Arrhythmogenic right ventricular dysplasia/cardiomyopathy in a Siberian husky

A seven-month-old male Siberian husky was presented with a recent history of anorexia, hindlimb weakness and syncope. Physical examination revealed severe tachycardia, tachypnoea and dyspnoea. Mucous membranes were pale and femoral pulses were weak. An electrocardiogram showed sustained ventricular tachycardia with a left bundle branch block configuration. Thoracic radiographs revealed slight right ventricular enlargement and two-dimensional echocardiography revealed mild right ventricular dilation at the cardiac apex and some hyperechogenic areas on the right side of the interventricular septum. Administration of intravenous lignocaine converted the ventricular tachycardia to sinus rhythm. The maintenance antiarrhythmic therapy consisted of oral procainamide and propranolol. Three weeks later the dog died suddenly. On postmortem examination, the right ventricular free wall was very thin at the apex, infundibulum and caudal aspect of the right ventricular parietal wall, similar to the 'triangle of dysplasia' of human patients. Histopathological examination revealed replacement of several areas of right ventricular free wall myocardium with connective tissue and fat. The right atrium and left ventricle were less severely affected by the same lesions. The clinical and pathological findings are similar to those reported in young people with arrhythmogenic right ventricular dysplasia/cardiomyopathy.     

URETEROLITHIASIS AND PAPILLOMA FORMATION IN THE URETER OF A GUINEA PIG

A 5-year-old guinea pig with suspected urolithiasis was presented for radiology and ultrasound examinations of the abdomen. Radiographically, an irregular-shaped mineral opacity was detected in the area of the urinary bladder. Ultrasonographically, pyelectasia of the right kidney, hydroureter with an ureterolith cranial to a thickened ureter wall close to the ureterovesical junction, and a thickened urinary bladder wall were detected. Histopathologically, the thickened ureter wall was found to be a papilloma. The ureter calculus consisted of 100% calcite.     

肉鸡腹水综合征患鸡右心组织钙沉积和Ca2+-ATPase活性变化

右心肥大衰竭是腹水综合征患鸡发病的重要环节之一,而心肌细胞内Ca^2＋浓度在调节心脏收缩和舒张功能及其生长方面都起着重要作用。本试验应用右心导管法测定AS患鸡右心压力变化情况,采用焦锑酸钾沉淀法、电镜酶细胞化学法研究AS患鸡右心组织Ca^2＋和钙泵（Ca^2＋-ATPase）活性变化及其精确定位。结果显示AS组肉鸡右心室舒张压极显著高于对照组（P〈0.01）,同时,右心室内压最大变化速率也极显著降低（P〈0.01）;对照组肉鸡右心组织偶见少量散在的Ca^2＋沉淀颗粒,低温诱发AS患鸡右心组织发生了明显的钙沉积;对照组肉鸡的右心组织Ca^2＋-ATPase以高电子密度颗粒分布于肌浆网、线粒体膜等处,AS患鸡心脏组织的Ca^2＋-ATPase的电子密度颗粒显著减少或缺失。本研究揭示,在低温条件下AS患鸡具有明显的右心舒张功能障碍,Ca^2＋浓度增高和Ca^2＋-ATPase功能抑制可能在其中起着重要作用。     

Naturally Occurring Biventricular Noncompaction in an Adult Domestic Cat

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non‐human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth‐eaten appearance to the inner wall of the mid‐ to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial‐lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.     

绵羊心壁组织学结构特征的研究

分别制作绵羊左、右心房,左、右心室石蜡组织切片,通过HE、改良PTAH染色法研究绵羊心壁的组织结构特征。结果发现绵羊心壁由心内膜、心肌膜和心外膜构成,心内膜中富含浦肯野纤维;心肌膜最厚,心肌纤维较细,呈螺旋状环绕分层排列;心外膜内可见大量脂肪细胞。改良PTAH染色将肌纤维染成紫蓝色,闰盘着色深蓝,纤维结缔组织染成玫瑰红色。研究结果表明,绵羊心肌纤维较细,肌纤维横纹清晰,闰盘较稀疏。H2O2因其氧化和漂白作用,在改良PTAH染色中有一定的作用。     

