Search

Hypertrophic cardiomyopathy (HCM) affects 15% of cats, and prevalence increases with age. Although many cats with HCM have normal life expectancy, some cats die suddenly, or develop congestive heart failure or arterial thromboembolism (ATE). High-risk cats can be recognized by left atrial enlargement on echocardiography, which can be missed on physical examination, as a heart murmur is often absent. Alternatively, plasma biomarkers can be measured as an initial screening test; echocardiography is indicated in cats with plasma NT-probrain natriuretic peptide concentrations exceeding 100 pmol/L. High-risk cats should be treated with clopidogrel to reduce the risk of ATE.

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.

Objective—To determine between-pony and within-pony variations and interobserver and intraobserver agreements of a technique for measurement of flow-mediated vasodilation (FMD) in healthy ponies. Animals—6 healthy pony mares (weight range, 236 to 406 kg; body condition score range, 3/9 to 7/9; age range, 14 to 25 years). Procedures—In each pony, the left median artery was occluded with a blood pressure cuff (inflated to > 300 mm Hg for 5 minutes). Two-dimensional ultrasonographic images of the artery were recorded for 30 seconds before cuff inflation and for 2 minutes after cuff deflation. Maximum luminal diameters of arteries were compared with their baseline diameters to calculate FMD (relative percentage increase in luminal size). Images were obtained from 6 ponies 1 time and from 1 pony 6 times. Independent analysis of images was performed by 2 investigators, 1 of whom analyzed images on 2 occasions. Results—Mean ± SD FMD in 6 ponies (1 time) was 12.57 ± 4.28% and in 1 pony (6 times) was 7.30 ± 2.11%. Between-pony and within-pony coefficients of variation were 34.09% and 28.84%, respectively. Interobserver agreement was fair (intraclass correlation coefficient, 0.47); intraobserver agreement was poor (intraclass correlation coefficient, 0.30). Conclusions and Clinical Relevance—FMD was identified and measured in ponies. Measurement of FMD is used to assess endothelial function in humans and has been investigated in dogs. Measurement of FMD in ponies appeared to be feasible and could be used to assess endothelial function (to determine predisposition for development of laminitis or cardiovascular diseases).

To evaluate whether the addition of a protease inhibitor (PI) to feline plasma improves the temporal stability of N-terminal pro-B-type natriuretic peptide (NT-proBNP).Forty-four EDTA blood samples were collected from 42 cats with cardiac disease or hyperthyroidism. Samples were separated within 15 min of collection and the plasma stored at -80 °C. Samples were thawed and each separated into 2 aliquots, one of which was mixed with PI. Each was subdivided into 5 aliquots, which remained at room temperature (RT) for zero, 24, 48, 96 or 120 h before being returned to storage at -80 °C. NT-proBNP was measured using a commercially-available ELISA.There was no difference in NT-proBNP measurements between plain and PI samples at time zero (P = 0.836) or 24 h (P = 0.293). At subsequent time-points NT-proBNP was higher in the PI than the plain samples (P 0.05). An overall effect of time at RT was detected for plain (P 0.001) and PI samples (P 0.001).The addition of PI to feline plasma significantly reduces, but does not eliminate, degradation of NT-proBNP at RT. This degradation occurs over a time course comparable to postal transportation of samples for laboratory analysis and may alter the clinical interpretation of results.

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.

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.

Objective—To determine aortic ejection velocity in healthy adult Boxers with soft ejection murmurs without overt structural evidence of left ventricular outflow tract obstruction and in healthy Boxers without cardiac murmurs. Design—Retrospective study. Animals—201 Boxers. Procedure—Dogs were examined independently by 2 individuals for evidence of a cardiac murmur, and a murmur grade was assigned. Maximal instantaneous (peak) aortic ejection velocity was measured by means of continuous-wave Doppler echocardiography from a subcostal location. Forty-eight dogs were reexamined approximately 1 year later. Results—A soft (grade 1, 2, or 3) left-basilar ejection murmur was detected in 113 (56%) dogs. Overall median aortic ejection velocity was 1.91 m/s (range, 1.31 to 4.02 m/s). Dogs with murmurs had significantly higher aortic ejection velocities than did those without murmurs (median, 2.11 and 1.72 m/s, respectively). Auscultation of a murmur was 87% sensitive and 66% specific for the identification of aortic ejection velocity > 2.0 m/s. An ejection murmur and aortic ejection velocity > 2.0 m/s were identified in 73 (36%) dogs. For most dogs, observed changes in murmur grade and aortic ejection velocity during a follow-up examination 1 year later were not clinically important. Conclusions and Clinical Relevance—Results suggested that ejection murmurs were common among healthy adult Boxers and that Boxers with murmurs were likely to have high (> 2.0 m/s) aortic ejection velocities. The cause of the murmurs in these dogs is unknown. (J Am Vet Med Assoc 2003;222:770–774)

