Association between systolic blood pressure and target organ damage in naturally occurring cases of systemic hypertension in the dog.

Chronic elevation in the systolic blood pressure (SBP) adversely affects the lifespan in the dog by causing injury to the eye, heart, kidney and brain. Understanding the association between SBP and target organ damage (TOD) helps in risk categorization and treatment planning. Therefore, a prospective study was undertaken to find the association between SBP and renal resistive index (RI) in naturally occurring cases of canine systemic hypertension. Based on the ACVIM guidelines 2018, dogs (n=135) were categorized into four risk groups of SBP, viz., A (minimal), B (low), C (moderate), and D (high). Ophthalmoscopy and echocardiography were used to assess ocular and cardiac changes, respectively. Nephrosonography, urinalysis, and RI were used to assess kidney damage. Odds ratio (OR) was used to quantify the risk of TOD for different categories of SBP. One-way Anova with Tukey's post-hoc test was used to test the effect of different SBP risk groups on urine protein creatinine ratio (UPC) and RI as well as the effect of number of TOD on the RI. Pearson's correlation test was done to see the relation of SBP with UPC and RI. Tortuous retinal vessels were common in group B with an OR of 11 (95% CI: 0.59-207). Retinal hemorrhage and left ventricular hypertrophy were common in group D with an OR of 13 (95% CI: 0.67-234) and 11 (95% CI: 0.61-207), respectively. A significant strong positive correlation of SBP with UPC (R2=0.65) and RI (R2=0.58) was observed. The renal RI significantly increased when the number of TOD was ≥ 2. It was concluded that SBP and RI are associated with the number and severity of TOD and might be valuable in risk classification in hypertensive dogs.

Heart failure in a cat due to hypertrophic cardiomyopathy phenotype caused by chronic uncontrolled hyperthyroidism.

A 16-year-old castrated male Persian cat was presented with weight loss, anorexia and dyspnoea. Tachycardia and tachypnoea were observed upon presentation. The cat was previously diagnosed with hyperthyroidism and left ventricular hypertrophy and received methimazole, but was subsequently not followed up and treated appropriately. Thoracic radiography revealed mild pleural effusion, interstitial lung pattern, moderate cardiomegaly and moderate-to-severe dilation of the pulmonary artery and pulmonary vein. On echocardiography, the left ventricular hypertrophy, identified earlier, shoed partial regression. Therefore, the previous myocardial hypertrophy was diagnosed as a hypertrophic cardiomyopathy phenotype related to hyperthyroidism. ST-segment elevation was identified on electrocardiography, and the thyroid profile examination revealed increased total thyroxine and free thyroxine and decreased thyroid-stimulating hormone levels, suggesting myocardial injury and uncontrolled hyperthyroidism, respectively. In addition, normal N-terminal pro-B-type natriuretic peptide and high cardiac troponin I levels were found. Based on these findings, the observed congestive heart failure was considered as a sequel of myocardial injury caused by uncontrolled hyperthyroidism. Clinical signs resolved after intravenous administration of furosemide and butorphanol, oxygen supply and thoracocentesis. Furosemide and pimobendan were additionally administered, and the cat was discharged. This case demonstrates that myocardial damage due to chronic uncontrolled hyperthyroidism may cause heart failure in cats.

Differences in Left Ventricular Enlargement Secondary to Chronic Volume Loading Between English Springer Spaniels and Two Similar Sporting Breeds.