Increased calcium deposits and decreased Ca2+-ATPase in right ventricular myocardium of ascitic broiler chickens

Right ventricular hypertrophy and failure is an important step in the development of ascites syndrome (AS) in broiler chickens. Cytoplasmic calcium concentration is a major regulator of cardiac contractile function and various physiological processes in cardiac muscle cells. The purpose of this study was to measure the right ventricular pressure and investigate the precise ultrastructural location of Ca(2+) and Ca(2+)-ATPase in the right ventricular myocardium of chickens with AS induced by low ambient temperature. The results showed that the right ventricular diastolic pressure of ascitic broilers was significantly higher than that of control broilers (P < 0.01), and the maximum change ratio of right intraventricular pressure (RV +/- dp/dt(max)) of ascitic broilers was significantly lower than that of the controls (P < 0.01). Extensively increased calcium deposits were observed in the right ventricular myocardium of ascitic broilers, whereas in the age-matched control broilers, calcium deposits were much less. The Ca(2+)-ATPase reactive products were obviously found on the sarcoplasmic reticulum and mitochondrial membrane of the control right ventricular myocardium, but rarely observed in the ascitic broilers. The data suggest that in ascitic broilers there is the right ventricular diastolic dysfunction, in which the overload of intracellular calcium and the decreased Ca(2+)-ATPase activity might be the important factors.     

Eisenmenger's complex in a Holstein-Friesian cow

A 4.5-year-old, Holstein-Friesian cow presented with a 1-month history of severe exercise intolerance. Rectal examination and transrectal ultrasonography revealed a large mass in the left retroperitoneum. The heart rate was 70 to 80/min. Premature ventricular complexes and ventricular bigeminy were present on an electrocardiogram. Erythrocytosis was present and blood gas analysis revealed marked hypoxaemia. An echocardiogram demonstrated a large ventricular septal defect, a partially dextroposed aorta, and concentric hypertrophy of the right ventricular free wall. Colour flow Doppler echocardiography and a contrast echocardiographic study demonstrated a right-to-left shunt through the ventricular septal defect. Eisenmenger's complex was diagnosed. The patient was euthanased. Necropsy confirmed the gross cardiac lesions identified by echocardiography and an abscess in the apex of the left ventricle. Severe pulmonary arterial lesions were present, consistent with a marked increased in pulmonary vascular resistance. Actinomyces pyogenes was cultured from abscesses of the retroperitoneum and the ventricular apex.     

A study on pathogenesis of sudden death syndrome in broiler chickens

Sudden death syndrome (SDS) in fast growing broiler chickens has been recognized as a patho-physiological entity for four decades, but its pathogenesis still remains unknown. More recent investigations provided evidence that link SDS to cardiac arrhythmia, but the mechanism triggering arrhythmogenesis and factors responsible for fatal outcome are poorly understood. In order to understand the chain of events leading to SDS in broilers, the present study focused on putative mechanisms that trigger arrhythmia and mechanisms that predispose the myocardium to fatal arrhythmia. Susceptibility of broilers to cardiac arrhythmia under stress conditions was evaluated using a simulated stress test with epinephrine. Detailed histopathological evaluation of the broiler heart was undertaken to identify structural features that may predispose the myocardium to fatal arrhythmia. The simulated stress challenge revealed that many broilers are highly susceptible to stress induced cardiac arrhythmia. In some broilers the stress challenge induced severe ventricular arrhythmia, and the life threatening nature of this arrhythmia was evidenced by the fact that several birds showing the most severe arrhythmic responses, died suddenly within several days after the stress challenge. Examination of hearts of broilers that died of SDS revealed microscopic lesions in the cardiomyocytes, and widespread changes in the sub-endocardial and mural His-Purkinje system (HPS). Immune staining for Caspase-3 confirmed that numerous Purkinje cells in the left ventricular myocardium from broiler chickens that died of SDS were undergoing apoptosis. The observed lesions suggest that the electrical stability of the myocardium was compromised. Taken together, our findings indicate that stress is a most likely trigger of cardiac arrhythmia in broilers, whereas the pathological changes seen in the myocardium and in the HPS in fast growing broilers provide a very conducive milieu for sustained ventricular arrhythmia. In cases where the electrical stability of the myocardium is compromised, even an episodic arrhythmic event may readily degenerate to catastrophic ventricular fibrillation and sudden death. We conclude that the combination of stress and changes in the cardiomyocytes and HPS are the key requisite features in the pathogenesis of SDS.     