Objective—To compare Doppler echocardiographic variables of left ventricular (LV) function with those obtained invasively via cardiac catheterization under a range of hemodynamic conditions. Animals—7 healthy anesthetized cats (1 to 3 years of age). Procedure—Cats were anesthetized and instrumented to measure the time constant of isovolumic relaxation (tau []), LV end-diastolic pressure (LVEDP), peak negative and positive rate of change of LV pressure, arterial blood pressure, and cardiac output. Echocardiographic variables of diastolic function (isovolumic relaxation time [IVRT], early LV flow propagation velocity [Vp], transmitral and pulmonary venous flow velocity indices, and LV tissue Doppler imaging indices) were measured simultaneously over a range of hemodynamic states induced by treatments with esmolol, dobutamine, cilobradine, and volume loading. Correlation between invasive and noninvasive measures of LV filling was determined by univariate and multivariate regression analyses. Results—Significant correlations were found between and IVRT, peak Vp, peak late transmitral flow velocity, and peak systolic pulmonary venous flow velocity. A significant correlation was found between LVEDP and early diastolic transmitral flow velocity (peak E) and the ratio of peak E to peak Vp, but not between LVEDP and peak Vp. Conclusion and Clinical Relevance—IVRT and Vp can be used as noninvasive indices of LV relaxation; Vp was independent of preload and heart rate in this study. The E:Vp ratio may be useful as an indicator of LV filling pressure. (Am J Vet Res 2003;64:93–103)

Objective—To compare measurements of blood flow in the common femoral artery obtained by duplex Doppler ultrasonography (DDU) and a reference ultrasonic transit-time flow (TTF) method and to examine the impact of Doppler spectral waveform measurement techniques on volumetric estimates. Animals—5 healthy female pigs. Procedure—Femoral arterial blood flow was measured simultaneously in anesthetized pigs by use of a TTF probe (left femoral artery) and transcutaneous DDU (right femoral artery). A range of flow states was induced pharmacologically by using xylazine, bradykinin, dobutamine, and isoflurane. Volumetric blood flow was calculated from DDU waveforms, using the product of the flow velocity integral (FVI), the cross-sectional vessel area, and heart rate. Three calculations of FVI were obtained by manually tracing the Doppler spectral envelopes at the outer envelope, the modal, and the inner envelope of the spectral dispersion pattern. Data analysis included calculation of Pearson correlation coefficients and Bland-Altman limits of agreement. Results—Blood flow measured by DDU was more closely correlated with TTF measurements when the modal or inner envelope tracing method was used ( r, 0.76 and 0.78; limits of agreement, –100 to 54.2 and –48.5 to 77.0 mL/min, respectively). Limits of agreement for the outer envelope tracing method were –238.5 to 64 mL/min. Conclusion and Clinical Relevance—Transcutaneous DDU is a reliable noninvasive technique for measuring blood flow in the femoral artery of pigs over a range of flow states. Tracing the inner envelope of the Doppler spectral dispersion pattern provided the best estimate of blood flow in this study. (Am J Vet Res 2003;64:43–50)

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.

Background Population characteristics and outcome of cats with arterial thromboembolism (ATE) managed in general practice (GP) have been poorly described. Hypothesis Cats with ATE presenting to GP are usually euthanized at presentation, but survival times >1 year are possible. Animals Cats with ATE managed by 3 GP clinics in the United Kingdom. Methods Records of cases presenting to GP over a 98-month period (2004–2012) were reviewed. Cats with an antemortem diagnosis of limb ATE were included. Outcome information was obtained. Results Over 98 months, 250 cats were identified with ATE. Prevalence was approximately 0.3%. At presentation, 153 cats (61.2%) were euthanized, with 68/97 (70.1%) of the remaining cats (27.2% of the total population) surviving >24 hours after presentation. Of these, 30/68 (44.1%) survived for at least 7 days. Hypothermia (HR, 1.44; 95% CI, 1.002–2.07; P = .049) and management by Clinic 2 (HR, 5.53; 95% CI, 1.23–24.8; P = .026) were independent predictors of 24-hour euthanasia or death. For cats surviving >24 hours, hypothermia (HR, 2.25; 95% CI, 1.12–4.48; P = .021) and failure to receive aspirin, clopidogrel, or both (HR, 8.26; 95% CI, 1.39–50; P = .001) were independent predictors of euthanasia or death within 7 days. For cats that survived ≥7 days, median survival time was 94 (95% CI, 42–164) days, with 6 cats alive 1 year after presentation. Conclusions Although 153/250 cats were euthanized at presentation, 6 cats survived >12 months. No factors were identified that predicted euthanasia on presentation.

