Congestive heart failure associated with myxomatous degeneration of the left atrioventricular valve in a parakeet

Congestive heart failure was diagnosed in a 27-year-old Indian ringneck parakeet with exercise-induced dyspnea. A grade IV/VI holosystolic murmur that radiated to the right sternal area was auscultated over the left side of the sternum. Radiography revealed progressive cardiomegaly, hepatomegaly, pulmonary edema, and accumulation of fluid within the coelomic cavity. Echocardiography revealed biatrial enlargement and enlargement of the right ventricle. Doppler recording revealed high velocity left and right atrioventricular valve regurgitation. Treatment with digoxin and furosemide alleviated clinical signs for approximately 10 months. Gross postmortem examination revealed cardiac enlargement and eccentric hypertrophy of both ventricles on cross-section. Pulmonary congestion and edema, hepatomegaly, hepatic congestion, and ascites were also evident. Histologic examination of the heart revealed myxomatous degeneration of the left atrioventricular valve, muscular hypertrophy of the right atrioventricular valve, and biventricular chronic myofiber degeneration and necrosis.     

Aorticopulmonary septal defect in a German shepherd dog

A 2-year-old, female German shepherd dog was referred with a 2-month history of dyspnea, ascites, and anorexia. On physical examination, an arrhythmia, tachypnea, and a continuous grade V/VI heart murmur were evidenced. Atrial fibrillation and tall R waves were noted on electrocardiography. Survey thoracic radiography revealed generalized cardiomegaly and enlarged pulmonary vessels. Echocardiography demonstrated severe dilatation of the left atrium and ventricle with reduced fractional shortening. Doppler echocardiography showed continuous and turbulent flow in the ascending aorta between the aorta and the pulmonary artery. Necropsy demonstrated an aorticopulmonary septal defect.     

Congestive heart failure and atrial fibrillation in a cat with myocardial fibro-fatty infiltration

Congestive heart failure and atrial fibrillation were diagnosed in a 4-year-old castrated Birman cat with progressive signs of dyspnea, tachypnea, and lethargy. Echocardiography revealed massive right-sided heart dilatation with ascites and hydrothorax. Electrocardiogram recording showed atrial fibrillation. Medical therapy with diuretics, benazepril, and antithrombotic agents was unsuccessful. The owner requested euthanasia. In post-mortem examination, changes associated with myocardial fibro-fatty infiltration were confirmed. Changes were most marked in the right ventricular wall but with left ventricular involvement was detected.     

Pulmonary hypertension and right-sided heart failure in an adult llama with hepatic disease

CASE DESCRIPTION: A 13-year-old llama was examined because of lethargy, inappetence, and syncope. CLINICAL FINDINGS: Physical examination revealed muffled heart and lung sounds and peripheral edema. Clinicopathologic abnormalities included lymphopenia, hyperglycemia, prerenal azotemia, mild hyponatremia, mild hypoalbuminemia, and high gamma-glutamyltransferase and creatine kinase activities. On ultrasonography, the liver appeared hyperechoic and ascites and pleural effusion were seen. Echocardiography revealed severe dilatation of the right atrium, right ventricle, and pulmonary artery; severe tricuspid regurgitation; and high right ventricular systolic pressure consistent with right-sided heart failure secondary to pulmonary hypertension. TREATMENT AND OUTCOME: Treatment with furosemide was attempted, but because of failing health, the llama was euthanized 4 weeks later. Macronodular cirrhosis of the liver, glomerulonephritis, and intimal fibrosis and medial hypertrophy of muscular pulmonary arteries were seen on histologic examination of postmortem specimens. CLINICAL RELEVANCE:Findings in this case were similar to those reported for human patients with portopulmonary hypertension secondary to hepatic cirrhosis. Pulmonary hypertension secondary to hepatic disease should be considered in the differential diagnosis of right-sided heart failure.     