Dilated cardiomyopathy of Doberman pinschers: retrospective histomorphologic evaluation of heart from 32 cases.

Dilated cardiomyopathy of Doberman Pinschers (DCDP) is a progressive disease often presenting with a history of episodic weakness and syncope, or with clinical signs of predominantly left-sided congestive heart failure. A systematic dissection and histomorphologic evaluation of the heart from 32 Doberman Pinschers with a clinical diagnosis of dilated cardiomyopathy revealed a highly specific location for the characteristic myocardial lesions. The lesions of DCDP were found only in the left ventricular free wall, and in 30 cases, the lesions were characterized by myofiber degeneration and atrophy, and replacement of myocardium by dense bundles of collagen and clusters of adipocytes. In the two remaining hearts, myofiber atrophy and degeneration were accompanied by collagen deposition, but not adipocytes. In stained longitudinal (base to apex) tissue sections of the left ventricle, the lesions of DCDP were usually apparent to the unaided eye; appearing as a central linear pale zone, aligned in the long axis of the ventricular free wall. The lesions did not contain inflammatory cell infiltrates and often involved > 50% of ventricular wall.     

Primary cardiac rhabdomyosarcoma in a cat

A seven-year-old domestic shorthair (DSH) cat was presented with anorexia and dyspnea. Pleural-pericardial effusion was detected with thoracic radiographs and echocardiography. Echocardiography demonstrated a large, soft-tissue mass in the right ventricular wall, protruding both into the pericardial space and into the right ventricle. Postmortem examination findings included a large mass in the right ventricular wall and multiple smaller masses on the external surface of the left ventricle and on the internal surface of the pericardium. Results of the histopathological and immunohistochemical examinations of the masses were consistent with rhabdomyosarcoma. This is the first reported case of primary cardiac rhabdomyosarcoma in the cat.     

Arrhythmogenic right ventricular cardiomyopathy in two cats

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disease characterised by infiltration of the myocardium by adipose and fibrous tissue. The disease is an important cause of sudden death in humans, but has rarely been described in animals. This report describes ARVC in two cats with right-sided congestive heart failure. One cat had also experienced previous episodes of syncope. Standard six-lead and 24-hour (Holter) electrocardiogram recording revealed complete atrioventricular block and multiform ventricular ectopics in both cats, with the addition of ventricular tachycardia, ventricular bigeminy and R-on-T phenomenon in one of them. On echocardiography, the right ventricle and atrium were massively dilated and hypokinetic. The survival times of the cats were three days and 16 days following diagnosis. Histopathology in one case revealed fibro-fatty infiltration of the myocardium, predominantly affecting the right ventricular free wall.     

Plexogenic pulmonary arteriopathy in a cat with non‐restrictive ventricular septal defect and chronic pulmonary hypertension

A 10‐week‐old, male, domestic long‐hair cat was medically managed for congenital heart disease over a period of 8 years. Regular clinical examinations, including sequential echocardiography, documented a non‐restrictive paramembranous ventricular septal defect, secundum‐type atrial septal defect and aortic dextroposition. Pulmonary arterial hypertension was diagnosed by the presence of high‐velocity tricuspid regurgitation, bidirectional low velocity flow across the ventricular septal defect, pulmonary arterial dilation and severe right ventricular hypertrophy without evidence of pulmonary outflow tract obstruction. The cat remained clinically stable until it died suddenly at 8 years of age. Histopathology of the lungs found evidence of plexogenic pulmonary arteriopathy. Despite severe pulmonary vascular lesions, other post‐mortem evidence of right heart failure was lacking and death was attributed to a fatal cardiac arrhythmia. In this case report of a cat with chronic pulmonary hypertension over 8 years, plexogenic lesions were found on histopathology. The microscopic findings resemble those previously reported in dogs.     

