoting feline aortic thromboembolism. The majority of pathological feline hearts have echocardiographic evidence of abnormal left ventricular filling, usually assessed with 2D and Doppler echocardiography and standard imaging tools. Actually, veterinary professionals have limited access to advanced computational techniques that would enable a better understanding of feline heart pathologies with improved morphological and haemodynamic descriptors. In this work, we applied state-of-the-art image processing and computational fluid simulations based on micro-computed tomography images acquired in 24 cases, including normal cats and cats with varying severity of cardiomyopathy. The main goal of the study was to identify differences in the LA/LAA morphologies and blood flow patterns in the analysed cohorts with respect to thrombus formation and cardiac pathology. The obtained results show significant differences between normal and pathological feline hearts, as well as in thrombus vs non-thrombus cases and asymptomatic vs symptomatic cases, while it was not possible to discern in congestive heart failure with thrombus and from non-thrombus cases. Additionally, in-silico fluid simulations demonstrated lower LAA blood flow velocities and higher thrombotic risk in the thrombus cases.

Micro-computed tomography (micro-CT) is a high-resolution imaging modality that provides accurate tissue characterization. Hypertrophic cardiomyopathy (HCM) occurs as a spontaneous disease in cats, and is characterized by myocardial hypertrophy, disarray and fibrosis, as in humans. While hypertrophy/mass (LVM) can be objectively measured, fibrosis and myocyte disarray are difficult to assess. We evaluated the accuracy of micro-CT for detection and quantification of myocardial disarray and fibrosis by direct comparison with histopathology. 29 cat hearts (12 normal and 17 HCM hearts) underwent micro-CT and pathologic examination. Myocyte orientation was assessed using structure tensor analysis by determination of helical angle (HA), fractional anisotropy (FA) and myocardial disarray index (MDI). Fibrosis was segmented and quantified based on comparison of gray-scale values in normal and fibrotic myocardium. LVM was obtained by determining myocardial volume. Myocardial segments with low FA, low MDI and disruption of normal HA transmural profile on micro-CT were associated with myocardial disarray on histopathology. FA was consistently lower in HCM than normal hearts. Assessment of fibrosis on micro-CT closely matched the histopathologic evaluation. LVM determined by micro-CT was higher in HCM than normal hearts. Micro-CT can be used to detect and quantify myocardial disarray and fibrosis and determine myocardial mass in HCM.

OBJECTIVE To describe arrhythmias associated with administration of lidocaine in dogs treated for supraventricular tachyarrhythmias. CASE SUMMARIES Four dogs with recent-onset supraventricular tachyarrhythmias: 3 dogs had atrial fibrillation (AF), and 1 had focal atrial tachycardia (FAT), which was thought to be AF at the time of assessment. The substrate of the supraventricular tachyarrhythmia was considered to be due to primary cardiomyopathy in 1 dog, high vagal tone in 2 dogs, and the change in hemodynamics from heavy sedation in 1 dog. Pharmacological cardioversion using lidocaine was only successful in the 2 dogs with vagally mediated AF. In these 2 cases, lidocaine administration resulted in a paroxysmal atrial flutter that was self-limiting and quickly led to sinus rhythm within 10 seconds in 1 dog but did not change over a 5-minute interval and required additional boluses in another dog. In the latter case, the dog showed severe bradycardia for 17.5 seconds prior to achieving sinus rhythm. The 2 unsuccessful cases both developed ventricular arrhythmias shortly after the lidocaine administration, with 1 case degenerating into ventricular fibrillation and cardiac arrest. NEW OR UNIQUE INFORMATION PROVIDED Arrhythmias associated with lidocaine should be considered when treating dogs with supraventricular tachyarrhythmia.

Supraventricular tachycardia (SVT) has not been well described in cats. The aim of this study was to describe the signalment, clinical findings, and outcome for cats with SVT versus cats with atrial fibrillation (AF).Forty-four client owned cats are included in the study. 23 cats with SVT and 21 with AF.This is a retrospective study. Clinical characteristics were compared between groups using a two-sample t-test or Mann-Whitney U test. Kaplan-Meier survival curves were generated to assess for impact of rhythm diagnosis, presence of ventricular arrhythmia, left atrial diameter, heart rate and congestive heart failure (CHF) status on cardiac death. Differences in survival between groups were compared using Mantel-Cox logrank comparison of Kaplan-Meier survival curves.Cats with supraventricular arrhythmias most commonly presented with respiratory distress (10 of 44 cats). Cats with AF had a slower median heart rate (220 [range: 180-260 beats per minute (bpm)] compared with cats with SVT (300 [range: 150-380] bpm, p 0.001). All cats with AF had structural heart disease, whereas 4 cats with SVT had no structural abnormalities. Left atrial diameter was significantly larger in cats with AF (23.7 (16.2-40.1) mm compared with 19.1 (12.8-31.4) mm in SVT cats; p = 0.02). Median survival was 58 days (1-780) in cats with AF and 259 days (2-2295) in cats with SVT (p = 0.1). Cats with signs of CHF had a shorter survival time (p = 0.001).Most cats with AF or SVT have advanced structural heart disease. Some cats with SVT had structurally normal hearts, suggesting that SVT in cats is not always a consequence of atrial enlargement.