Cor triatriatum sinister in a cat

A heart murmur was detected in a five-month-old Persian chinchilla cat. The animal was referred to Nihon University Animal Medical Center where radiographic examination revealed an enlarged heart with dilation of pulmonary arteries and veins and pulmonary oedema. Echocardiography revealed partition of the left atrium, with turbulent blood flow within the left atrium. The patient was placed under continuous care at the facility, but died at seven months of age. Postmortem examination revealed that the left atrium was partitioned by a fibromuscular septum, with a 1 mm diameter perforation, consistent with a diagnosis of cor triatriatum sinister.     

Mitral valve and tricuspid valve dysplasia in a 9‐week‐old Standardbred colt

A 9‐week‐old Standardbred colt was presented for investigation of dull demeanour, exercise intolerance and heart murmurs. Cardiac auscultation revealed a grade 5/6 holosystolic murmur and a grade 5/6 pansystolic murmur over the left and right cardiac apex respectively, and an irregularly irregular cardiac rhythm. Electrocardiographic examination findings were consistent with atrial fibrillation and tachycardia. Echocardiographic examination identified marked atrioventricular regurgitation and atrial dilation bilaterally, thickening of the mitral and tricuspid valves and dilation of the pulmonary artery consistent with pulmonary hypertension. No ventricular or atrial septal defect was present. Cardiomegaly and diffuse pulmonary oedema were evident on examination of lateral thoracic radiographs. Dysplasia of the mitral and tricuspid valves, eccentric cardiomegaly and pulmonary oedema were confirmed by post mortem examination. Dysplasia of the atrioventricular valves represents a rare cause of biventricular failure in the horse.     

Primary cardiac fibrosarcoma with pulmonary metastasis in a Labrador Retriever

A 6-year-old, neutered male Labrador Retriever was diagnosed with congestive heart failure, and an echocardiogram revealed a large mass inside the pericardial sac associated with the left ventricle. At necropsy, the dog had marked ascites, mild hydrothorax, marked hydropericardium, and an 11.0 x 7.0 x 6.0 cm, tan and red, firm, well-demarcated mass attached to the left ventricular free wall. The mass was diagnosed as a fibrosarcoma based on the morphologic appearance and supportive immunohistochemical staining. To our knowledge, this is the first case report of a primary fibrosarcoma involving the left ventricular free wall myocardium, epicardium, and pericardium with a pulmonary metastasis in a dog.     

Congestive heart failure associated with hyperthyroidism in cats

Hyperthyroidism was diagnosed in 4 cats with congestive heart failure. Dyspnea and anorexia were observed in 3 of the 4 cats. In each cat, a holosystolic left and/or right apical heart murmur was auscultated. In 3 cats, a prominent extra heart sound (gallop rhythm) was auscultated. All cats had a palpably large thyroid lobe(s) and weight loss. The laboratory and ECG changes were similar to those reported for feline hyperthyroidism. Moderate-to-severe pleural effusion and cardiomegaly were detected via radiography in all cats. Some cats had radiographic signs of pulmonary venous engorgement and pulmonary edema. Echocardiography revealed cardiac dilatation and low left ventricular shortening fraction (wall motion) in all cats. Three cats responded initially to cardiac drugs and propylthiouracil or thyroidectomy. One of these died later, presumably from an adverse reaction to propylthiouracil, and the others died from recurrent congestive heart failure (1) or postoperative cardiac arrest (1). One cat did not respond to treatment, and died 2 days after diagnosis.     

Pathogenesis of ascites in broilers raised at low altitude: aetiological considerations based on echocardiographic findings