INTRODUCTION: English springer spaniels have larger, rounder ventricles than most other breeds. How this geometry impacts responses to volume overload remains unknown. We compared left ventricular size between English springer spaniels and two similarly sized sporting breeds (Border collies and Labrador retrievers) in naturally occurring chronic left ventricular volume loading conditions (mitral regurgitation and patent ductus arteriosus [PDA]) to examine whether differences in remodelling responses exist between these breeds. ANIMALS, MATERIALS AND METHODS: We searched records for cases of mitral regurgitation and PDA in three breeds. We recorded age, sex, presence of congestive heart failure (CHF), body weight and specific echocardiographic variables. We compared normalised measures of left ventricular size between breeds. Cases with CHF were further examined as a separate group. RESULTS: One-hundred-and-ninety-one dogs were included: 110 with degenerative mitral valve disease, 42 with mitral dysplasia and 39 with PDA. One third of all cases had CHF. All measures of left ventricular size were larger in English springer spaniels in mitral regurgitation cases (P<0.001), whereas PDA cases did not differ. English springer spaniels with PDA resulting in CHF had larger systolic dimensions and volumes than similarly affected non-English Springer Spaniel dogs (P=0.003). CONCLUSIONS: English springer spaniels have greater left ventricular dimensions when exposed to chronic mitral regurgitation, compared with Border collies and Labrador retrievers, but not when exposed to volume overload from a PDA. English springer spaniels differ in their left ventricular morphology from two other sporting breeds, supporting previous studies that they have a unique cardiac morphotype.

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

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

Echocardiographic values for normal conditioned and unconditioned North American whippets.

BACKGROUND: Echocardiographic reference intervals have not been reported for North American whippets, or for whippets that have undergone pet-level athletic training. OBJECTIVES: To develop normal echocardiographic reference intervals for North American whippets and investigate differences in echocardiographic parameters based on athletic conditioning in pet whippets engaged in competitive sports. ANIMALS: One-hundred healthy North American whippets. METHODS: Dogs were examined at national shows between 2005 and 2009. Echocardiographic reference intervals were constructed and the effect of athletic conditioning on parameters of structure and function was assessed. RESULTS: Two dimensional, M-mode, Doppler and tissue Doppler reference ranges for healthy North American whippets are presented. Measures of left ventricular (LV) chamber diameter were larger in conditioned whippets (N = 25) and remained significantly larger than in unconditioned whippets (N = 16) when normalized for weight using allometric equations. Calculated LV mass was higher in conditioned dogs than in unconditioned dogs, and this difference persisted when LV mass was normalized by weight. Mitral E velocity was higher in conditioned dogs than in unconditioned dogs, whereas E/A and measures related to systolic function were not different. CONCLUSIONS AND CLINICAL IMPORTANCE: Pet whippets in peak athletic condition have larger hearts than do less conditioned whippets, but measures of systolic function are similar. Whippet pet athletes may show eccentric LV hypertrophy at peak condition. Normal values for cardiac size and function in North American whippets might be considered abnormal if population-specific whippet reference intervals are not used in analysis.

Prognostic relevance of left cardiac enlargement in dogs with preclinical myxomatous mitral valve disease.

INTRODUCTION: According to the most recent consensus guidelines on canine myxomatous mitral valve disease (MMVD), dogs with only left atrial enlargement (LAE) or left ventricular enlargement are classified as stage B1. The concomitant presence of LAE and left ventricular enlargement is needed to be classified as stage B2. The primary aim of the study was to evaluate the prognosis in stage B1 and stage B2 according to the revised definition. The secondary aim was to assess the prognostic relevance of LAE in stage B1. ANIMALS: A total of 440 dogs with MMVD, 276 in stage B1 and 164 in stage B2. MATERIALS AND METHODS: Retrospective and observational study. The left atrium-to-aorta ratio and the left ventricular end-diastolic diameter normalized were used to define cardiac dimensions. The long-term outcome was assessed by telephone interviews with owners and referring vets. Both cardiac-related and all-cause mortality were evaluated. RESULTS: Stage B1 dogs had a longer median survival time than stage B2, considering both cardiac-related death (2344 vs. 1341 days; P<0.001) and all-cause mortality (1832 vs. 855 days; P<0.001). Age, left atrium-to-aorta ratio, and the left ventricular end-diastolic diameter normalized were independent predictors of cardiac-related death and all-cause mortality. Among stage B1, dogs with LAE lived shorter than those without LAE (1183 vs. 1882 days; P=0.005) considering all-cause mortality. DISCUSSION AND CONCLUSIONS: Stage B1 dogs lived longer than stage B2 dogs. Among stage B1, LAE had prognostic relevance considering all-cause mortality. This finding could add useful prognostic information in the management of preclinical MMVD.