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.

Introduction Hypertrophic cardiomyopathy (HCM) has a variable prognosis; left atrial size, presence of clinical signs and left ventricular systolic function have been shown to predict outcomes. Mitral annular plane systolic excursion (MAPSE) and tricuspid annular plane systolic excursion (TAPSE) assess longitudinal ventricular systolic function and are decreased in cats with HCM. The aim of the study was to ascertain whether MAPSE and TAPSE have prognostic value in HCM and if cats with pleural effusion have lower MAPSE and TAPSE than cats with pulmonary oedema. Animals One hundred eighty-four client-owned cats diagnosed with HCM. Methods This is a retrospective study. Echocardiography was used to diagnose HCM (end-diastolic left ventricular wall thickness ≥ 6 mm) and to measure MAPSE and TAPSE. Survival information was obtained. Results No multivariable model including MAPSE or TAPSE could be generated in this population. Cats with pleural effusion ± pulmonary oedema had lower MAPSE measured at the interventricular septum (MAPSE IVS) and TAPSE, compared with cats with pulmonary oedema only. MAPSE IVS was the only factor predicting pleural effusion on multivariable regression model. Conclusions Lower MAPSE and TAPSE were not independently associated with outcomes on multivariable analysis. Cats with pleural effusion ± pulmonary oedema had lower TAPSE and MAPSE IVS than cats with pulmonary oedema, and MAPSE IVS was the only predictive factor associated with the development of pleural effusion in this population.

BACKGROUND: Hypertrophic cardiomyopathy is the most prevalent heart disorder in cats and principal cause of cardiovascular morbidity and mortality. Yet, the impact of preclinical disease is unresolved.HYPOTHESIS/OBJECTIVES: Observational study to characterize cardiovascular morbidity and survival in cats with preclinical nonobstructive (HCM) and obstructive (HOCM) hypertrophic cardiomyopathy and in apparently healthy cats (AH).ANIMALS: One thousand seven hundred and thirty client-owned cats (430 preclinical HCM; 578 preclinical HOCM; 722 AH).METHODS: Retrospective multicenter, longitudinal, cohort study. Cats from 21 countries were followed through medical record review and owner or referring veterinarian interviews. Data were analyzed to compare long-term outcomes, incidence, and risk for congestive heart failure (CHF), arterial thromboembolism (ATE), and cardiovascular death.RESULTS: During the study period, CHF, ATE, or both occurred in 30.5% and cardiovascular death in 27.9% of 1008 HCM/HOCM cats. Risk assessed at 1, 5, and 10 years after study entry was 7.0%/3.5%, 19.9%/9.7%, and 23.9%/11.3% for CHF/ATE, and 6.7%, 22.8%, and 28.3% for cardiovascular death, respectively. There were no statistically significant differences between HOCM compared with HCM for cardiovascular morbidity or mortality, time from diagnosis to development of morbidity, or cardiovascular survival. Cats that developed cardiovascular morbidity had short survival (mean ± standard deviation, 1.3 ± 1.7 years). Overall, prolonged longevity was recorded in a minority of preclinical HCM/HOCM cats with 10% reaching 9-15 years.CONCLUSIONS AND CLINICAL IMPORTANCE: Preclinical HCM/HOCM is a global health problem of cats that carries substantial risk for CHF, ATE, and cardiovascular death. This finding underscores the need to identify therapies and monitoring strategies that decrease morbidity and mortality.

This report, issued by the ACVIM Specialty of Cardiology consensus panel, revises guidelines for the diagnosis and treatment of myxomatous mitral valve disease (MMVD, also known as endocardiosis and degenerative or chronic valvular heart disease) in dogs, originally published in 2009. Updates were made to diagnostic, as well as medical, surgical, and dietary treatment recommendations. The strength of these recommendations was based on both the quantity and quality of available evidence supporting diagnostic and therapeutic decisions. Management of MMVD before the onset of clinical signs of heart failure has changed substantially compared with the 2009 guidelines, and new strategies to diagnose and treat advanced heart failure and pulmonary hypertension are reviewed.

