Trypanosoma cruzi infection diagnosed in dogs in nonendemic areas and results from a survey suggest a need for increased Chagas disease awareness in North America.

OBJECTIVE: To describe the clinical presentation and outcome in dogs diagnosed with Trypanosoma cruzi infection in nonendemic areas and to survey veterinary cardiologists in North America for Chagas disease awareness. ANIMALS: 12 client-owned dogs; 83 respondents from a veterinary cardiology listserv. PROCEDURES: A retrospective, multicenter medical records review to identify dogs diagnosed with American trypanosomiasis between December 2010 and December 2020. An anonymous online survey was conducted August 9 to 22, 2022. RESULTS: Diagnosis was made using indirect fluorescent antibody titer (n = 9), quantitative PCR assay (1), or postmortem histopathology (2). Time spent in Texas was < 1 year (n = 7) or 2 to 8 years (5). Time in nonendemic areas prior to diagnosis was < 1 year (n = 10) and > 3 years (2). Eleven had cardiac abnormalities. Of the 12 dogs, 5 had died unexpectedly (range, 1 to 108 days after diagnosis), 4 were still alive at last follow-up (range, 60 to 369 days after diagnosis), 2 were euthanized because of heart disease (1 and 98 days after diagnosis), and 1 was lost to follow-up. Survey results were obtained from 83 cardiologists in North America, of which the self-reported knowledge about Chagas disease was limited in 49% (41/83) and 69% (57/83) expressed interest in learning resources. CLINICAL RELEVANCE: Results highlight the potential for encountering dogs with T cruzi infection in nonendemic areas and need for raising awareness about Chagas disease in North America.

Utility of cardiac MRI to diagnose myocardial ischemia and fibrosis in dogs with cardiomegaly secondary to myxomatous mitral valve disease.

OBJECTIVE: To assess whether cardiac MRI or various biomarkers can be used to detect myocardial ischemia and fibrosis in dogs with cardiomegaly secondary to myxomatous mitral valve disease (MMVD). ANIMALS: 6 dogs with cardiomegaly secondary to naturally occurring stage B2 MMVD being treated only with pimobendan with or without enalapril and 6 control dogs with no cardiac disease. All dogs were ≥ 5 years old with no systemic illness. PROCEDURES: Serum cardiac troponin I and concentrations were measured, and dogs were anesthetized for cardiac MRI with ECG-triggered acquisition of native T1- and T2-weighted images. Gadolinium contrast was administered to evaluate myocardial perfusion and late gadolinium enhancement (LGE). Mean T1 and T2 values and regions of LGE were measured with dedicated software. Extracellular volume (ECV) was estimated on the basis of Hct and T1 values of myocardium and surrounding blood. Subjective analysis for myocardial perfusion deficits was performed. RESULTS: Dogs with MMVD had significantly (P = .013) higher cardiac troponin I concentrations than control dogs, but galectin-3 concentrations did not differ (P = .08) between groups. Myocardial fibrosis was detected in 4 dogs with MMVD and 3 control dogs; no dogs had obvious myocardial perfusion deficits. Native T1 and T2 values, postcontrast T1 values, and ECV values were not significantly different between groups (all P > .3). CLINICAL RELEVANCE: Results suggest that some dogs with cardiomegaly secondary to MMVD may not have clinically relevant myocardial fibrosis.

Retrospective evaluation of hypertrophic cardiomyopathy in 68 dogs.