The ACVIM consensus statement definition of left ventricular enlargement in myxomatous mitral valve disease does not always represent left ventricular enlargement.

OBJECTIVE: To determine how frequently the current criteria for left ventricular enlargement in dogs misclassify healthy dogs as having left ventricular enlargement; to examine the effect of breed on diastolic left ventricular normalized dimensions (LVIDDN); to propose appropriate scaling exponents and reference limits for dogs. ANIMALS: Echocardiographic data from 1,124 healthy adult dogs, including 454 dogs weighing <20 kg. METHODS: We calculated power regression parameters (allometric scaling), including exponents and proportionality constants, for various subsets of the dogs (all dogs, dogs < 20 kg, generic dogs, and individual breeds with >10 observations) and derived upper reference limits for LVIDDN. We determined the proportions of dogs that would be identified as having left ventricular enlargement with each regression model compared to previously published reference limits or guidelines. We then identified breeds failing to conform to generic dog models. RESULTS: The American College of Veterinary Internal Medicine-recommended scaling exponent (0.294) and criterion for identifying left ventricular enlargement (1.7) identified >10% of apparently healthy dogs as having left ventricular enlargement, with specific breeds being misclassified up to 50% of the time. However, with a scaling exponent of 0.33, a constant of 1.7 represented a normal left ventricular size in 97.5% of healthy dogs in both generic and non-conforming breeds. CONCLUSIONS: Left ventricular internal dimension in diastole normalized to bodyweight is breed-dependent. A constant of 1.7 with a scaling exponent of 0.294 does not always represent ventricular enlargement; a scaling exponent of 0.33, with breed-specific reference limits for breeds that fail to conform to allometric models of generic dogs, reduces the misclassification of healthy dogs as having left ventricular enlargement.

Congenital supravalvular aortic stenosis in a kitten.

A three-month-old, male intact Norwegian forest cat without any clinical signs was referred to the cardiology service of the author's teaching hospital for evaluation of a cardiac murmur. The murmur was systolic with an intensity of 4 out of 6 with the point of maximal intensity at the left heart base. Echocardiography revealed a moderate mitral valve regurgitation and a moderate dynamic left ventricular outflow tract obstruction both resulting from systolic anterior motion of the mitral valve (SAM). Moreover, left ventricular concentric hypertrophy was noted. Oral atenolol therapy was initiated. Recheck examination 3.5 months later revealed unchanged murmur characteristics in the still asymptomatic kitten. Echocardiography showed no SAM, but there was a severe fixed aortic stenosis apparent caused by a discrete supravalvular lesion, 4 mm distal to the valve, with an hourglass morphology. Supravalvular aortic stenosis is a rare congenital anomaly in cats, which has not been reported antemortem yet.

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.

[Reversible left ventricular hypertrophy and congestive heart failure due to suspected myocarditis in a cat in the course of FLUTD]. / Reversible linksventrikuläre Muskelhypertrophie und Herzversagen durch vermutete Myokarditis bei einer Katze im Zuge einer FLUTD.