Background Epidemiologic knowledge regarding noncardiovascular and all‐cause mortality in apparently healthy cats (AH) and cats with preclinical hypertrophic cardiomyopathy (pHCM) is limited, hindering development of evidence‐based healthcare guidelines. Objectives To characterize/compare incidence rates, risk, and survival associated with noncardiovascular and all‐cause mortality in AH and pHCM cats. Animals A total of 1730 client‐owned cats (722 AH, 1008 pHCM) from 21 countries. Methods Retrospective, multicenter, longitudinal, cohort study. Long‐term health data were extracted by medical record review and owner/referring veterinarian interviews. Results Noncardiovascular death occurred in 534 (30.9%) of 1730 cats observed up to 15.2 years. Proportion of noncardiovascular death did not differ significantly between cats that at study enrollment were AH or had pHCM (P = .48). Cancer, chronic kidney disease, and conditions characterized by chronic weight‐loss‐vomiting‐diarrhea‐anorexia were the most frequently recorded noncardiovascular causes of death. Incidence rates/risk of noncardiac death increased with age in AH and pHCM. All‐cause death proportions were greater in pHCM than AH (65% versus 40%, respectively; P

Objectives Hypertrophic cardiomyopathy (HCM) appears to be common in cats and, based on pilot data, a prevalence of 15% has been hypothesized. The objectives were to screen a large population of apparently healthy adult cats for cardiac disease, and identify factors associated with a diagnosis of HCM. Animals A total of 1007 apparently healthy cats ≥6 months of age. Methods In this prospective, cross-sectional study, the inclusion criteria were: apparently healthy cats, aged ≥6 months, available for rehoming over a 17-month period from two rehoming centres. Hypertensive or hyperthyroid cats were excluded. Body weight, body condition score, auscultation, systolic blood pressure and two-dimensional (2-D) echocardiography were evaluated. Cats with left ventricular end-diastolic wall thickness ≥6 mm on 2-D echocardiography were considered to have HCM. Results Complete data were obtained in 780 cats. Heart murmur prevalence was 40.8% (95% confidence interval (CI) 37.3–44.3%), 70.4% of which were considered functional. The prevalence of HCM was 14.7% (95% CI 12.3–17.4%), congenital disease 0.5% (95% CI 0.1–1.3%), and other cardiomyopathies 0.1% (95% CI 0.0–0.7%). The HCM prevalence increased with age. The positive predictive value of a heart murmur for indicating HCM was 17.9–42.6% (higher in old cats), and the negative predictive value was 90.2–100% (higher in young cats). The factors associated with a diagnosis of HCM in binary logistic regression models were male sex, increased age, increased body condition score and a heart murmur (particularly grade III/VI or louder). Conclusions Hypertrophic cardiomyopathy is common in apparently healthy cats, in contrast with other cardiomyopathies. Heart murmurs are also common, and are often functional.

Hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats, and it can lead to increased morbidity and mortality. Cats are often screened for HCM because of the presence of a heart murmur, but screening for breeding purposes has also become common. These cats are usually purebred cats of breeding age, and generally do not present with severe disease or with any clinical signs. This type of screening is particularly challenging because mild disease may be difficult to differentiate from a normal phenotype, and the margin for error is small, with potentially major consequences for the breeder. This article reviews HCM screening methods, with particular emphasis on echocardiography.

Objectives To evaluate vena contracta and other echocardiographic measures of myxomatous mitral valve disease (MMVD) severity in a multivariable analysis of survival in dogs. Animals 70 dogs diagnosed with MMVD from stored echocardiographic images that met study inclusion criteria. Methods Left heart dimensions were measured as well as mitral regurgitant jet area/left atrial area (JAR), early mitral filling velocity (E vel ), extent of mitral valve prolapse in right and left views (Prol R , Prol L ), Prol indexed to aortic diameter (Prol R :Ao, Prol L :Ao), presence of a flail leaflet (Flail R , Flail L ), and mitral regurgitation vena contracta diameter (VC R , VC L ) indexed to aortic diameter (VC R :Ao, VC L :Ao). Follow-up from referring veterinarians was obtained by questionnaire or telephone to determine survival times. Inter- and intra-observer agreement was evaluated with Bland–Altman plots and weighted Kappa analysis. Survival was analyzed using Kaplan–Meier curves, logrank tests and Cox's proportional hazards. Results Logrank analysis showed VC L :Ao, VC R :Ao, Flail L, Prol R :Ao, Prol L :Ao, left ventricular internal dimension in diastole indexed to aortic diameter (LVIDD:Ao) >2.87, left atrium to aorta ratio (LA/Ao) >1.6, and E vel >1.4 m/s were predictors of cardiac mortality. In a multivariable analysis, the independent predictors of cardiac mortality were E vel >1.4 m/s [hazard ratio (HR) 5.0, 95% confidence interval (CI) 2.5–10.3], Flail L (HR 3.1, 95% CI 1.3–7.9), and Prol R :Ao (HR 2.8, 95% CI 1.3–6.3). Conclusions Echocardiographic measures of mitral regurgitation severity and mitral valve pathology provide valuable prognostic information independent of chamber enlargement in dogs with MMVD.