BACKGROUND: There is a lack of clinical data on hypertrophic cardiomyopathy (HCM) in dogs. HYPOTHESIS/OBJECTIVES: To investigate signalment, clinical signs, diagnostic findings, and survival in dogs with HCM. ANIMALS: Sixty-eight client-owned dogs. METHODS: Retrospective multicenter study. Medical records were searched between 2003 and 2015. The diagnosis of left ventricular (LV) hypertrophy was made by echocardiographic examination. RESULTS: Three hundred and forty-five dogs with LV hypertrophy were identified, of which 277 were excluded. The remaining 68 dogs were 0.3 to 14 years old and predominantly <10 kg (85%), and without a sex predilection. Twenty-four % were Shih Tzu and 24% terrier breeds. Most (80%) had a systolic heart murmur. Owner-determined exercise intolerance (37%) and syncope (18%) were most commonly reported signs. The majority (84%) of dogs had symmetrical LV hypertrophy, whereas asymmetrical septal and LV free wall hypertrophy was observed in 9% and 6% of dogs, respectively. Isolated basal interventricular septal hypertrophy was not observed. Commonly recorded were systolic anterior motion of the mitral valve (60%) and LV diastolic dysfunction (89% of dogs where diastolic function was evaluated). Six dogs died unexpectedly, and 3 developed congestive heart failure. Known survival times were between 1 day and 114 months after diagnosis. CONCLUSIONS AND CLINICAL IMPORTANCE: Hypertrophic cardiomyopathy in dogs should be considered as a differential diagnosis if LV hypertrophy is identified. Small breed dogs are overrepresented, and it is uncommon for dogs with HCM to develop CHF although sudden death can occur.

Effects of pimobendan in cats with hypertrophic cardiomyopathy and recent congestive heart failure: Results of a prospective, double-blind, randomized, nonpivotal, exploratory field study.

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 (<10 mg/kg/d) with or without clopidogrel. The primary endpoint was a successful outcome (ie, completing the 180-day study period without a dose escalation of furosemide). RESULTS: The proportion of cats in the full analysis set population with a successful outcome was not different between treatment groups (P = .75). For nonobstructive cats, the success rate was 32% in pimobendan-treated cats versus 18.2% in the placebo group (odds ratio [OR], 2.12; 95% confidence interval [CI], 0.54-8.34). For obstructive cats, the success rate was 28.6% and 60% in the pimobendan and placebo groups, respectively (OR, 0.27; 95% CI, 0.06-1.26). No difference was found between treatments for the secondary endpoints of time to furosemide dose escalation or death (P = .89). Results were similar in the per-protocol sets. Adverse events in both treatment groups were similar. CONCLUSIONS AND CLINICAL IMPORTANCE: In this study of cats with HCM and recent CHF, no benefit of pimobendan on 180-day outcome was identified.

Effects of pimobendan on left atrial transport function in cats.

BACKGROUND: Arterial thromboembolism is a sequela of hypertrophic cardiomyopathy (HCM) in cats related to left atrial (LA) enlargement and dysfunction. HYPOTHESIS: Pimobendan improves LA transport function in cats. ANIMALS: Twenty-two client-owned cats with HCM and 11 healthy cats. METHODS: Prospective, double-blind, randomized, placebo-controlled clinical cohort study. Cats were randomized to receive either pimobendan (0.25 mg/kg PO q12h) or placebo for 4 to 7 days. Nineteen echocardiographic variables of LA size and function were evaluated. Statistical comparisons included t tests, analysis of variance, and multivariable analyses. RESULTS: Peak velocity of left auricular appendage flow (LAapp peak; mean ± SD, 0.85 ± 0.20 vs 0.71 ± 0.22 m/s; P = .01), maximum LA volume (P = .03), LA total emptying volume (P = .03), peak velocity of late diastolic transmitral flow (A peak velocity; 0.77 ± 0.12 vs 0.62 ± 0.17 m/s; P = .05), and A velocity time integral (A VTI; 3.05 ± 0.69 vs 3.37 ± 0.49; P = .05) were increased after pimobendan. Mean change after pimobendan was larger in cats with HCM compared to healthy cats for LA fractional shortening (2.1% vs -2.1%; P = .05), A VTI (0.58 vs 0.01 cm; P = .01), LAapp peak (0.20 vs 0.02 m/s; P = .02), LA kinetic energy (3.51 vs -0.10 kdynes-cm; P = .05), and LA ejection force (1.93 vs -0.07 kdynes; P = .01) in the multivariable model. The stronger effect of pimobendan in cats with HCM was independent of LA size. CONCLUSIONS AND CLINICAL IMPORTANCE: We identified positive, albeit minor, effects of pimobendan on LA function in cats with HCM. Whether or not treatment with pimobendan decreases the risk of cardiogenic embolism deserves further study.