A 2.5-year-old castrated male domestic shorthair cat with a past pertinent history of FLUTD treatment 8 days earlier was presented during the night due to apathy and anorexia. Radiographs, ECG, blood pressure measurement and echocardiography revealed left-sided congestive heart failure, left ventricular concentric hypertrophy, left atrial dilation, severe diastolic dysfunction, hypotension, and vagotonus-associated sinus bradycardia with a first degree AV-block as well as a right bundle brunch block. NT-ProBNP and troponin I concentrations were elevated (NT-ProBNP > 1500 pmol/l, Troponin I 32.87 ng/ml). Presumptive diagnosis was acute myocarditis. Bartonella henselae PCR and Toxoplasma gondii IgM titer were negative. Initial IgG titer amounted to 1:32 (reference range: < 1:32) and on later testing this was negative. FeLV and FIV tests exhibited negative results. Coronavirus testing was not performed because the cat was vaccinated accordingly. A metastatic infection with Proteus mirabilis, which had been isolated from the urine, appeared possible. Alternatively, a hypersensivity reaction to drugs or a stress-induced myocarditis was taken into consideration. The hospitalized cat was treated with furosemide (initialy and in the course of further treatment), theophyllin (initially), continuous infusion with lactated Ringer's solution, pimobendan, and the addition of enrofloxacin to the ongoing amoxicillin/clavulanic acid administration. After 4 days, the cat's general condition improved satisfactorily and blood pressure returned to normal range. Left ventricular hypertrophy resolved, however, diastolic dysfunction as well as left atrial dilation persisted. Within the next 8 weeks, echocardiographic findings and cardiac biomarkers returned to near normal values. All medication was tapered and finally discontinued. During the last recheck examination 7 months following initial presentation, no cardiac changes were apparent.

Cardiac extracellular volume fraction in cats with preclinical hypertrophic cardiomyopathy.

BACKGROUND: Cardiac magnetic resonance imaging (CMR) allows for detection of fibrosis in hypertrophic cardiomyopathy (HCM) by quantification of the extracellular volume fraction (ECV). HYPOTHESIS/OBJECTIVES: To quantify native T1 mapping and ECV in cats. We hypothesize that native T1 mapping and ECV will be significantly increased in HCM cats compared with healthy cats. ANIMALS: Seventeen healthy and 12 preclinical HCM, age-matched, client-owned cats. METHODS: Prospective observational study. Tests performed included indirect blood pressure, CBC, biochemical analysis including total thyroid, urinalysis, transthoracic echocardiogram, and CMR. Cats were considered healthy if all tests were within normal limits and a diagnosis of HCM was determined by the presence of left ventricular concentric hypertrophy ≥6 mm on echocardiography. RESULTS: There were statistically significant differences in LV mass (healthy = 5.87 g, HCM = 10.3 g, P < .0001), native T1 mapping (healthy = 1122 ms, HCM = 1209 ms, P = .004), and ECV (healthy = 26.0%, HCM = 32.6%, P < .0001). Variables of diastolic function including deceleration time of early diastolic transmitral flow (DTE), ratio between peak velocity of early diastolic transmitral flow and peak velocity of late diastolic transmitral flow (E : A), and peak velocity of late diastolic transmitral flow (A wave) were significantly correlated with ECV (DTE; r = 0.73 P = .007, E : A; r = -0.75 P = .004, A wave; r = 0.76 P = .004). CONCLUSIONS AND CLINICAL IMPORTANCE: Quantitative assessment of cardiac ECV is feasible and can provide additional information not available using echocardiography.

Increased insulin-like growth factor 1 concentrations in a retrospective population of non-diabetic cats diagnosed with hypertrophic cardiomyopathy.

OBJECTIVES: The aim of the study was to document whether a proportion of non-diabetic cats with left ventricular hypertrophy (LVH) previously diagnosed with hypertrophic cardiomyopathy (HCM) have elevated circulating insulin-like growth factor 1 (IGF-1) concentrations. METHODS: A retrospective analysis of residual blood samples obtained at the time of echocardiographic diagnosis of HCM from a population of 60 non-diabetic cats were analysed for circulating IGF-1 concentrations using a validated radioimmunoassay and compared with a control group of 16 apparently healthy cats without LVH. Clinical and echocardiographic data for cats with an IGF-1 level >1000 ng/ml were compared with those with an IGF-1 level <800 ng/ml. RESULTS: In total, 6.7% (95% confidence interval 1.8-16.2%) of cats with HCM had an IGF-1 level >1000 ng/ml. The prevalence of an IGF-1 level >1000 ng/ml in the control group was zero. CONCLUSIONS AND RELEVANCE: A small proportion of non-diabetic cats previously diagnosed with HCM had an IGF-1 concentration at a level that has been associated with feline hypersomatotropism (fHS) in the diabetic cat population. Further prospective research is required to confirm or refute the presence of fHS in non-diabetic cats with LVH and increased IGF-1.

