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.

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.

[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.

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.

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.

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.

Sensibilidade e especificidade do exame eletrocardiográfico na detecção de sobrecargas atriais e/ou ventriculares em gatos da raça Persa com cardiomiopatia hipertrófica / Sensitivity and specificity of electrocardiographic examination in detecting ventricular or atrial overloads in Persian cats with hypertrophic cardiomyopathy

A cardiomiopatia hipertrófica (CMH) é a principal cardiopatia dos felinos e é caracterizada por hipertrofia miocárdica concêntrica, sem dilatação ventricular. O ecocardiograma é o melhor meio diagnóstico não invasivo para a diferenciação das cardiomiopatias e é considerado padrão ouro para a detecção de hipertrofia ventricular presente na CMH. Alterações eletrocardiográficas também são comuns em animais com CMH e o eletrocardiograma (ECG) é um teste de triagem para detecção de hipertrofia ventricular em humanos, sendo um exame rápido e facilmente disponível. Em gatos, poucos estudos foram realizados quanto à sensibilidade e especificidade do ECG na detecção de hipertrofia ventricular. Com a intenção de avaliar o uso do ECG como ferramenta de triagem para diagnóstico de CMH em felinos, gatos da raça Persa (n=82) foram avaliados por meio de exames ecocardiográfico e eletrocardiográfico. Animais com bloqueios e/ou distúrbios de condução foram excluídos da análise estatística (n=22). Posteriormente, os animais incluídos foram classificados em: normais (n=38), suspeitos (n=6) e acometidos pela CMH (n=16)...

Hypertrophic cardiomyopathy (HCM) is the most common feline heart disease and is characterized by increased cardiac mass with a hypertrophied and not dilated left ventricle. The echocardiography is the best noninvasive diagnostic tool for the differentiation of cardiomyopathies and is considered the gold standard for detection of ventricular hypertrophy present in HCM. Electrocardiographic changes are also common in animals with HCM and the electrocardiogram (ECG) is quick, easy and highly available screening test for the detection of ventricular hypertrophy in humans. In cats, few studies have been conducted regarding the sensitivity and specificity of ECG in detecting ventricular hypertrophy. With the intention of evaluating the use of ECG as a screening tool for diagnosis of HCM in cats, Persian cats (n=82) were evaluated by echocardiographic and electrocardiographic examinations. Animals with blocks and/or conduction disturbances were excluded from statistical analysis (n=22). Subsequently the animals included were classified as normal (n=38), suspicious (n=6) and affected by HCM (n=16)...

[Mitral valve dysplasia in a cat causing reversible left ventricular hypertrophy and dynamic outflow tract obstruction]. / Mitraalklepdysplasie als oorzaak voor een reversibele hypertrofie en dynamische uitstroombaanobstructie van de linker ventrikel bij een kat.

A 6-month-old male European shorthair cat was examined because of a 2/6 systolic left apical cardiac murmur. Echocardiography revealed severe concentric left ventricular hypertrophy and severe dynamic left ventricular outflow tract obstruction (pressure gradient of 85 mmHg) caused by systolic anterior motion (SAM) of the septal mitral valve leaflet. After 2 months of oral treatment with atenolol, the cardiac murmur had disappeared. Echocardiography showed only slight thickening of the interventricular septum and resolution of the pressure gradient. The cat was discharged and its owner was advised to continue atenolol lifelong. Echocardiographic findings of a combination of left ventricular concentric hypertrophy and dynamic left ventricular outflow tract obstruction can be caused by hypertrophic obstructive cardiomyopathy (HOCM) or mitral valve dysplasia in the absence of hypertension and fixed aortic stenosis. In the case of HOCM, left ventricular hypertrophy is the primary process. In the case of mitral valve dysplasia, systolic anterior motion of the mitral valve is the primary problem, which leads to dynamic left ventricular outflow tract obstruction and ultimately to left ventricular concentric hypertrophy, due to pressure overload. If the left ventricular outflow tract obstruction is reduced with an oral beta-receptor blocker the secondary left ventricular hypertrophy may resolve. This would not happen in the case of hypertrophic obstructive cardiomyopathy. To the best of the authors' knowledge, this is the first documented case of severe dynamic left ventricular outflow tract obstruction and severe left ventricular hypertrophy in a cat successfully treated with oral atenolol.

Signs of left heart volume overload in severely anaemic cats.

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<0.005) and severely anaemic cats also had a larger median left ventricular end-diastolic diameter (1.80cm versus 1.27cm, respectively; P<0.05). No difference was found between the groups in VHS or frequency of radiographic signs of CHF. Despite the small sample size, these preliminary findings suggest that severely anaemic cats are more likely to have enlarged left heart dimensions than mildly anaemic cats.

Left ventricular hypertrophy is prevalent in Sprague-Dawley rats.