Acquired left-to-right shunting through a valve-incompetent foramen ovale in a cat with hypertrophic cardiomyopathy and congestive heart failure.

CASE SUMMARY: An 8-year-old spayed female domestic shorthair cat was presented for a recheck evaluation of hypertrophic cardiomyopathy and chronic kidney disease. Three years prior to presentation, the patient was diagnosed with obstructive hypertrophic cardiomyopathy and started on atenolol. The left ventricular outflow tract obstruction subsequently resolved. Biochemical analysis a week prior to presentation demonstrated severe azotemia. Transthoracic echocardiograph revealed pericardial effusion, pleural effusion, severe left ventricular concentric hypertrophy, severe left atrial enlargement and continuous left-to-right flow through the interatrial septum near the fossa ovalis. The patient was euthanized owing to poor prognosis, and gross examination at necropsy revealed a valve-incompetent patent foramen ovale secondary to severe left atrial dilation. RELEVANCE AND NOVEL INFORMATION: To our knowledge, this is the first report of an acquired left-to-right shunt through a valve-incompetent foramen ovale in a cat with hypertrophic cardiomyopathy. Severe left atrial dilation was suspected to cause interatrial shunting through the valve-incompetent foramen ovale, and this finding may be relevant to echocardiographic evaluations in other cats.

Comparison of Two Commercially Available Immunoassays for the Measurement of Bovine Cardiac Troponin I in Cattle With Induced Myocardial Injury.

Background: Multiple cardiac troponin I (cTnI) immunoassays are commercially available. Overall, assays have not been standardized, and inter-assay differences in the detection of the analyte cardiac troponin I can be clinically relevant. Objective: To compare the diagnostic accuracy of the commercially available Abbott i-STAT®1 cTnI immunoassay (i-STAT) and the previously validated ADVIA Centaur TnI-Ultra immunoassay (Centaur) in cattle. Hypothesis: There will be significant differences in bovine serum cTnI results measured by the Centaur and i-STAT methods. Animals: Ten dairy cows with experimentally induced myocardial injury due to monensin administration. Thirty apparently healthy dairy cows with no history of monensin exposure served as controls. Methods: Blood was collected at various time points after administration of a single dose of monensin (20 to 50 mg/kg) via orogastric tube. A total of 112 blood samples were collected. Cardiac TnI concentration was analyzed with the two methods and the association between methods analyzed via linear regression. Bland-Altman analysis to evaluate agreement between methods was performed on samples divided into groups (cTnI < 1.0 ng/mL and cTnI ≥ 1.0 ng/mL). Results: Analyzer results were linearly correlated with each other (R 2 = 0.931). Samples with cTnI concentrations <1.0 ng/mL had a bias of -0.13 ± 0.20 ng/mL and samples with cTnI concentrations >1.0 ng/mL had a bias of -9.81 ± 13.26 ng/mL. Conclusions and clinical importance: The results of this study reveal that cTnI concentrations determined with the i-STAT are systematically lower compared to the concentrations determined by the Centaur.

Detection of congestive heart failure by Doppler echocardiography in cats with hypertrophic cardiomyopathy.

