Ventricular systolic dysfunction in dogs diagnosed with hypoadrenocorticism

In human patients with hypoadrenocorticism, a secondary dilated cardiomyopathy is noted that has been reported to resolve with replacement steroid therapy. A similar secondary dilated cardiomyopathy in dogs with hypoadrenocorticism has not been previously described. We present three dogs concurrently diagnosed with hypoadrenocorticism and ventricular dilation with systolic dysfunction. Two dogs were presented with clinical signs consistent with biventricular congestive heart failure and a third dog was presented with signs of acute hypoadrenocorticism without congestive heart failure. All dogs recovered to normal cardiac size and function with therapy. Hypoadrenocorticism should be considered as a differential diagnosis in dogs that present with ventricular dilation and systolic dysfunction if there are other indicators in the clinical and laboratory testing. Additionally, a thorough cardiac evaluation should be recommended for dogs that are found to have a heart murmur at the time of diagnosis of hypoadrenocorticism.     

An update on treatment and prognostic indicators in canine myxomatous mitral valve disease

Mitral regurgitation caused by myxomatous mitral valve disease is the most common cause for congestive heart failure and cardiac-related mortality in dogs. Typically, it takes several years for the disease to progress from mild, clinically silent myxomatous mitral valve disease to severe disease with signs of congestive heart failure. A proportion of dogs will never progress into congestive heart failure before they die from other causes or old age. Some variables have been shown to be predictive of onset of congestive heart failure and they might be useful to identify dogs that need more frequent monitoring and eventually treatment. Results from several controlled clinical trials are available concerning medical treatment of dogs with myxomatous mitral valve disease with or without congestive heart failure. These trials provide estimates of treatment effects and also allow identification of other variables with prognostic value for the outcome after the onset of congestive heart failure. Use of prognostic variables together with qualitative and quantitative results from clinical drug trials may aid the clinician and owner to plan and decide on optimal management of the myxomatous mitral valve disease dog. The purpose of this article is to review the current knowledge of prognostic variables and therapy for this common condition in dogs.     

Heart failure in two West Highland white terriers caused by congenital angiomatous cardiac anomaly

The paper describes the clinical and pathological characteristics of an unusual cystic congenital cardiac anomaly that caused clinical signs of congestive heart failure, respiratory distress and cardiac arrhythmias in two West Highland white terrier puppies. In both dogs a definitive diagnosis was made postmortem.     

Tricuspid valve stenosis caused by fibrous adhesions to an endocardial pacemaker lead in a dog

Acquired tricuspid valve stenosis (TVS) is a rare complication of endocardial lead placement in humans that has not been described in the veterinary literature. We describe a 6.5-year-old Border terrier that was presented with right-sided congestive heart failure 5.5 years after placement of a transvenous pacemaker. Severe TVS was confirmed by cardiac ultrasonography and appeared to be secondary to excessive endocardial pacemaker lead within the right atrium. Repositioning of the lead proved impossible and subsequent postmortem examination demonstrated fusion of the tricuspid valve (TV) leaflets around the endocardial lead with associated narrowing of the tricuspid valve orifice. In addition, the loop of the endocardial lead was anchored by thick fibrous tissue to the right atrial wall. This case report suggests that if sufficient endocardial lead is left inside the heart, in dogs undergoing transvenous pacemaker therapy, the redundant lead can become adherent to the tricuspid valve apparatus and cause valvular stenosis.     

Echocardiographic and clinical signs of canine dilated cardiomyopathy

The clinical signs, electrocardiograms and echocardiograms of 12 dogs with dilated cardiomyopathy of large breeds and congestive heart failure were reviewed. There was a high prevalence of males (11 dogs) and of the Doberman breed (7 dogs). Seven dogs had atrial fibrillation. The echocardiograms revealed significant increases in left ventricular and left atrial dimensions. The shortening fraction (%ΔD), aortic root excursion and left ventricular wall excursion were all significantly decreased, documenting a decrease in contractile function of the left ventricle that, together with the cardiac enlargement characterize this disease. The advantages of obtaining these functional parameters non-invasively are emphasized.     