This study reports novel insight into the aetiology of pulmonary hypertension and ascites in broiler chickens. The scope of measurements was focused on anatomical and functional parameters, and blood flow patterns in leghorns (resistant to ascites), fast-growing broilers (susceptible to ascites), broilers developing ascites, and ascitic broilers evaluated in vivo using echocardiography, and further examined in the context of postmortem findings. Both, in vivo observed features and postmortem findings, showed clear differences between broilers and leghorns, and between normal and ascitic broilers. Abnormalities in the heart chamber geometry and blood flow patterns were detected upon echocardiographic examination in all ascitic broilers. Right and left atrio-ventricular (AV) valve regurgitation were common findings in ascitic broilers and some apparently normal broilers, with left AV valve insufficiency being a predominant feature with respect to degree and frequency of occurrence. Blood flow disturbances were not detected in leghorns. Left ventricular fractional shortening (functional parameter) was considerably reduced (P < 0.01) in ascitic birds (mean: 21.7 +/- 2.0 SE) in comparison with normal broilers (mean: 39.1 +/- 3.6 SE), or leghorns (mean: 43.3 +/- 2.4 SE). The presented findings indicate that pathological and functional changes in the left ventricle and atrium play a significant role in the pathogenesis of ascites in broilers. Severe dilation of the left atrium and pulmonary veins seen on postmortem examination, as well as regurgitant blood flow in the left atrium, demonstrated by Doppler study in ascitic birds, provide evidence that chronically elevated pressure in the left atrium is involved in the aetiology of pulmonary hypertension and ascites in fast-growing broilers.     

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.     

Congenital cardiac disease in dogs

Ventricular septal defect (VSD) generally occurs high in the membranous septum rather than lower in the muscular portion. The English Bulldog and Siberian Husky may be predisposed. Clinical signs include a holosystolic or crescendo-decrescendo murmur best heard low on the right side at the 3rd-4th intercostal space and, with large defects, pulmonary congestion, exercise intolerance, cyanosis and ascites. The ECG is normal unless the right ventricle is hypertrophied, which causes right axis deviation and other electrocardiographic signs of right-sided heart enlargement. Plain film thoracic radiographs reveal signs of right-sided heart enlargement but often are not diagnostic. Nonselective angiocardiography is often not useful in diagnosing VSD with a left-to-right shunt of blood. Selective angiocardiography, in which contrast medium is injected directly into the left ventricle via a catheter, is the method of choice for diagnosis of VSD. Dogs with a small VSD remain asymptomatic, but those with large defects require surgical correction with a prosthetic septal pathic or pulmonary artery band.     

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 .     

Suspected monensin toxicosis in feedlot cattle

Suspected monensin toxicosis was seen in feedlot cattle aged 6 to 9 months. Twenty cattle died following inclusion of monensin in the feed at 400g/tonne, which was 13 times the recommended level. The deaths occurred over 2 weeks. Clinical signs were inappetance, respiratory distress and sudden death. Post-mortem features were those of right-sided heart failure and included dependent subcutaneous oedema, ascites, hydrothorax, and periancinar hepatocyte congestion and necrosis. However, in contrast to previous reports no myocardial necrosis was found, but focal skeletal muscle necrosis was observed. Additional findings were marked pulmonary oedema accompanied by fibrin and erythrocyte exudation into alveoli and interlobular lymphatics. From these findings it appears that monensin, as well as affecting both cardiac and skeletal muscle, has a primary effect on lung vasculature.     

Diagnosis of pulmonary thromboembolism in a cat using echocardiography and pulmonary scintigraphy

A 10-year-old male cat was presented with sudden onset of respiratory difficulties. Clinical examinatlon revealed an acute dyspnoea with cyanosis associated with a left systolic heart murmur. Standard thoracic radiographs excluded pulmonary oedema and showed very few pulmonary changes given the intensity of the respiratory compromlse. Echocardiographic examination revealed hypertrophic cardiomyopathy and a thrombus In the right pulmonary artery. Pulmonary sclntlgraphy confirmed a pulmonary thromboembolism with hypovascularisatlon of the left cranial lobe and of the ventral segment of the right lobe. Conservative treatment was instituted using an antibiotic (doxycycllne), anticoagulants (heparin, coumadine) and a calcium lnhlbitor (diltiazem). The cat was given absolute rest. The general condition of the animal improved.     

Demonstration of Clostridium septicum infection in a goose flock.