BACKGROUND: Left-sided congestive heart failure (CHF) is characterized by increased filling pressures and related Doppler echocardiographic (DE) filling patterns. HYPOTHESIS: Doppler echocardiographic variables of left ventricular filling derived from transmitral flow, pulmonary vein flow, and tissue Doppler can be used to detect CHF in cats with hypertrophic cardiomyopathy (HCM). ANIMALS: Forty-seven client-owned cats. METHODS: Prospective clinical cohort study. Cats underwent physical examination, thoracic radiography, analysis of N-terminal pro-brain natriuretic peptide (NT-proBNP), and transthoracic echocardiography and were divided into 3 age-matched groups: Group 1 (apparently healthy control), Group 2 (preclinical HCM), and Group 3 (HCM and CHF). Measured and calculated variables included respiratory rate, DE estimates, serum NT-proBNP concentration, and radiographic CHF score. Groups were compared using ANOVA, and receiver operating characteristic (ROC) curve and multivariate analyses were used to identify diagnostic cutoffs for the detection of CHF. RESULTS: Fifteen cats were in Group 1, 17 in Group 2, and 15 in Group 3. The ROC analysis indicated that the ratio of peak velocity of early diastolic transmitral flow to peak velocity of late diastolic transmitral flow (area under the curve [AUC], 1.0; diagnostic cutoff, 1.77; P = .001), ratio of left atrial size to aortic annular dimension (AUC, 0.91; diagnostic cutoff, 1.96; P = .003), left atrial diameter (AUC, 0.89; cutoff, 18.5 mm; P = .004), diastolic functional class (AUC, 0.89; cutoff, class 2; P = .005), respiratory (AUC, 0.79; cutoff, 36 breaths per minute [brpm]; P = .02), and the ratio of the peak velocity of fused early and late transmitral flow velocities to the peak velocity of the fused early and late diastolic tissue Doppler waveforms (AUC, 0.74; cutoff, 15.1; P = .05) performed best for detecting CHF. CONCLUSIONS AND CLINICAL IMPORTANCE: Various DE variables can be used to detect CHF in cats with HCM. Determination of the clinical benefit of such variables in initiating treatments and assessing treatment success needs further study.

Long-term incidence and risk of noncardiovascular and all-cause mortality in apparently healthy cats and cats with preclinical hypertrophic cardiomyopathy.

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 < .001) because of higher cardiovascular mortality in pHCM cats. Comparing AH with pHCM, median survival (study entry to noncardiovascular death) did not differ (AH, 9.8 years; pHCM, 8.6 years; P = .10), but all-cause survival was significantly shorter in pHCM (P = .0001). CONCLUSIONS AND CLINICAL IMPORTANCE: All-cause mortality was significantly greater in pHCM cats due to disease burden contributed by increased cardiovascular death superimposed upon noncardiovascular death.

Cutting balloon and high-pressure balloon dilation for palliative treatment of congenital double-chambered right ventricle and primary infundibular stenosis in a Golden retriever dog.

Combined cutting balloon and high-pressure balloon dilation was performed in a dog with a double-chambered right ventricle and severe infundibular stenosis of the right ventricular outflow tract. The peak systolic pressure gradient across the stenosis decreased by 65% after dilation (from 187 mmHg before to 66 mmHg after) affirming the intervention as successful. However, early re-stenosis occurred within 3 months leading to exercise intolerance, exercise-induced syncope, and right-sided congestive heart failure. Cutting balloon followed by high-pressure balloon dilation provided temporary but not long-term relief of right ventricular obstruction in this dog.

The role of spatial organization of Ca2+ release sites in the generation of arrhythmogenic diastolic Ca2+ release in myocytes from failing hearts.