Background Type 1 polysaccharide storage myopathy (PSSM1), an equine glycogen storage disorder caused by a gain of function mutation (R309H) in the gene encoding glycogen synthase (GYS1), is associated with the accumulation of amylase-resistant alpha-crystalline polysaccharide inclusions within skeletal muscle. Several glycogenoses in humans have a cardiac phenotype, and reports exist of horses with PSSM and polysaccharide inclusions in cardiac muscle. Hypothesis/Objectives To investigate the hypothesis that horses with PSSM1 display a cardiac phenotype. Our objectives were to compare plasma cardiac troponin I (cTnI) concentration and the incidence of cardiac arrhythmias in PSSM1 homozygotes, heterozygotes, and control horses. Methods One hundred and twenty-five Belgian and Percheron horses under the same management were genotyped for the R309H GYS1 mutation. From these, 8 age-, breed-, and sex-matched cohorts of each genotype were identified. Plasma cTnI concentration and incidence of cardiac arrhythmias (determined by 24-hour Holter ECG) were compared between the groups. Results Although some PSSM1-affected horses had mildly increased plasma cTnI concentrations, there was no significant difference in cTnI concentrations between groups. There were no significant differences in the incidence of ectopic beats, cardiac conduction intervals or mean heart rate between groups. Conclusions and clinical importance We found no evidence of clinically relevant cardiac myocyte injury or arrhythmias in horses with PSSM1. Additional study is required to determine whether myocardial function may be compromised in this disorder.

Objectives This pilot study was performed to investigate murmur prevalence and to explore the association between auscultatory and echocardiographic findings in apparently healthy cats in order to design a larger study. Animals, materials and methods Adult cats in 4 rehoming centres were screened by auscultation and echocardiography (echo) over 2 periods of 2 weeks each. In the first period, echo was attempted only in cats with murmurs. In the second period, all cats underwent auscultation by 2 observers and echo. LVH was defined in 5 ways: maximal diastolic left ventricular (LV) wall thickness ≥6 mm or ≥5.5 mm with 2D (LVH 6 2D , LVH 5.5 2D , respectively) or M-Mode echo (LVH 6 MM or LVH 5.5 MM respectively), or LV wall thickness ≥6 mm (2D) for >50% of a wall segment (LVH 50% ). Results 67/199 (34%) cats had a murmur. Interobserver agreement on murmur presence was moderate ( κ 0.47). 61 cats with a murmur and 31 cats without underwent both auscultation and echo. Depending on the criteria, LVH was present in 31 (LVH 6 2D ), 21 (LVH 50% ) and 11 (LVH 6 MM ) scanned cats. 18–62% of cats with murmurs had LVH, depending on the echo criteria used. Agreement was best between observers in identifying LVH using LVH 6 2D and LVH 50% ( κ = 1.0). Conclusions Heart murmurs are common in apparently healthy cats. The prevalence of LVH varies depending on the criteria used.

Background In humans, acromegaly due to a pituitary somatotrophic adenoma is a recognized cause of increased left ventricular (LV) mass. Acromegalic cardiomyopathy is incompletely understood, and represents a major cause of morbidity and mortality. We describe the clinical, echocardiographic and histopathologic features of naturally occurring feline acromegalic cardiomyopathy, an emerging disease among domestic cats. Methods Cats with confirmed hypersomatotropism (IGF-1>1000ng/ml and pituitary mass; n = 67) were prospectively recruited, as were two control groups: diabetics (IGF-1

A 4-yr-old male ferret (Mustela putorius furo) was presented with a 3-day history of pelvic limb ataxia and weakness. A cellulitis associated with a deep bite wound was identified and initially treated with antibiotics and anti-inflammatory medication. Two weeks later, a grade IV/VI cardiac murmur was identified on physical examination. Echocardiographic examination revealed irregular thickening of the aortic valve leaflets, with normal chamber dimensions and normal systolic function. The ferret's physical condition rapidly deteriorated and it was subsequently euthanatized. Myxomatous degeneration of the aortic valve leaflets, with ulceration and vegetative lesions, and multiorgan infarctions were identified during necropsy. A bacterial etiologic agent was not identified from blood culture or histopathology. Lesions present were consistent with nonbacterial thrombotic endocarditis, a novel condition in the ferret.