Evaluation of N-terminal prohormone of brain natriuretic peptide and cardiac troponin-I levels in cats with systolic anterior motion of the mitral valve in the absence of left ventricular hypertrophy.

OBJECTIVES: To identify the prevalence of systolic anterior motion of the mitral valve (SAM) in apparently healthy cats in the absence of left ventricular hypertrophy (LVH) and examine the relationship between specific cardiac biomarker concentrations and echocardiographic parameters in these individuals. ANIMALS: eighty client-owned cats. MATERIALS AND METHODS: retrospective study; inclusion criteria were the presence of SAM on conscious echocardiography and concurrent measurement of plasma N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and serum cardiac troponin-I (cTnI). Cats were excluded if they had LVH, left atrial enlargement or systemic disease. The percentages of cats with NT-proBNP and cTnI concentrations above the normal reference range were calculated. The correlation between each biomarker concentration and left ventricular myocardial wall thickness, left atrial size and maximum left ventricular outflow tract velocity was evaluated. RESULTS: Thirty-four of 80 patients with SAM showed no evidence of cardiac remodelling (LVH or left atrial enlargement). Of these patients, 30 of 34 had elevated NT-proBNP, and cTnI was elevated in 13 of 27 (48.1%) cats where this biomarker was measured in association with the NT-proBNP assay. A positive correlation was observed between concentration of plasma NT-proBNP and maximum left ventricular outflow tract velocity (rs = 0.67, p<0.0001). No significant correlations were found between the concentration of biomarkers and the remaining echocardiographic parameters. CONCLUSIONS: SAM is frequently observed in cats even in the absence of cardiac remodelling, and these individuals often demonstrate elevated plasma NT-proBNP and serum cTnI concentrations. Plasma NT-proBNP elevation is correlated with the severity of the left ventricular outflow obstruction caused by SAM.

Pressure-induced left ventricular hypertrophy in canine model of aortic stenosis using nylon tie

The aim of this study was to develop an experimentally-induced canine model of left ventricular hypertrophy through banding of the ascending aorta using nylon ties. Seven clinically normal dogs free of cardiovascular disease were used. Nylon tie was used in banding the mid-ascending aorta. Clinical, radiographic and echocardiographic evaluations were done at 1.5, 3 and 6 months. Dogs were euthanized at 6 months for post mortem and histopathological evaluation. Clinically, dogs did not exhibit any signs of cardiovascular disease at 1.5 or 3 months, while at 6 months two dogs (28.6 %) exhibited mild weight loss, exercise intolerance and heart murmurs. Radiographic evaluation revealed significant increase in cardiac size only at 6 months based on measurement of the cardiothoracic area evaluation. Echocardiography revealed increased left ventricular wall thickness starting from 1.5 month, although this increase was statistically significant at 3 and 6 months (p > 0.05). Left ventricular hypertrophy was confirmed by post mortem examination. Histopathological sections of left ventricle in all dogs demonstrated myocyte hypertrophy and interstitial fibrosis. This model simulates the naturally occurring ventricular hypertrophy using a rapid and economic technique. Such models are required to understand pathogenesis of heart disease and to develop effective treatment strategy.

VGLL4 plays a critical role in heart valve development and homeostasis.

Heart valve disease is a major clinical problem worldwide. Cardiac valve development and homeostasis need to be precisely controlled. Hippo signaling is essential for organ development and tissue homeostasis, while its role in valve formation and morphology maintenance remains unknown. VGLL4 is a transcription cofactor in vertebrates and we found it was mainly expressed in valve interstitial cells at the post-EMT stage and was maintained till the adult stage. Tissue specific knockout of VGLL4 in different cell lineages revealed that only loss of VGLL4 in endothelial cell lineage led to valve malformation with expanded expression of YAP targets. We further semi-knockout YAP in VGLL4 ablated hearts, and found hyper proliferation of arterial valve interstitial cells was significantly constrained. These findings suggest that VGLL4 is important for valve development and manipulation of Hippo components would be a potential therapy for preventing the progression of congenital valve disease.