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.

WE are currently enrolling cases for a cardiac MRI (cMRI) clinical study in order to validate a new echocardiographic scoring system for assessing the severity of degenerative mitral valve disease in asymptomatic dogs. Up to now, it has been very difficult to assess the accuracy of …

To compare flow-mediated vasodilation (FMD) measurements in brachial and femoral arteries of healthy dogs habituated to the assessment method, evaluate repeatability of these measurements, and investigate effects of blood pressure cuff inflation time on femoral artery FMD measurements.11 healthy adult Miniature Schnauzers.Arterial luminal diameter and blood flow velocity integral (FVI) were measured before and after cuff inflation of 5 minutes' (brachial and femoral arteries) or 3 minutes' duration (femoral artery) in separate experiments. A blood pressure cuff was inflated to200 mm Hg distal to each imaging site to increase local blood flow to induce reactive hyperemia. Changes in FVI after cuff deflation, FMD, and between-dog and within-dog coefficients of variation (CVs) were determined.After cuff inflation of 5 minutes' duration, greater changes were detected in median change in FVI and FMD of brachial arteries (174.0% and 8.0%, respectively), compared with values determined for femoral arteries (32.0% and 2.1%, respectively). Between-dog CV for brachial artery FMD was 34.0%, compared with 89.6% for femoral arteries, and within-dog CV was 32.5% for brachial arteries versus 51.6% for femoral arteries after cuff inflation of 5 minutes' duration.In healthy Miniature Schnauzers, FMD was greater and more repeatable in brachial arteries than in femoral arteries. Reactive hyperemia was inconsistently induced in femoral arteries following 3- or 5-minute cuff inflation times. Brachial, but not femoral, artery FMD measurement is a potentially useful research technique for measurement of endothelial function in dogs.

Objectives To measure flow-mediated vasodilation (FMD) in healthy dogs and in client-owned dogs with chronic valvular disease (CVD) and to investigate possible correlations between markers of CVD severity and FMD. Animals Twelve dogs with CVD and 11 healthy weight-matched dogs. Methods Brachial artery FMD following 5 min inflation of a cuff around the antebrachium was measured in 12 dogs with CVD and 11 healthy weight-matched dogs. Measurements were also obtained in the healthy dogs 5 min after cuff placement but without inflation (‘sham cuff placement’). Dogs with CVD underwent echocardiography to confirm and characterize their disease. Results In healthy dogs (median age 4 [2–6] years), median FMD was 7.7% versus 3.4% with sham cuff placement (P = 0.003). In dogs with CVD (median age 8 [4–16] years) median FMD was 5.5% versus 7.7% in healthy dogs (P = 0.131). FMD showed an inverse correlation with left ventricular end-diastolic diameter normalized for body weight (r = −0.76, P = 0.0043). Conclusions Brachial FMD in dogs with early CVD inversely correlates with severity of left ventricular remodelling.

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.

To determine if serum cardiac troponin I (cTnI) concentrations can distinguish cardiac from non-cardiac causes of respiratory distress (RD) in cats.53 cats. cTnI concentrations were measured in 30 cats with non-cardiac respiratory distress (RD-NC) and compared to 23 cats with RD due to congestive heart failure (RD+CHF).The RD+CHF group had higher median cTnI concentration (0.94 ng/ml interquartile range IQR 0.54-4.00, range0.20-90.14) than the RD-NC group (0.2 ng/ml IQR0.2-0.33, range0.20-41.1, p0.001). The area under the curve (AUC) was 0.842 (95% CI 0.728-0.955) for the receiver operator curve (ROC) analysis of the accuracy of cTnI concentrations to discriminate RD+CHF from RD-NC cats. A cut-off ofor = 0.81 ng/ml discriminated RD+CHF from RD-NC cats with a sensitivity and specificity of 65.2% and 90.0% respectively. However considerable overlap in cTnI concentrations between the 2 groups was identified.Serum cTnI concentrations were different in RD+CHF compared to RD-NC cats. However the overlap in cTnI concentrations between the 2 groups reduced the clinical efficacy of the assay which therefore should not be used as a stand-alone test but in combination with other diagnostics such as echocardiography and radiography.