In heart failure (HF), dysregulated cardiac ryanodine receptors (RyR2) contribute to the generation of diastolic Ca2+ waves (DCWs), thereby predisposing adrenergically stressed failing hearts to life-threatening arrhythmias. However, the specific cellular, subcellular, and molecular defects that account for cardiac arrhythmia in HF remain to be elucidated. Patch-clamp techniques and confocal Ca2+ imaging were applied to study spatially defined Ca2+ handling in ventricular myocytes isolated from normal (control) and failing canine hearts. Based on their activation time upon electrical stimulation, Ca2+ release sites were categorized as coupled, located in close proximity to the sarcolemmal Ca2+ channels, and uncoupled, the Ca2+ channel-free non-junctional Ca2+ release units. In control myocytes, stimulation of ß-adrenergic receptors with isoproterenol (Iso) resulted in a preferential increase in Ca2+ spark rate at uncoupled sites. This site-specific effect of Iso was eliminated by the phosphatase inhibitor okadaic acid, which caused similar facilitation of Ca2+ sparks at coupled and uncoupled sites. Iso-challenged HF myocytes exhibited increased predisposition to DCWs compared to control myocytes. In addition, the overall frequency of Ca2+ sparks was increased in HF cells due to preferential stimulation of coupled sites. Furthermore, coupled sites exhibited accelerated recovery from functional refractoriness in HF myocytes compared to control myocytes. Spatially resolved subcellular Ca2+ mapping revealed that DCWs predominantly originated from coupled sites. Inhibition of CaMKII suppressed DCWs and prevented preferential stimulation of coupled sites in Iso-challenged HF myocytes. These results suggest that CaMKII- (and phosphatase)-dependent dysregulation of junctional Ca2+ release sites contributes to Ca2+-dependent arrhythmogenesis in HF.

Synchronous Diaphragmatic Flutter Secondary to Primary Hypoparathyroidism in a Dog.

A 3 yr old, spayed, female miniature mchnauzer was presented for rhythmic, spontaneous contractions of the abdominal wall and across the costal arches. The rate of contractions coincided with the heart rate and increased during exercise. The dog was diagnosed with primary hypoparathyroidism based on low plasma ionized calcium and serum parathyroid hormone (PTH) concentrations. Fluoroscopic exam confirmed the diagnosis of a synchronous diaphragmatic flutter. Treatment of the hypocalcemia led to resolution of the diaphragmatic flutter.

Iatrogenic embolization and transcatheter retrieval of a ventricular septal defect occluder in a dog.

A 7-month-old Irish Setter underwent transcatheter therapy of a muscular ventricular septal defect (VSD) and pulmonary valve stenosis. Standard devices for muscular VSD closure could not span the interventricular septum due to right ventricular hypertrophy, and an Amplatzer post-infarction muscular VSD occluder with a wider waist was successfully implanted. Following VSD closure, inflation of the balloon dilation catheter during balloon pulmonary valvuloplasty resulted in iatrogenic embolization of the VSD occluder to the left ventricular outflow tract. Retrieval and reimplantation of the device was achieved using a snare catheter. This report describes a potential complication and management during intracardiac device implantation in a dog. Additionally, the case illustrates that the Amplatzer post-infarction muscular VSD occluder holds potential value in animals with a hypertrophied interventricular septum that cannot be spanned using a conventional device.

Echocardiographic assessment of right ventricular systolic function in conscious healthy dogs following a single dose of pimobendan versus atenolol.

OBJECTIVE: To quantify drug-induced changes in right ventricular (RV) systolic function after administration of pimobendan and atenolol. ANIMALS: 80 healthy privately-owned dogs. METHODS: Using a prospective, blinded, fully-crossed study design with randomized drug administration, RV systolic function was determined twice at two time periods; before and 3 h after administration of pimobendan (0.25 mg/kg PO) or atenolol (1 mg/kg PO). Indices of RV systolic function included tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC), pulsed-wave tissue Doppler-derived systolic myocardial velocity of the lateral tricuspid annulus (S'), and speckle-tracking-derived global longitudinal RV free wall strain and strain rate. The effect of treatment on percent change from baseline RV function was analyzed with a linear mixed model including the covariates heart rate, body weight, age, gender, drug sequence, and time period. RESULTS: All indices showed a significant (p < 0.0001) increase and decrease from baseline following pimobendan and atenolol, respectively. Significant differences from baseline were attributed to drug treatment (p < 0.0001); whereas, effects of other covariates were not significant. The greatest percent changes, but also highest variability, were observed for S' and strain rate (p < 0.0001). Post-atenolol, a significantly greater proportion of dogs exceeded the repeatability coefficient of variation for FAC and S' compared to TAPSE (p ≤ 0.007). CONCLUSIONS: Echocardiographic indices in healthy dogs tracked expected changes in RV systolic function following pimobendan and atenolol and warrant study in dogs with cardiovascular disease.