Diagnostic and prognostic utility of surface electrocardiography in cats with left ventricular hypertrophy.

OBJECTIVES: To assess the ability of electrocardiography (ECG) to predict left ventricular hypertrophy (LVH) in the cat and to investigate the prognostic value of selected ECG variables in cats with LVH. ANIMALS: Fifty-seven privately owned cats: 22 clinically healthy cats and 35 cats with LVH. MATERIAL AND METHODS: This is a clinical cohort study. Echocardiographic diagnosis and surface ECG were available. Electrocardiography analysis included rhythm diagnosis and specific electrocardiographic measurements. In cats with LVH, cause of death and outcome data were recorded and analyzed using Kaplan-Meier curves. RESULTS: The presence of arrhythmia had sensitivity and specificity of 31% and 100%, respectively, for identifying LVH. Among ECG measurements, duration of QT interval (QT) and QT interval corrected for heart rate (QTc) was statistically different between healthy cats and cats with LVH (p = 0.007). Overall, the most accurate cutoffs to identify LVH were QT > 170 ms (sensitivity and specificity 48.3% and 91%, respectively) and QTc > 188 ms (sensitivity and specificity 62% and 77%, respectively). In healthy cats, the highest QT and QTc values were 180 ms and 200 ms, respectively. Mean survival time was 58 days and indeterminable for cats with QT > 180 ms and QT ≤ 180 ms, respectively (p = 0.042) and 125 days and indeterminable for cats with QTc > 200 ms and QTc ≤ 200 ms, respectively (p = 0.017). CONCLUSIONS: Arrhythmias as well as prolonged QT and QTc are useful ECG parameters in identifying LVH and predicting survival in affected cats.

Transient Myocardial Thickening in Cats Associated with Heart Failure.

BACKGROUND: Cats with hypertrophic cardiomyopathy (HCM) and congestive heart failure (CHF) can have resolution of both left ventricular hypertrophy and CHF. OBJECTIVES: To describe the clinical characteristics of cats with transient myocardial thickening (TMT) and CHF compared with a control population of cats without resolution of HCM. ANIMALS: A total of 21 cats with TMT, 21 cats with HCM. METHODS: Retrospective study. Clinical records at 4 veterinary centers were searched for TMT cases and a control group of cats with HCM and CHF. TMT was defined as initial maximal left ventricular wall thickness (LVWT) ≥6 mm with left-sided CHF, with subsequent resolution of CHF, reduction in left atrium/aorta (LA/Ao), and LVWT<5.5 mm. HCM was defined as persistent LVWT ≥6 mm. RESULTS: Cats with TMT were younger (2 [0.4-11.4] years) than cats with HCM (8 [1.6-14] years) (P < 0.0001), and antecedent events were more common (15/21 versus 6/21, respectively) (P = 0.01). In cats with TMT, LVWT normalized from 6.8 [6.0-9.7] mm to 4.8 [2.8-5.3] mm and LA/Ao decreased from 1.8 [1.6-2.3] to 1.45 [1.2-1.7] after a mean interval of 3.3 (95% CI: 1.8-4.7) months. CHF recurred in 1 of 21 TMT and 15 of 21 cats with HCM. Cardiac treatment was discontinued in 20 of 21 cats with TMT and 0 of 21 HCM cats. All cats with TMT survived, whereas 8 of 19 cats with HCM died during the study period. CONCLUSIONS AND CLINICAL IMPORTANCE: TMT occurs in younger cats, and antecedent events are common. The prognosis is better in cats with CHF associated with TMT than HCM.

Echocardiographic and electrocardiographic parameters during the normal postpartum period in toy breeds of dogs.