To review the pathophysiology, clinical signs, diagnosis, and treatment of pulmonary thromboembolism (PTE) in small animals.Human and veterinary clinical studies, reviews, texts, and recent research in canine and feline PTE diagnosis and thromboembolic therapeutics.In humans, clinical probability assessment and point-of-care D-dimer-based algorithms are widely used. Computed tomography pulmonary angiography is the gold standard for PTE diagnosis in humans. Echocardiography is increasingly used for bedside assessment of affected patients. In low-risk human patients anticoagulants alone are recommended while patients with cardiogenic shock are treated with thrombolytics followed by anticoagulation.PTE is associated with numerous predisposing conditions causing hypercoagulability, blood flow stasis, or endothelial injury. Identifying at-risk patients is key to diagnosis in small animals. Thromboelastography provides a method for identifying hypercoagulable patients. Computed tomography pulmonary angiography may replace selective pulmonary angiography as the imaging technique of choice for PTE diagnosis. PTE therapy consists of supportive treatment combined with appropriate, individualized thromboembolic pharmacotherapy for acute treatment and chronic management. Thrombolytic therapy for PTE remains controversial but may be indicated in hemodynamically unstable acute PTE. Thromboprophylaxis in specific conditions is rational although evidence of efficacy is limited. Prognosis depends upon degree of cardiopulmonary compromise and patient response to therapy. Mortality rates in small animals are unknown.New diagnostic techniques and advances in therapy offer significant potential for improvements in the identification and treatment of PTE in small animals. Further study must be directed to validating new diagnostic modalities and evaluating therapeutic regimes.

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.

Dilated cardiomyopathy (DCM) is characterized by reduced systolic function, heightened sympathetic tone, and high morbidity and mortality. Little is known regarding the safety and efficacy of beta-blocker treatment in dogs with DCM.Carvedilol improves echocardiographic and neurohormonal variables in dogs with DCM over a 4-month treatment period.Prospective, placebo-controlled, double-blinded randomized study. Dogs with DCM underwent echocardiography, ECG, thoracic radiographs, and neurohormonal profiling, followed by titration onto carvedilol (0.3 mg/kg q12h) or placebo over a 4-week period and subsequently received 3 months of therapy. Primary study endpoints included left ventricular volume and function.Sixteen dogs received carvedilol and 7 received placebo. At study end, 13 carvedilol dogs and 5 placebo dogs were alive. There was no difference in the mean percentage change in left ventricular volume at end-diastole (LVVd), left ventricular end-systolic volume (LVVs), and ejection fraction (EF) between treatment groups, suggesting that both groups experienced similar amounts of disease progression. Carvedilol treatment did not result in significant changes in neurohormonal activation, radiographic heart size, heart rate, or owner perceived quality-of-life. Baseline B-type natriuretic peptide (BNP) predicted dogs in the carvedilol-treated group that maintained or improved their EF over the study duration.Carvedilol administration did not improve echocardiographic or neurohormonal indicators of heart function. The lack of effect may be related to severity of disease, carvedilol dose, or brevity of follow-up time. Statistical power of the present study was adversely affected by a high fatality rate in study dogs and small sample size.

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.

Objective—To determine the influence of age, body weight (BW), heart rate (HR), sex, and left ventricular shortening fraction (LVSF) on transmitral and pulmonary venous flow in clinically normal dogs. Animals—92 client-owned dogs 3 months to 19 years old. Procedure—Transthoracic Doppler echocardiography recordings of transmitral flow and pulmonary venous flow were obtained in conscious unsedated dogs. Influence of age, BW, HR, sex, and LVSF on diastolic variables was assessed, using statistical methods such as ANOVA on ranks and univariate and multivariate forward stepwise linear regression analyses. Results—Age significantly influenced isovolumic relaxation time (IVRT; r = 0.56), ratio between peak velocity of the early diastolic mitral flow wave-to-peak velocity of late diastolic mitral flow wave (E:A; r = –0.44), deceleration time of early diastolic mitral flow (DTE; r = 0.26), and peak velocity of atrial reversal pulmonary venous flow wave (AR-wave; r= 0.37). Significant changes of mitral inflow and pulmonary venous flow variables were evident only in dogs > 6 and > 10 years old, respectively. Body weight significantly influenced DTE ( r = 0.63), late diastolic flow duration ( r= 0.60), and AR duration ( r= 0.47), whereas HR significantly affected DTE ( r = –0.34), IVRT ( r= –0.33), and peak velocity of AR ( r= 0.24). Sex or LVSF (range 22 to 48%) did not influence any echocardiographic variables. Conclusions and Clinical Relevance—Age, BW, and HR are important factors that affect filling of the left atrium and left ventricle in clinically normal dogs. (Am J Vet Res 2001;62:1447–1454)