Ischaemic heart disease in the dog: a review of 65 cases

Sixty-five dogs are reviewed with histopathologically confirmed intramural arteriosclerosis. Clinical data (clinical signs, electrocardiographic findings and ultrasound parameters) on these animals were collected from nine small animal clinics in Sweden: 16 dogs had died suddenly, with few or no previous clinical signs; 13 dogs died or were euthanased during or shortly after general anaesthesia or sedation; 30 dogs developed acute (14) or chronic (16) congestive heart failure; and six dogs died or were euthanased for causes unrelated to cardiac disease. Electrocardiography of 23 of the dogs revealed several types of arrhythmias, with atrial fibrillation and sinus tachycardia being most commonly detected. Ultrasonographic examinations of 24 dogs found a relatively high number (19) with decreased indices of contractility. Dogs that had died suddenly and in relation to general anaesthesia or sedation had a higher incidence (25 of 29) of purely arteriosclerotic changes in the myocardial vessels, whereas just over half the dogs with congestive heart failure (16 of 30) had other concomitant heart lesions (in most cases endocardiosis). The incidence of myocardial infarcts was high (51 of 65 cases). It is postulated that arteriosclerosis in the dog may be an important reason for sudden death and death during general anaesthesia. Coronary arterial disease should also be a consideration in the clinical evaluation of dilated cardiomyopathy and may contribute to the decreased myocardial contractility when it is present in dogs with mitral regurgitation.     

Right ventricular aneurysm and atrial septal defect in a cat

This case report shows the development of a right ventricular aneurysm in a cat with a large atrial septal defect. Despite this complex cardiac pathology, the cat lived normally for more than 4 years and developed fatal congestive heart failure.     

Canine hypertrophic cardiomyopathy.

Necropsy findings in 10 dogs with naturally occurring cardiac disease closely resembled hypertrophic cardiomyopathy in human beings and cats. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Ratios of septum to free wall thickness in the 10 dogs ranged from 1.1 to 1.5, and 6 had ratios greater than or equal to 1.3. Marked cardiac muscle cell disorganization in the ventricular septum, characteristic of human patients with hypertrophic cardiomyopathy, was found in only 2 of the 10 dogs. Death occurred while the dogs were under anesthesia during the course of operative procedures (5 dogs) or unexpectedly in animals without previous manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. Two of these 4 dogs with heart failure and 1 dog that died during unrelated surgery, but without prior signs of heart disease, had electrocardiographic evidence of complete heart block.     

Can ventricular function be assessed by echocardiography in chronic canine mitral valve disease?

Mitral regurgitation (MR) related to chronic degenerative valvular disease is the most important cause of heart failure in dogs. Ultrasound examination of the heart can identify valve lesions, confirm the presence of valvular regurgitation, document cardiac remodeling, estimate intracardiac pressures, and quantify systolic ventricular function. These findings can influence prognosis or selection of medical therapy. Reductions in ventricular systolic function may be detected on serial echocardiographic examinations in some dogs with MR. However the changes in ventricular loading that accompany MR often complicate these measurements. For example, shortening and ejection fractions are often increased in severe MR, even in the setting of congestive heart failure. Echocardiography with Doppler is also used to assess ventricular diastolic function and filling pressures. This information helps predict the risk of congestive heart failure. However these findings are often rendered ambiguous by age-related impairment of ventricular relaxation, elevations in left atrial pressure due to MR, and effects of volume overload on myocardial tissue velocities. These factors limit the usefulness of ventricular filling and tissue velocities, as well as derived ratios such as the E/E' ratio, for predicting congestive heart failure in MR. More advanced Doppler and tissue echocardiographic methods, as well as prospective clinical studies, are needed to reduce the ambiguity involved with assessment of ventricular function and filling pressures in the setting of MR.     

Association between exogenous atrial natriuretic peptide and hemodynamics in dogs with congestive heart failure produced by experimental mitral regurgitation

Association between exogenous atrial natriuretic peptide (ANP) and hemodynamic changes was ascertained in 3 dogs with overt congestive heart failure (CHF(+)) and 3 dogs without congestive heart failure (CHF(-)) caused by experimental mitral regurgitation (MR). The hemodynamic measurements were recorded in all dogs during and after 1 hr infusion of ANP at the rate of 0.1 (low dose), 0.5 (medium dose) and 1.0 (high dose) microg/kg/min, respectively. Heart rate, mean arterial pressure, pulmonary capillary wedge pressure (PCWP) and systemic vascular resistance decreased significantly during and after ANP infusion even with low dose in the CHF(+). Stroke volume, stroke volume index and cardiac output in the CHF(+) during and after ANP infusion showed an increasing trend as compared with the CHF(-). Double product, an indicator of myocardial oxygen consumption, significantly decreased during and after ANP administration at all doses in the CHF(+). These findings indicate that even at low dose, exogenous ANP improves cardiac performance and reduces myocardial oxygen consumption in the CHF(+), and suggest that ANP has beneficial effects in the treatment of dogs with overt congestive heart failure resulting from MR.     