Ultrastructural and molecular changes in the left and right ventricular myocardium associated with ascites syndrome in broiler chickens raised at low altitude

The present study examines ultrastructural and molecular changes in ventricular myocardium associated with ascites cases in fast-growing broilers raised at low altitude. Extensive ultrastructural lesions were seen in the left and right ventricular myocardium of broilers with fulminant heart failure and ascites. Significant changes included lesions in the myofibril contractile apparatus, altered mitochondria, marked reduction in the myofibril component, and changes in the extracellular matrix (ECM) architecture. No lesions were observed in hearts of slow growing broilers, but mild to moderate changes (predominantly in the left ventriculum) were apparent in the hearts from some clinically normal, fast-growing broilers. SDS-PAGE profiles of washed myofibrils showed several distinctly different bands in preparations from left ventricular myocardium of ascitic birds. Western blot analysis of these samples revealed several fragments of myosin heavy chain, M-protein, and titin. Based on gelatinolytic activity, matrix metalloproteinases (MMP) in the cytosolic fraction of ventricular myocardium homogenates were identified as MMP-2. The relative activity of this enzyme appears to be considerably higher in preparations from broilers, particularly in the preparations from the left ventriculum of fast-growing broilers, in comparison to leghorns or slow growing broilers. The nature and distribution of the changes in the heart indicate that chronic cardiomyopathic process in the left ventricular myocardium occurs during the development of ascites. It is postulated that progressive deterioration of the left heart pump function caused by initial lesions in the left ventricular myocardium is a significant factor in the development of pulmonary hypertension and the pathogenesis of ascites in broilers raised at low altitude.     

Age‐ and Gender‐Dependent Changes of Bovine Myocardium Architecture

Growth, gravidity and lactation put high demands on the performance of the myocardium. The aim of this study, which was performed in 40 female and 20 male bovines ranging from 1 to 4.5 years old, was to determine gross and microscopic morphometric data of bovine myocardium to establish a comparative measure of myocardial growth during juvenile development. During the developmental stage of young adulthood, age‐related increases in female myocardial characteristics included cardiac mass, left and right ventricular mass and the ratio of cardiac mass to loose connective tissue. Age‐related decreases were observed in the number of myocyte nuclei per mm² and the thickness of the right ventricular wall. Sex differences in these parameters were found between 2‐year‐old bulls (N = 20) and 2‐year‐old heifers (N = 10), with males having heavier hearts, thicker ventricular walls, less myocytes in the left ventricle and less connective tissue in both ventricles. Age and sex had no influence on the ratio of capillaries to myocytes, estimated at 0.98 in the adult bovine. Capillary density does not change during juvenile development, but cross‐sectional capillary area does adapt to myocyte cross‐sectional area, accounting for this relatively constant ratio.     

Negative inotropic effect of diazepam in isolated guinea pig heart

The inotropic effect of diazepam, a benzodiazepine derivative, and its mechanism of action were examined using guinea pig heart and single ventricular cell preparations. In Langendorff hearts and right ventricular free-wall preparations, diazepam (10 to 100 microM) produced a monophasic negative inotropic effect in a concentration dependent manner. Neither a central type (flumazenil 1 microM) nor a peripheral type (PK11195 10 microM) of benzodiazepine receptor antagonist antagonized the monophasic negative inotropic effects of diazepam. Diazepam (10 to 100 microM) shortened action potential duration of papillary muscle in a concentration dependent manner. In isolated single ventricular cells, diazepam (30 and 100 microM) inhibited the calcium current (I(Ca)) in a concentration dependent manner. Diazepam produced a significant decrease in I(Ca) elicited by first depolarizing pulses, however, the decrease of I(Ca) was not augmented during a train of depolarizing pulses. Thus, diazepam appears to produce a tonic block of cardiac calcium channels and the mode of inhibition is clearly different from the use-dependent block of verapamil. From these results, it was concluded that diazepam produces a monophasic negative inotropic effect that is independent of the benzodiazepine receptor, and is probably mediated through an inhibition of I(Ca) in guinea pig heart preparations.     