The aim of this study was to evaluate echocardiographic and electrocardiographic parameters during the normal canine postpartum period. Twenty clinically healthy pregnant bitches of toy breeds (11 Miniature poodles, five Yorkshire terriers, two Maltese terriers and two Bichons Frises) were evaluated on days -3, 3, 10, 17, 24, 38, 52 and 80 relative to parturition (day 0). During the first postpartum week, the width of the interventricular septum in systole, the shortening fraction and the left atrium size decreased, while the left ventricle internal diameter in systole and end systolic stress increased. There were progressive decreases in the velocity of circumferential fibre shortening, stroke volume, cardiac output, and mitral E and A wave values. Systolic blood pressure increased markedly during the first postpartum week to gradually increase thereafter. Heart rate and corrected QT interval progressively decreased, while P wave amplitude increased. QRS complex amplitude decreased in the second week after parturition and then increased during the following weeks. In conclusion, there were changes in systolic function and some structural adaptive changes in the bitch during the first 80days postpartum. In addition, maternal heart rate and corrected QT interval decreased, while P wave and QRS amplitudes increased.

Left atrial volume and function in dogs with naturally occurring myxomatous mitral valve disease.

OBJECTIVE: Myxomatous mitral valve disease (MMVD) induces progressive left atrial (LA) enlargement. The LA modulates left ventricular filling and performance through its reservoir, conduit, and contractile function. Assessment of LA size and function may provide valuable information on the level of cardiac compensation. Left atrial function in dogs with naturally occurring MMVD remains largely unexplored. The objective of this study was to evaluate LA volume and function in dogs with naturally occurring MMVD. ANIMALS: This prospective study included 205 client-owned dogs of different breeds, 114 healthy dogs, and 91 dogs with MMVD of different disease severities. METHODS: Using two-dimensional echocardiography, the biplane area-length method was applied to assess LA volume and calculate volumetric indices of LA reservoir, conduit, and contractile function. RESULTS: Left atrial volume and LA stroke volume increased, whereas LA reservoir and contractile function decreased with increasing disease severity. A maximal LA volume <2.25mL/kg was the optimal cut off identified for excluding congestive heart failure in dogs with chronic MMVD with a sensitivity of 96% and a specificity of 100%. An active LA emptying fraction <24% and/or a LA expansion index <126% were suggestive of congestive heart failure in dogs with chronic MMVD with a sensitivity of 77% and a specificity of 89% and a sensitivity of 82% and a specificity of 82%, respectively. CONCLUSION: Dogs with MMVD appear to have larger LA volumes with poorer LA function. Deteriorating LA function, characterized by a decreasing reservoir and active contractile function, was evident in dogs with MMVD with increasing disease severity.

Antemortem Screening for Left Ventricular Hypertrophy in Rhesus Macaques (Macaca mulatta).

Concentric left ventricular hypertrophy (LVH) is a hallmark finding in hypertrophic cardiomyopathy that leads to diastolic dysfunction and variable cardiac consequences as severe as congestive heart failure and sudden cardiac death. LVH was diagnosed postmortem in a large colony of rhesus macaques (Macaca mulatta), but methods to screen and diagnose LVH in living animals are desired. We hypothesized that targeted echocardiography of macaques with a familial association of LVH would yield antemortem LVH diagnoses. We also hypothesized that cardiac biomarker levels would be higher in sudden-death LVH or occult LVH than controls and that cardiac troponin I (cTnI) levels would be higher in macaques housed outdoors than indoors. Sera were assayed for cardiac biomarkers (cTnI, C-reactive protein, creatinine kinase-MB, creatine phosphokinase, and LDH), in conjunction with echocardiography, after diagnosis by postmortem exam or from animals with different levels of exercise due to indoor compared with outdoor housing. None of the investigated biomarkers were associated with LVH. cTnI levels were significantly higher in serum collected from outdoor than indoor macaques. In addition, LVH was diagnosed in 29.4% of subjects with a familial association of LVH. These findings suggest that exercise may increase cTnI levels in rhesus macaques and that targeted echocardiography of rhesus macaques with a familial association of LVH was the most useful variable examined for disease surveillance.