Evaluation of circulating amino terminal-pro-B-type natriuretic peptide concentration in dogs with respiratory distress attributable to congestive heart failure or primary pulmonary disease

OBJECTIVE: To evaluate assessment of circulating amino terminal-pro-B-type natriuretic peptide (NT-proBNP) concentration as a means to discriminate between congestive heart failure and primary pulmonary disease in dogs. DESIGN: Prospective case series. ANIMALS: 46 dogs with signs of respiratory distress or coughing. PROCEDURES: All dogs underwent physical and thoracic radiographic examinations. Dogs with evidence of heart disease (eg, murmur, arrhythmia, or large cardiac silhouette detected by radiography) also underwent echocardiography. Dogs with no evidence of heart disease or failure were included if they underwent bronchoalveolar lavage (with cytologic examination and bacterial culture of the lavage fluid). Blood samples for NT-proBNP assay were obtained within 12 hours of the diagnosis of heart failure or prior to bronchoalveolar lavage in dogs with primary pulmonary disease. Circulating concentrations of NT-proBNP were compared between groups and correlated with radiographic and echocardiographic measures of cardiac size. RESULTS: Congestive heart failure and primary pulmonary disease were diagnosed in 25 and 21 dogs, respectively. Dogs with congestive heart failure had significantly higher median serum or plasma NT-proBNP concentration (2,554 pmol/L; interquartile [25% to 75%] range, 1,651.5 to 3,475.5 pmol/L) than dogs with primary pulmonary disease (357 pmol/L; interquartile range, 192.5 to 565.5 pmol/L). Radiographic vertebral heart score and echocardiographic left atrial-to-aortic diameter ratio were not correlated with NT-proBNP concentration. Left ventricular end-diastolic diameter (measured echocardiographically) and NT-proBNP concentration were weakly correlated. CONCLUSIONS AND CLINICAL RELEVANCE: Serum or plasma NT-proBNP concentration assessment may be useful for discrimination of congestive heart failure from primary pulmonary disease in dogs with respiratory distress or cough.     

Arrhythmogenic right ventricular cardiomyopathy in a dog

An 8-month-old Labrador retriever bitch was evaluated for sudden-onset, progressive abdominal distension. Physical examination revealed an exaggerated inspiratory effort, severe ascites, bilateral jugular vein distension, and hypokinetic femoral arterial pulses. Thoracic auscultation detected tachycardia with muffled heart sounds, without audible cardiac murmurs. Thoracic radiographs identified severe right ventricular enlargement and pleural effusion. The electrocardiogram was consistent with incomplete right bundle branch block or right ventricular enlargement. Echocardiography demonstrated severe right ventricular and atrial dilation, secondary tricuspid regurgitation, and thinning and hypocontractility of the right ventricular myocardium. Left heart chamber sizes were slightly decreased, with normal left ventricular contractility. A diagnosis of arrhythmogenic right ventricular cardiomyopathy was reached, based on the characteristic clinical, electrocardiographic, radiographic and echocardiographic findings, and the exclusion of other causes of isolated right ventricular failure. Treatment effected good control of clinical signs, until acutely decompensated congestive right heart failure led to euthanasia after 4 months. Arrhythmogenic right ventricular cardiomyopathy is a well-described clinical entity in humans, and has previously been documented in 3 male dogs. The condition is characterised by progressive fibro-adipose replacement of right ventricular myocardium, while the left ventricle usually remains unaffected. It should be considered a differential diagnosis in any young dog presented with isolated right heart failure, syncope, or unexplained ventricular tachyarrhythmias. This article reports the 1st case of arrhythmogenic right ventricular cardiomyopathy in a female dog, and highlights its echocardiographic features.     

Aortic body carcinoma and myocardial infarction in a dobermann pinscher

Dilated cardiomyopathy is the usual cause of congestive heart failure in the dobermann pinscher and was the presumptive diagnosis in an eight-year-old female dobermann pinscher presented for dyspnoea and syncope. This was supported by thoracic radiography and electrocardiographic evidence of ventricular tachycardia. An echocardiogram revealed a left atrial tumour as the principal cause of cardiac failure. Pathological examination confirmed that the tumour was a large aortic body carcinoma in an unusual location. Multifocal myocardial infarctions were also found. This unusual case demonstrates the importance of a complete cardiological examination as part of a diagnostic work up and confirms the necessity of echocardiography as one of the examination methods.     

Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study

Background: Myxomatous mitral valve disease (MMVD) continues to be an important cause of morbidity and mortality in geriatric dogs despite conventional therapy. Hypothesis: Pimobendan in addition to conventional therapy will extend time to sudden cardiac death, euthanasia for cardiac reasons, or treatment failure when compared with conventional therapy plus benazepril in dogs with congestive heart failure (CHF) attributable to MMVD. Animals: Two hundred and sixty client‐owned dogs in CHF caused by MMVD were recruited from 28 centers in Europe, Canada, and Australia. Methods: A prospective single‐blinded study with dogs randomized to PO receive pimobendan (0.4–0.6 mg/kg/d) or benazepril hydrochloride (0.25–1.0 mg/kg/d). The primary endpoint was a composite of cardiac death, euthanized for heart failure, or treatment failure. Results: Eight dogs were excluded from analysis. One hundred and twenty‐four dogs were randomized to pimobendan and 128 to benazepril. One hundred and ninety dogs reached the primary endpoint; the median time was 188 days (267 days for pimobendan, 140 days for benazepril hazard ratio = 0.688, 95% confidence limits [CL] = 0.516–0.916, P= .0099). The benefit of pimobendan persisted after adjusting for all baseline variables. A longer time to reach the endpoint was also associated with being a Cavalier King Charles Spaniel, requiring a lower furosemide dose, and having a higher creatinine concentration. Increases in several indicators of cardiac enlargement (left atrial to aortic root ratio, vertebral heart scale, and percentage increase in left ventricular internal diameter in systole) were associated with a shorter time to endpoint, as was a worse tolerance for exercise. Conclusions and Clinical Importance: Pimobendan plus conventional therapy prolongs time to sudden death, euthanasia for cardiac reasons, or treatment failure in dogs with CHF caused by MMVD compared with benazepril plus conventional therapy.     

Diagnosis and treatment of congestive heart failure secondary to dilated cardiomyopathy in a hedgehog

A one‐year‐old African pygmy hedgehog (Atelerix albiventris) was evaluated for severe respiratory distress. Physical examination findings included marked dyspnoea, cyanosis and tachypnoea. Radiographic findings included an enlarged heart and pulmonary oedema, and dilated cardiomyopathy was confirmed via echocardiogram. The patient was treated for congestive heart failure because of dilated cardiomyopathy with furosemide, enalapril, pimobendan and l‐carnitine. Within 24 hours of treatment, the pulmonary oedema and cyanosis had resolved. Following discharge, clinical improvement was noted by the owner and echocardiogram confirmed improved fractional shortening. Cardiomyopathy has been reported at post‐mortem examination in hedgehogs, but there are no reports of ante‐mortem diagnosis and treatment. Performing baseline cardiac assessment in hedgehogs is recommended, and treatment with l‐carnitine and pimobendan may improve outcome, as carnitine deficiency is a possible cause of cardiomyopathy in hedgehogs. Successful emergency treatment of congestive heart failure in the hedgehog of this report may be effective for other hedgehogs presented with similar clinical signs .     

Hybrid cutting balloon dilatation for treatment of cor triatriatum sinister in a cat

A hybrid surgical approach and balloon dilatation were performed successfully in a cat with cor triatriatum sinister and clinical signs of congestive heart failure. Left lateral thoracotomy was used to access the heart and cutting balloon followed by standard balloon dilatation were utilized to dilate the perforation in the anomalous left atrial membrane. Clinical signs resolved completely after dilation of the anomalous left atrial membrane. Based upon the outcome of this case, balloon dilatation appears to be a viable treatment option for cats affected with cor triatriatum sinister.     

Therapeutic trial of granulocyte-colony stimulating factor for dilated cardiomyopathy in three dogs

Three dogs were presented to us for evaluation of cardiac problems. Electrocardiographic recordings revealed severe tachyarrhythmia and atrial fibrillation with ventricular tachycardia in 2 of the 3 dogs. The echocardiographic findings of the 3 dogs revealed markedly decreased fractional shortening and a marked increase in E-point septal separation. Based on the results of electrocardiographic and echocardiographic evaluation, the 3 dogs were diagnosed as dilated cardiomyopathy (DCM). The dogs were treated with conventional cardiac medication, but cardiac function did not improve and the clinical signs remained. We subsequently attempted treatment with granulocyte-colony stimulating factor (G-CSF; 10 microg/kg, subcutaneously). The specific purpose of G-CSF therapy for DCM was to improve cardiac function and a significant improvement in cardiac function was confirmed. The three dogs had no treatment side effects. This case report suggests that G-CSF might have therapeutic effects for medically refractory DCM in dogs.     

Use of the loop diuretic torsemide in three dogs with advanced heart failure

Diuretics are a mainstay of therapy in dogs with heart failure. In dogs with advanced heart failure, moderate to high doses of loop diuretics such as furosemide are used with diminishing effects as profound activation of neuroendocrine systems promote signs of congestive heart failure. The loop diuretic torsemide has several characteristics that make it suitable for treatment of advanced heart failure including longer half-life, increased potency of diuretic action, and anti-aldosterone effects. This case report details the administration of torsemide in 3 dogs with advanced heart failure and apparent furosemide resistance.