A double-blind, randomized, placebo-controlled study was conducted to examine the effect on heart failure class and survival of pimobendan, an oral calcium-sensitizing inodilator, in dogs with dilated cardiomyopathy (DCM). Pimobendan (0.3-0.6 mg/kg body weight/d) or placebo was administered to English Cocker Spaniels (CSs; n = 10) and Doberman Pinschers (DPs: n = 10) that had DCM in addition to background therapy of furosemide, enalapril, and digoxin. Addition of pimobendan to standard triple therapy was associated with a significant improvement in heart failure class, regardless of breed (P < .02, Mann-Whitney rank sum test). Overall, 8 of 10 animals in the pimobendan-treated group, and 1 of 10 animals in the placebo group improved their heart failure status by at least I modified New York Heart Association functional class after initial stabilization (P = .005, Fisher's exact test). Pimobendan had no significant effect on survival in the CSs (P = 0.77, log-rank test), but DPs treated with pimobendan had significantly longer survival times compared with placebo (P < .02, log-rank test), with a median survival time of 329 days in the pimobendan group compared with 50 days in the placebo group, and a hazard ratio of 3.4 (95% confidence interval 1.4-39.8). Pimobendan resulted in significant improvement in heart failure class when added to standard therapy in this group of dogs with DCM, and may have contributed to improved survival in DPs.

Objective To evaluate left ventricular (LV) diastolic function in boxer dogs with aortic stenosis (AS). Background LV relaxation, elastic recoil, filling and stiffness have been found to be abnormal in people with AS and were related to disease severity, clinical signs and prognosis. Methods 2-D, M-mode and Doppler echocardiography was done in 74 boxers with AS (55 with mild AS, 7 with moderate AS and 12 with severe AS) and compared with reference values from 66 normal boxers. Measurements included isovolumic relaxation time (IVRT), peak early (E) and late (A) transmitral filling velocities, mitral E wave deceleration time, peak systolic, and early and late (AR) diastolic pulmonary wenous flow velocities and related variables. In addition, left atrial (LA) function, LV dimensions and hypertrophy and LV systolic performance were assessed. Results Eight dogs (15%) with mild AS had abnormal LV diastolic function, compared with 16 dogs (84%) with moderate or severe AS. Two dogs (3%) had also systolic abnormalities. The flow pattern of delayed relaxation, pseudonormal mitral inflow and restrictive flow were found in 10, 11 and 3 dogs, respectively. IVRT and E:A were heterogeneous in dogs with moderate or severe AS, being either high, normal, or low. Peak AR velocity was significantly higher (p ≤ 0.05) in dogs with severe AS, and the A duration:AR duration ratio was significantly lower (p ≤ 0.05) in dogs with moderate and severe AS compared with the other dogs, suggesting decreased LV compliance, increased LV end-diastolic pressure, and normal or increased LA systolic function. Bivariate linear regression analysis revealed significant correlations between the severity of AS based on Doppler and LV hypertrophy (IVSd: r = 0.61, p ≤ 0.001 and LVPWd: r = 0.46, p ≤ 0.001) and AS severity and A duration: AR duration (r = -0.64, p ≤ 0.001). Conclution In most boxer dogs with moderate or severe AS, LV diastolic function is abnormal even in the presence of normal systolic performance.

To investigate the effect of various genetic and environmental modifiers on left ventricular (LV) wall thickness in a cohort of cats genotyped for the myosin binding protein C3 mutation (MYBPC3).Sixty-four Ragdoll cats.All cats were screened for HCM with echocardiography and genotyping for the HCM-associated MYBPC3:R820W mutation. Cats were also genotyped for previously identified variant polymorphisms of the angiotensin-converting enzyme (ACE) and cardiac beta-adrenergic receptor (ADRB1) genes. Plasma N-terminal pro-B-type natriuretic peptide and cardiac troponin I were also measured. Associations were evaluated between genotype (MYBPC3 negative/positive, and ACE and ADRB1 negative/heterozygous/homozygous), patient factors (body weight, age and sex) and echocardiographic measurements of LV wall thickness.Male cats had greater maximum wall thickness (LVmax; 5.8 mm, IQR 5.1-6.4 mm) than females (4.7 mm, IQR 4.4-5.3 mm, p = 0.002). Body weight positively correlated with LVmax (ρ = 0.604, p0.001). The MYBPC3:R820W-positive cats had a greater LVmax (5.44 mm, IQR 4.83-6.28 mm) than the negative cats (4.76 mm, IQR 4.36-5.32 mm, p = 0.001). Also, the ACE polymorphism genotype was associated with LVmax: the homozygous cats (5.37 mm, IQR 5.14-6.4 mm) had greater LVmax than the heterozygous cats (4.73 mm, IQR 4.41-5.55 mm, p = 0.014). Only the MYBPC3 genotype and body weight were independently associated with wall thickness in multivariable analysis.This study provides evidence that the MYBPC3:R820W mutation is independently associated with LV wall thickness in Ragdoll cats. Body weight is also independently associated with maximum LV wall thickness, but is not currently accounted for in HCM screening. In addition, other genetic modifiers may be associated with variation in LV wall thickness in Ragdolls.