Pulmonary artery dissection in eight dogs with patent ductus arteriosus.

OBJECTIVES: To describe a series of dogs with pulmonary artery dissection and patent ductus arteriosus (PDA). ANIMALS: Eight dogs. METHODS: Retrospective case series. RESULTS: Pulmonary artery dissection was diagnosed in 8 dogs, 3 were Weimaraners. Four dogs presented in left-sided congestive heart failure, 4 presented for murmur evaluation and without clinical signs, and 1 presented in right-sided congestive heart failure. In 7 dogs the dissection was first documented concurrent with a diagnosis of uncorrected PDA. In the other dog, with pulmonary valve stenosis and PDA, the dissection was observed on autopsy examination 17 months after balloon pulmonary valvuloplasty and ductal closure. Median age at presentation for the 7 dogs with antemortem diagnosis of pulmonary artery dissection was 3.5 years (range, 1.5-4 years). Three dogs had the PDA surgically ligated, 2 dogs did not undergo PDA closure, 1 dog failed transcatheter occlusion of the PDA with subsequent surgical ligation, 1 dog underwent successful transcatheter device occlusion of the PDA, and 1 dog had the PDA closed by transcatheter coil delivery 17 months prior to the diagnosis of pulmonary artery dissection. The 2 dogs that did not have the PDA closed died 1 and 3 years after diagnosis due to heart failure. CONCLUSIONS: Pulmonary artery dissection is a potential complication of PDA in dogs, the Weimaraner breed may be at increased risk, presentation is often in mature dogs, and closure of the PDA can be performed and appears to improve outcome.

Echocardiographic assessment of right ventricular systolic function in conscious healthy dogs: repeatability and reference intervals.

OBJECTIVES: To determine the feasibility, repeatability, intra- and interobserver variability, and reference intervals for 5 echocardiographic indices of right ventricular (RV) systolic function: tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC), pulsed wave tissue Doppler imaging-derived systolic myocardial velocity of the lateral tricuspid annulus (S'), and speckle-tracking echocardiography-derived global longitudinal RV free wall strain and strain rate. To explore statistical relationships between RV systolic function and age, gender, heart rate, and bodyweight. ANIMALS: 80 healthy adult dogs. METHODS: Dogs underwent 2 echocardiographic examinations. Repeatability and intra-observer and inter-observer measurement variability were quantified by average coefficient of variation (CV). Relationships between RV function and age, heart rate and bodyweight were estimated by regression analysis. RESULTS: All indices were acquired with clinically acceptable repeatability and intra- and inter-observer variability (CVs < 10%). No differences were identified between male and female dogs. Allometric scaling by bodyweight demonstrated significant, clinically relevant correlations between RV function and bodyweight (all p ≤ 0.001) as follows: TAPSE - strong positive correlation (r(2) = 0.75); S' - moderate positive correlation (r(2) = 0.31); strain rate - moderate negative correlation (r(2) = 0.44); FAC and strain - weak negative correlations (r(2) = 0.22 and 0.14, respectively). Strain rate and FAC were positively correlated with heart rate (r(2) = 0.35 and 0.31, respectively). Allometric scaling generated bodyweight-based reference intervals for these RV systolic function indices. CONCLUSIONS: Echocardiographic indices of RV systolic function are feasible to obtain, repeatable, and affected by bodyweight. Studies of these indices in dogs with cardiovascular disease are needed.

Echocardiographic evaluation of left ventricular diastolic function in cats: Hemodynamic determinants and pattern recognition.