Laryngeal rhabdomyoma in a dog

A 3‐year‐old, female spayed Australian Shepherd dog was presented to Veterinary Healthcare Associates in Winter Haven, FL with a history of respiratory stridor, difficulty swallowing, and a change in bark for approximately 3 months. Radiographs revealed a soft tissue mass caudal to the epiglottis. Oral and computerized tomographic (CT) examinations were performed under general anesthesia and revealed a small firm mass in the caudal larynx on the right side. Cytologic evaluation of a fine‐needle aspirate of the mass revealed cells consistent with a rhabdomyoma, oncocytoma, or granular cell tumor. Histopathologic interpretation was rhabdomyoma or oncocytoma. Histochemical staining with periodic acid‐Schiff was mostly negative with a low number of weakly positive cells and with phosphotungstic acid‐hematoxylin was strongly positive with visible cross striations. Tumor cells did not express pancytokeratin AE1/AE3, were strongly immunoreactive for myoglobin and muscle‐specific actin, and did not express vimentin except for a low number of weakly immunoreactive cells. These findings confirmed a diagnosis of rhabdomyoma. Primary neoplasia of the larynx is rare, and widely varying types of neoplasms have been documented in this location. Due to the cytologic and histologic similarities between rhabdomyoma, oncocytoma, and granular cell tumor, these neoplasms should be differentiated using histochemical staining and immunohistochemical analysis.     

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.     

Comparative assessment of right ventricular performance from the pressure-volume relationship in double-muscled and conventional calves.

Forty-one and 55 records of right-sided and systemic arterial pressures, cardiac output, and end-diastolic and end-systolic right ventricular volumes were collected from a group of 6 conventional and 6 double-muscled calves, respectively. In each group, the mean right ventricular pressure-volume loop was constructed. Global cardiac performance was significantly lower in the double-muscled than in the conventional calves. The right ventricular end-diastolic and end-systolic volumes, as well as the diastolic portion of the mean pressure-volume loop, were similar in the 2 groups. Those results suggest that the reduced cardiac performance of double-muscled calves is not due to a lowered ventricular preload and that diastolic properties of their myocardium are similar to those of conventional calves. When expressed on a body weight basis, however, the right ventricular end-diastolic and end-systolic volumes were lower in the double-muscled than in conventional calves. When expressed as a function of probable metabolic demand, therefore, the volumetric capacity of the cardiac pump appears to be reduced in double-muscled calves. The significantly lower right ventricular ejection fraction, maximal rate of ventricular pressure rise and right ventricular peak-systolic pressure to end-systolic volume ratio measured in double-muscled as compared with conventional calves suggest that reduced myocardial contractility may also be partly responsible for the significantly lower stroke index of the former calves. The cardiac pump of double-muscled cattle thus seems to be less effective than that of conventional cattle because of reduced volumetric capacity and lowered strength of contraction.     

Multiple cardiac anomalies in a cat.

A 7-week-old domestic shorthair cat was examined because of congestive heart failure. Echocardiography and angiography were used to identify multiple cardiac anomalies. Because of the uncorrectable nature of the defects, the cat was euthanatized. Necropsy revealed persistent left vena cava, patent foramen ovale, and a right atrial/left ventricular canal. The right atrioventricular valve was replaced by a small ostium, and no chordae tendinae or papillary muscles were observed around the ostium. The pulmonary trunk originated from the right atrium. The right ventricular free wall was approximately 1 mm thick.     

Coronary arteriosclerosis with myocardial atrophy in a 13-year-old dog

Myocardial ischemia, an uncommon cause of sudden death in dogs, usually results in infarction and fibrosis of the myocardium. Necropsy examination of a 13-year-old German Shepherd dog that died suddenly demonstrated multifocal myocardial thinning and loss in the left and right ventricular free wall and right atrium. Histopathologic examination confirmed the myocardial thinning to be sites of myocyte atrophy and loss, with loose reticulin-positive fibrovascular tissue and adipocytes and little fibrosis. Many intramural coronary arteries were irregularly thickened and partially occluded by segmental intimal and medial deposits of periodic acid-Schiff-positive, Congo red-negative amorphous extracellular material. This finding is consistent with hyaline arteriosclerosis. These vascular lesions likely lead to insufficient perfusion of the affected myocardium and gradual loss of myofibers without the acute necrosis and fibrosis characteristic of infarction.