Norwegian Forest cats (NFCs) are often listed as a breed predisposed to cardiomyopathy, but the characteristics of cardiomyopathy in this breed have not been described. The aim of this preliminary study was to report the features of NFC cardiomyopathy based on prospective echocardiographic screening of affected family groups; necropsy findings; and open-source breed screening databases. Prospective examination of 53 NFCs revealed no murmur or left ventricular (LV) outflow tract obstruction in any screened cat, though mild LV hypertrophy (defined as diastolic LV wall thickness ≥5.5mm) was present in 13/53 cats (25%). Gross pathology results and histopathological sections were analysed in eight NFCs, six of which had died of a cardiac cause. Myocyte hypertrophy, myofibre disarray and interstitial fibrosis typical of hypertrophic cardiomyopathy were present in 7/8 cats, but endomyocardial fibrosis suggestive of restrictive cardiomyopathy was also present in the same cats. Pedigree data analysis from 871 NFCs was supportive of a familial cardiomyopathy in this breed.

M-mode echocardiography was used to assess apical mitral annulus motion (MAM) in 103 normal dogs and 101 dogs with cardiac disease, to obtain information on systolic left ventricular long axis function. In normal dogs, a close relationship was found between MAM and body weight (r = 0.80, P0.001). There was a weak correlation between MAM and heart rate (r = -0.25, P0.05), but no correlation between MAM and age or left ventricular shortening fraction (P0.05). Mean MAM (95% confidence intervals) were established for normal dogs of differing body weight, and were 0.70 cm (0.65 to 0.75) in dogs15 kg, 1.08 cm (1.03 to 1.13) in dogs weighing 15 to 40 kg, and 1.51 cm (1.21 to 1.81) in dogs40 kg. "Cut-off" values to define decreased MAM for normal dogs of differing body weight were 0.45 cm (dogs15 kg), 0.80 cm (dogs 15-40 kg), and 1.20 cm (dogs40 kg). In dogs with cardiac disease, median MAM was normal in mitral valve endocardiosis or aortic stenosis, but significantly decreased (P0.05) in dilated cardiomyopathy. All dogs with mitral valve endocardiosis (n = 54) or aortic stenosis (n = 26) had MAM above the above-mentioned "cut-off" values, suggesting normal or increased left ventricular longitudinal systolic shortening, whereas 81% (17/21) of dogs with dilated cardiomyopathy had MAM below the "cut-off" value, indicating decreased long axis systolic function. It is concluded that MAM may be used to evaluate systolic left ventricular long axis performance in dogs and may add useful information on global left ventricular contraction dynamics.

A study was undertaken to investigate the relationship between murmur intensity, murmur duration, duration to peak intensity and frequency components with degree of aortic stenosis in boxers. Measurements were made from phonocardiograms obtained from 35 boxers with ejection-type murmurs, and values were compared with those obtained for aortic flow velocity measured by Doppler echocardiography. Murmur intensity graded by auscultation was significantly correlated with aortic flow velocity (P

Objective—To identify clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and echocardiographic evidence of left ventricular systolic dysfunction. Design—Retrospective study. Animals—48 mature Boxers. Procedure—Medical records were reviewed for information on age; sex; physical examination findings; and results of electrocardiography, 24-hour ambulatory electrocardiography, thoracic radiography, and echocardiography. Results—Mean age of the dogs was 6 years (range, 1 to 11 years). Twenty (42%) dogs had a systolic murmur, and 9 (19%) had ascites. Congestive heart failure was diagnosed in 24 (50%) dogs. Seventeen (35%) dogs had a history of syncope. Mean fractional shortening was 14.4% (range, 1% to 23%). Mean left ventricular systolic and diastolic diameters were 4.5 cm (range, 3 to 6.3 cm) and 5.3 cm (range, 3.9 to 7.4 cm), respectively. Twenty-eight (58%) dogs had a sinus rhythm with ventricular premature complexes (VPCs), and 20 had supraventricular arrhythmias (15 with atrial fibrillation and 5 with sinus rhythm and atrial premature complexes). Sixteen of the dogs with supraventricular arrhythmias also had occasional VPCs. Morphology of the VPCs seen on lead II ECGs was consistent with left bundle branch block in 25 dogs, right bundle branch block in 8, and both in 11. Conclusions and Clinical Relevance—Results suggest that Boxers with cardiomyopathy and left ventricular dysfunction frequently have arrhythmias of supraventricular or ventricular origin. Whether ventricular dysfunction was preceded by electrical disturbances could not be determined from these data, and the natural history of myocardial disease in Boxers requires further study. (J Am Vet Med Assoc 2005;226:1102–1104)