Left ventricular (LV) diastolic dysfunction is highly prevalent in cats and is a functional hallmark of feline cardiomyopathy. The majority of cats with hypertrophic, restrictive, and dilated cardiomyopathy have echocardiographic evidence of abnormal LV filling, even during the occult (preclinical) phase. Moderate and severe diastolic dysfunction is an indicator of advanced myocardial disease, is associated with clinical signs including exercise intolerance and congestive heart failure, affects outcome, and influences therapeutic decisions. Therefore, identification and quantification of LV diastolic dysfunction are clinically important. Surrogate measures of diastolic function determined by transthoracic two-dimensional, M-mode, and Doppler echocardiographic (DE) methods have been used widely for such purpose. Major functional characteristics of LV diastole, including global function, relaxation and untwist, chamber compliance, filling volume, and the resultant filling pressures can be semi-quantified by echocardiographic methods, and variables retrieved from transmitral flow, pulmonary vein flow, and tissue Doppler recordings are most frequently used. Although there is still a critical lack of well-designed studies in the field, knowledge has steadily accumulated over the past 20 years, reference ranges of diastolic echocardiographic variables have been determined, epidemiological studies have been conducted, and new treatments of diastolic dysfunction in cats have been evaluated. This report will give the reader a summary of the current status in the field of feline diastology with focus on the noninvasive diagnostic methods and interpretation of echocardiographic surrogate measures of LV diastolic function. Lastly, a grading system using a composite of left atrial size and various DE variables potentially useful in the functional classification of LV diastole in cats is introduced.

Sudden death of a horse with supraventricular tachycardia following oral administration of flecainide acetate.

OBJECTIVE: To describe a case of supraventricular tachycardia and sudden death in a horse following administration of flecainide acetate. CASE SUMMARY: An 8-year-old Hanoverian warmblood gelding was treated for chronic, naturally occurring, supraventricular tachycardia with digoxin, procainamide hydrochloride, quinidine sulfate, and flecainide acetate. After oral administration of flecainide, polymorphic ventricular tachycardia (torsades de pointes) and ventricular fibrillation developed, leading to cardiovascular collapse and death. NEW OR UNIQUE INFORMATION PROVIDED: Atrial fibrillation is the most commonly diagnosed dysrhythmia associated with poor performance in horses, while atrial tachycardia is rarely documented. Here, we describe a case of sudden death in a horse with atrial tachycardia following the oral administration of flecainide acetate, after the lack of response to other antiarrhythmic drugs. Information provided in this case report is new and will make clinicians aware of the potential complications of flecainide alone or in combination with other drugs, in horses with cardiac dysrhythmias.

Radiographic and echocardiographic assessment of left atrial size in 100 cats with acute left-sided congestive heart failure.

The aims of this study were to evaluate left atrial size in cats with acute left-sided congestive heart failure. We hypothesized that left atrial size as determined by thoracic radiography can be normal in cats with acute left-sided congestive heart failure. One hundred cats with acute left-sided congestive heart failure in which thoracic radiography and echocardiography were performed within 12 h were identified. Left atrial size was evaluated using right lateral and ventrodorsal radiographs. Measurements were compared to two-dimensional echocardiographic variables of left atrial size and left ventricular size. On echocardiography, left atrial enlargement was observed in 96% cats (subjective assessment) whereas maximum left atrial dimension was increased (>15.7 mm) in 93% cats. On radiographs left atrial enlargement (subjective assessment) was found in 48% (lateral view), 53% (ventrodorsal view), and 64% (any view) of cats whereas left atrial enlargement was absent in 36% of cats in both views. Agreement between both methods of left atrial size estimation was poor (Cohen's kappa 0.17). Receiver operating characteristic curve analysis identified a maximum echocardiographic left atrial dimension of approximately 20 mm as the best compromise (Youden index) between sensitivity and specificity in the prediction of radiographic left atrial enlargement. Left atrial enlargement as assessed by thoracic radiography may be absent in a clinically relevant number of cats with congestive heart failure. Therefore, normal left atrial size on thoracic radiographs does not rule out presence of left-sided congestive heart failure in cats with clinical signs of respiratory distress.

Effect of treatment with atenolol on 5-year survival in cats with preclinical (asymptomatic) hypertrophic cardiomyopathy.

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.