Clostridium septicum infection causing 5.0 to 5.2% mortality is reported for the first time in the literature from six-week-old growing geese in three flocks comprising 5,200, 5,500 and 5,900 geese, respectively. The affected birds exhibited weakness, uncoordinated movement, ataxia and, frequently, oblique position of the head and neck (torticollis) as well as signs indicative of dysequilibrium. The affected birds died within 18-24 h. Gross pathological examination revealed anaemia, hepatitis with map-like necroses of irregular outline (Fig. 1), acute enteritis, pulmonary oedema and cardiac dilatation. Light and electron-microscopic examination showed that the sinusoids of the liver were markedly dilated (Fig. 2) and filled with serous exudate and gas (Figs 2 and 3), and the hepatocytes surrounding them exhibited severe oedema (Fig. 4). Among the hepatocytes, ciliated bacteria 7-10 mu in length and 1-3 mu in width, bounded by a well-defined cell wall and often showing signs of spore formation were observed (Figs 5 and 6). By bacteriological examination the pathogen was isolated, its properties were studied, and the clinical entity of malignant oedema was experimentally reproduced by intramuscular injection of guinea-pigs and rabbits. The applied antibiotic (oxytetracycline) and furazolidone therapy proved effective.     

Early clinical and morphologic alterations in the pathogenesis of furazolidone-induced toxicosis in ducklings

Clinical and pathologic alterations during the development of furazolidone-induced toxicosis were investigated in a group of 35 newly hatched male Pekin ducklings fed a ration containing 700 mg of furazolidone/kg of feed for 27 days. A control group (n = 25) was fed the same ration without added furazolidone. Every 3 days, ducklings were weighted and palpated for ascites and 3 were chosen at random for euthanasia to determine the severity of lesions and to obtain hearts for gross measurements and ultrastructural study. Clinical alterations in treated ducklings consisted of decreased feed consumption with lower weight gain and nervous signs. Gross pathologic alterations included cardiomegaly with dilatation of all chambers and thinning of the myocardium, pericardial effusion, pulmonary edema and congestion, ascites, and testicular enlargement. Gross lesions were not observed before day 8. The earliest lesion (day 9) was cardiac chamber dilatation, with the left ventricle and left atrium most commonly and most severely dilated. Hearts from ducklings euthanatized on days 6, 12, 18, 24, and 27 were examined ultrastructurally. Myofibrillar lysis was first observed on day 12 in 1 duckling (of 3) and in at least 1 duckling from subsequent euthanasia periods. Myofibrillar lysis did not appear to be uniform among the cardiac chambers.     

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.     

Excessive moderator bands in the left ventricle of 21 cats

Excessive numbers of moderator bands bridging the left ventricular septum and free wall and entangling papillary muscles were associated with heart failure and death in 21 cats. Clinical findings included dyspnea, anorexia, hypothermia, cardiomegaly, pleural effusion, plumonary edema, heart murmurs, gallop rhythm, electrocardiographic abnormalities (especially conduction disturbances), increased left ventricular end-diastolic pressure, angiocardiographic evidence of left ventricular restriction, and aortic thromboembolism. Pathologic changes included a morphologically distinct network of abnormal numbers of moderator bands in the left ventricle, left ventricular hypertrophy (younger cats--mean age, 4 years) or dilatation (older cats--mean age, 8.7 years), left atrial enlargement and hypertrophy, and pulmonary edema with heart failure cells in the alveoli. Heart weights of affected cats were significantly less than those of cats with congestive, hypertrophic, and restrictive cardiomyopathy (endocardial fibrosis), but were not significantly less than heart weights of clinically normal cats. Pathologic changes were characteristic of the syndrome grossly and histologically, but clinical findings were not clearly definable.     

An unusual presentation of suspected oedema disease of swine in Kenya

From a group of 11 recently weaned pigs, 4 were reported to be sick. Clinical examination of the sick pigs revealed marked dyspnoea, bluish-red discolouration of the skin, incoordination and difficulty in walking. Bacteriological examination of the gut contents of 2 pigs that had died earlier yielded pure cultures of haemolytic Escherichia coli. Post mortem examination of the remaining 2 pigs that died subsequently revealed progressive pulmonary collapse. One of these also showed subcutaneous oedema of the head and marked oedema of the mesentery of the spiral colon and oedema of the brain. Microscopically there was pulmonary alveolar collapse and degenerative changes in the liver. On the basis of the clinical signs, isolation of haemolytic E. coli and the post mortem findings, a diagnosis of oedema disease was made.