Objectives A mutation identified in the myosin binding protein C3 gene (MYBPC3 R820W) has been associated with hypertrophic cardiomyopathy (HCM) in Ragdoll cats. Ragdolls with HCM are reported to have a poor prognosis and homozygous cats seem particularly likely to develop severe HCM, although the outcome in Ragdolls tested for the MYBPC3 mutation has not been reported. We aimed to determine the influence of genotype on survival in Ragdoll cats using a questionnaire, and hypothesized that homozygous Ragdolls had shorter lifespans and were more likely to suffer cardiac death than heterozygous or wild-type (WT) cats. Animals 251 client owned Ragdoll cats. Methods A questionnaire for breeders/owners of MYBPC3 genotyped Ragdolls included items related to genotype, age, sex, current status (alive/dead), and date and circumstances of death. Death was categorized as cardiac or non-cardiac. Survival was analyzed using Kaplan–Meier curves and log rank tests. Results Completed questionnaires were received for 236 cats (156 WT, 68 heterozygous, 12 homozygous). Median survival time for homozygous cats was 5.65 years (95%CI 0.4–10.9 years) compared to heterozygous (>16.7 years) or WT (>15.2 years). Homozygous cats were more likely to die from cardiac death ( p = 0.004 vs. WT; p = 0.003 vs. heterozygous) and had significantly shorter time to cardiac death (vs. WT p p Conclusions Ragdoll cats homozygous for the MYBPC3 R820W mutation have a shorter survival time than WT or heterozygous cats. This suggests a mode of inheritance that follows an incomplete dominance pattern.

Objectives To investigate the effect of treatment with atenolol on 5-year survival in cats with preclinical hypertrophic cardiomyopathy (HCM). Animals 63 Client-owned cats with preclinical HCM and 31 healthy control cats. Methods Prospective, observational, open-label, clinical cohort study. Cats with HCM were diagnosed by echocardiography, treated with atenolol (6.25–12.5 mg q12h, PO; n = 42) or untreated ( n = 21), and were observed for 5 years after enrollment. The study end point was death from any cause. Cats of similar body weight, age, gender, and breed without evidence of heart disease were studied concurrently and served as controls. Results During the observational period, 27 cats with HCM died; 14 (22%) due to cardiac disease and 13 (21%) due to non-cardiac disease. Ten control cats (32%) died of non-cardiac disease. There was no significant difference ( P = 0.307) in all-cause mortality between control and HCM. Cardiac mortality was higher in cats with HCM compared to control cats ( P = 0.005). There was no significant difference in all-cause mortality ( P = 0.729) and cardiac mortality ( P = 0.897) between cats with HCM treated or untreated with atenolol. Age and left atrial size at diagnosis were the only predictors of 5-year outcome. Conclusions Our study failed to demonstrate an effect of atenolol on 5-year survival in cats with preclinical HCM.

A 6 year-old Labrador retriever was presented after being struck by a car. A ventricular arrhythmia, attributed to myocardial trauma, developed 12 h post-trauma. Echocardiography revealed lesions consistent with a subaortic paramembranous ventricular septal defect (VSD) with shunting of blood from the left ventricle to the right atrium (Gerbode defect). A right-to-left shunting atrial septal defect (ASD) was visualised. Pleural and peritoneal effusions developed within 48 h. Fifteen days post-trauma flow across the ASD was left-to-right while left-to-right shunting across the VSD persisted. No cavitary effusions were detected at 15 days post-trauma or subsequently.

Anaemia induces haemodynamic compensatory mechanisms resulting in volume overload and increased left heart dimensions in humans and dogs. The aims of this retrospective study were to investigate the effects of anaemia on echocardiographic left heart dimensions, vertebral heart size (VHS) and radiographic evidence of congestive heart failure (CHF) in cats. Fifteen cats fulfilled the inclusion criteria and were classified as mildly anaemic (haematocrit (Hct)>18–24%) or severely anaemic (Hct≤18%). Eight out of eight severely anaemic cats had left atrial enlargement compared with 1/6 mildly anaemic cats (P

Although most cardiac diseases have an adverse effect on cardiac output, it is congestive heart failure (CHF) that is usually responsible for clinical signs in dogs and cats. CHF can be defined as abnormal fluid accumulation as a result of heart disease. Increased atrial pressures lead to increased capillary hydrostatic pressure, and fluid accumulates in the interstitial spaces (pulmonary oedema) or body cavities (pleural effusion or ascites). Congestive signs are more common than signs of low cardiac output because the main priority of the cardiovascular system is provision of adequate systemic arterial blood pressure, and this is tightly regulated. Arterial blood pressure is maintained in the face of reduced cardiac output via activation of a number of neurohormonal mechanisms. These include increased sympathetic tone, as well as other mechanisms that help to increase cardiac output (such as sodium and water retention) or increase systemic vascular resistance. Importantly, support of arterial blood pressure is often at the expense of increased filling (atrial) pressures, increased risk of pulmonary oedema or effusions, and increased myocardial work. This chapter considers Treatment according to stage of heart disease; and Specific treatments.