Unrecognized cardiovascular abnormalities may confound the interpretation of research data collected using rats. However, although SPF rat colonies are screened for microbes and kept under standardized environmental conditions, their cardiovascular status is largely unknown. We recently performed surgery on anesthetized 80-d-old Sprague-Dawley rats and observed a high mortality that could not be attributed to the procedures or preceding treatments. Upon necropsy, cardiomyopathy was readily apparent in a substantial proportion of these rats. To further evaluate the nature of this condition, we evaluated the histology and morphology of hearts from both Sprague-Dawley and Lewis rats. Compared with Lewis rats, Sprague-Dawley rats had greater left ventricular wall thickness and larger cardiomyocyte cell size. Severe left ventricle hypertrophy was present in 38% of young adult Sprague-Dawley rats. These findings may have implications for research models that use Sprague-Dawley rats.

Evaluation of the renin-angiotensin system in cardiac tissues of cats with pressure-overload cardiac hypertrophy.

OBJECTIVE: To clarify regulation of the renin-angiotensin (RA) system in cardiac tissues by measuring angiotensin-converting enzyme (ACE) and chymase activities in cats with pressure-overload cardiac hypertrophy. ANIMALS: 13 adult cats. PROCEDURES: Pressure-overload cardiac hypertrophy was induced by coarctation of the base of the ascending aorta in 6 cats, and 7 cats served as untreated control animals. Cats were examined before and 3 months and 2 years after surgery. Two years after surgery, cardiac hypertrophy was confirmed by echocardiography, and the blood pressure gradient was measured at the site of constriction. Cats were euthanized, and ACE and chymase activities were measured in cardiac tissues. RESULTS: Mean +/- SD pressure gradient across the aortic constriction was 63 +/- 6 mm Hg. Chymase activity predominated (75% to 85%) in the RA system of the cardiac tissues of cats. Fibrosis in the wall of the left ventricle was detected in cats with hypertrophy, and fibrosis of the papillary muscle was particularly evident. CONCLUSIONS AND CLINICAL RELEVANCE: Chronic pressure overload on the heart of cats can activate the RA system in cardiac tissues. A local increase in angiotensin II was one of the factors that sustained myocardial remodeling.

Effects of enalapril in cats with pressure overload-induced left ventricular hypertrophy.

In order to evaluate the effect of enalapril on haemodynamics and renal function in a pressure overload model, we prepared eight feline models of left ventricular hypertrophy (LVH) by banding of the aortic arch. The LVH cats were assigned to the placebo group or the enalapril group (0.5 mg/kg, PO, sid) 3 months following surgery, and each received its respective drug for 4 weeks. Each week, blood pressure, angiotensin converting enzyme (ACE) activity in blood, and creatinine clearance were measured, and complete blood count (CBC), biochemical examination of the blood, echocardiography, and chest radiography were carried out. The interventricular septum thickness (IVSd, IVSs), fractional shortening (FS), and ejection fraction (EF) increased significantly in the LVH cats following surgery (P<0.05). There was no significant difference between the placebo group and the enalapril group with respect to general physical parameters, CBC, biochemical parameters and renal function. In the enalapril group, systolic arterial pressure, mean arterial pressure, and ACE activity in blood decreased significantly following administration (P<0.05). In addition, the left ventricular free wall thickness in diastole and IVSd decreased significantly following administration (P<0.05). These results suggest that, in a pressure overload model, enalapril (0.5 mg/kg, sid) inhibits cardiac hypertrophy, reduces blood pressure, and does not adversely affect renal function.

Effect of pravastatin on left ventricular mass by activation of myocardial K ATP channels in hypercholesterolemic rabbits.

Epidemiological studies showed that hypercholesterolemia was associated with a higher left ventricular mass. Myocardial ATP-sensitive potassium (K(ATP)) channels have been implicated in the development of cardiac hypertrophy. We investigated the effect of pravastatin on hypercholesterolemia-induced ventricular hypertrophy and whether the attenuated hypertrophic effect was via activation of myocardial K(ATP) channels. In this study, we evaluated the hemodynamic, biochemical, and morphological responses to pravastatin in cholesterol-fed (1%) rabbits. Male New Zealand White rabbits were randomized to either vehicle, nicorandil (an agonist of K(ATP) channels), pravastatin, glibenclamide (an antagonist of K(ATP) channels), or a combination of nicorandil and glibenclamide or pravastatin and glibenclamide for 8 weeks. The left ventricular weight and left ventricular myocyte sizes increased 8 weeks after cholesterol-feeding in comparison to that in normocholesterolemic rabbits. Pravastatin administration significantly decreased the left ventricular weight by 12% and cardiomyocyte cell areas by 30%. Hyperlipidemic rabbits in the nicorandil- and pravastatin-treated groups significantly attenuated cardiomyocyte hypertrophy, as compared with the vehicle-treated group (3162 +/- 277 microm(2), 3372 +/- 228 microm(2) versus 4388 +/- 163 microm(2) in the vehicle group, both P < 0.0001, respectively). Nicorandil-induced effects were abolished by administering glibenclamide. Similarly, pravastatin-induced beneficial effects were reversed by the addition of glibenclamide, implicating K(ATP) channels as the relevant target. The results of the present study suggest a pathogenetic role of K(ATP) channels in hypercholesterolemia-induced ventricular hypertrophy. The antihypertropic effects of pravastatin may be related to activation of K(ATP) channels, and result in an amelioration of cardiomyocyte hypertrophy development by an atherogenic diet.