Successful management of the animal with cardiorespiratory disease depends on accurate anatomical localization of disease and efficient diagnostic planning. Determination of the history of the complaint, assessment of the pattern of breathing, and careful examination and auscultation will assist in determining the site responsible for generation of cardiorespiratory complaints. This chapter considers History; General physical examination; Cardiac auscultation; Thoracic auscultation and percussion; and Clinical signs of heart failure.

Objective— To report successful surgical treatment of double chambered right ventricle (DCRV) in a cat. Study Design— Clinical report. Animals— Cat with DCRV. Methods— DCRV was diagnosed in a 5-month-old male Maine Coon cat using echocardiography and angiocardiography. At 2 years, despite medical therapy, chylothorax developed. A section of the right ventricular free wall that spanned the fibromuscular obstruction was excised under total venous inflow occlusion (TVIO) using the incised pericardial patch technique. Results— Short-term recovery was complicated by return of chylothorax but this resolved after thoracocentesis and diuretic therapy. Three years after surgery, the cat is free of clinical signs and no longer on any medical therapy. Conclusions— Partial right ventriculectomy can be performed under TVIO through an incised pericardial patch. Clinical Relevance— DCRV in cat can be successfully treated by partial right ventriculectomy performed under TVIO through an incised pericardial patch.

Quinidine is effective for treatment of atrial fibrillation (AF) in horses, but often accelerates ventricular response rate. Diltiazem effectively controls heart rate response to AF in other species. This investigation determined the effects of diltiazem on cardiac rate and rhythm, left ventricular (LV) function, central hemodynamics, and peripheral blood flow in normal, standing, nonsedated horses. A dose-finding study was performed. Afterward, 8 healthy horses were treated with diltiazem IV every 30 minutes to achieve cumulative dosages of 0 (saline control), 1, 1.5, and 2 mg/kg. Plasma diltiazem concentration, heart rate and rhythm (by electrocardiography), LV function and central hemodynamics (by cardiac catheterization), LV dimensions (by echocardiography), and forelimb blood flow (by Doppler sonography) were determined during each treatment period. Diltiazem plasma concentrations between 390 and 910 ng/mL were achieved, with considerable variation among horses. Cardiac effects of diltiazem included intermittent depression of the sinus and atrioventricular (AV) nodes and mild impairment of systolic and diastolic LV function. Vascular effects of diltiazem included arterial vasodilatation, increased limb blood flow, and decreased systemic vascular resistance. Baroreceptor reflex-mediated sympathetic activation increased sinus node rate and presumably blunted the depressive effects of diltiazem on myocardial and nodal tissues. Two horses developed transient high-grade sinus arrest with severe systemic hypotension. Diltiazem appears relatively safe in healthy horses, but dosage may be limited by hypotension from vasodilatation and direct suppression of sinus node discharge. Because of its inhibitory effects on AV nodal conduction, diltiazem may prove useful for heart rate control in horses with AF.

Pimobendan is an oral inodilator compound available in many countries for use in canine heart failure. It combines calcium-sensitizing effects with PDE III inhibition, resulting in positive inotropic effects and veno- and ergic signal transduction pathway in the failing heart, the calcium-sensitizing effects may assume greater importance in patients with heart failure. Clinical studies in human patients have shown sustained improvement in hemodynamics and exercise tolerance, with favorable neurohormonal effects. One study showed a nonsignificant trend toward increased mortality [20], but proarrhythmic effects have not ben observed. Studies in naturally occurring canine heart failure suggest that pimobendan's effects are at least comparable to those of ACE inhibitors, if not superior. Pimobendan is likely to play an increasing role in the future in the treatment of canine heart disease.

Objective— To compare the incidence of residual patent ductus arteriosus (PDA) flow after ligation using 2 different dissection techniques: a standard dissection and a method described by Jackson and Henderson. Study Design— A randomized, prospective study. Animals— Thirty-five dogs admitted for surgical correction of a left to right shunting PDA. Methods— Dogs were randomly assigned: 19 to a standard dissection technique (group S) and 16 to the Jackson and Henderson dissection group (group JH). Results— Gender ratio, age at surgery, and diameter of the ductus were not statistically different between groups. Breed distribution was also similar. Because 1 dog had fatal intraoperative hemorrhage, only 34 dogs were available for residual flow comparisons. Twenty-one percent of group S dogs had residual flow compared with 53% in group JH. Whereas no intraoperative complications occurred in group S, 3 were encountered in group JH. Conclusions— The incidence of residual flow was higher when the Jackson and Henderson dissection was used for PDA ligation compared with a standard method of dissection. This was probably because of entrapment of loose connective tissue within the medial aspect of the ligature, impeding complete closure of the ductus. Clinical Relevance— Ideal PDA closure should result in no residual ductal flow to prevent possible adverse long-term sequelae, such as recanalization and infective endocarditis.