Tricuspid atresia in a foal

An Arabian crossbred foal was examined because of a suspected congenital cardiac anomaly. There was a grade V/V crescendo-decresendo holosystolic murmur and thrill in the left 4th intercostal space. The foal was slightly cyanotic and polycythemic. Electrocardiography suggested left ventricular hypertrophy. Angiography and cardiac and vascular pressure recordings led to a diagnosis of pulmonic stenosis. The foal died after cardiac bypass and corrective surgery. Postmortem examination revealed an enlarged right atrium, atresia of the tricuspid orifice, a large, fenestrated patent foramen ovale, eccentric left ventricular hypertrophy, and a large interventricular septal defect. The right ventricle had a small lumen and a relatively thick wall. There was valvular and supravalvular pulmonic stenosis, with poststenotic dilatation of the pulmonary artery. A single coronary artery originated from the anterior sinus of the aorta.     

Endocardial fibroelastosis in a dog

Endocardial fibroelastosis is an uncommon congenital heart disease in dogs that may be manifested by signs of left-sided congestive heart failure. A three-month-old, male, Fila Brasileiro dog developed signs of generalised heart failure. Physical examination revealed normal temperature, ascites, and pale and cyanotic mucous membranes. The pup died just after radiography which revealed ascites, hepatomegaly, severe cardiac enlargement and pulmonary oedema. At necropsy, serosanguineous fluid in the thorax and abdomen, pulmonary oedema, right ventricular dilatation, hypertrophy and dilatation of the left ventricle, and mitral valve incompetence were observed. The histopathological examination demonstrated that the thickening of the endocardium of the left atrium and left ventricle was due to the presence of elastic and collagen fibres, although there were no signs of an inflammatory process.     

Norepinephrine stores in the hypertrophied bovine heart.

Influence of hypertrophy on the cardiac stores of norepinephrine (NE) and epinephrine in different chambers of the heart were studied in calves with experimental left or right ventricular enlargement. In the control calves, concentration of NE was markedly higher in the atrial than in the ventricles, the left atrial body had a lower concentration than the right atrial body. The same was true of the left ventricular tissue compared to the right ventricular tissue. Marked depression of the cardiac NE concentration was observed in all chambers in the groups with right and left ventricular enlargement. The magnitude of changes was roughly related to the severity of the stenosis. Depletions in the concentration of NE were not noticed in the operated nonresponsive calves. By contrast, epinephrine was in small concentrations in control calves, amounting on the average to less than 10% of the amount of NE concentration in the same cardiac tissues. However, alterations in cardiac epinephrine values were not observed in the cardiac tissues obtained from animals with cardiac hypertrophy.     

Cardiac dimensions in severely anemic neonatal pigs

The effects of chronic severe anemia on weights and chamber volumes of hearts were studied in 9 spontaneously anemic neonatal pigs (mean hematocrit = 10.1%) and 10 healthy piglets (mean hematocrit = 28.3%) of approximately the same age and similar body weights. All cardiac chamber weights, as well as total heart weight/body weight ratios, were significantly higher in the anemic pigs than in the healthy pigs (P less than 0.001). The left ventricular free wall/right ventricular free wall weight ratio was identical in the 2 groups. Calculated left ventricular volume/body weight ratio also was significantly greater in the anemic pigs (P less than 0.05). It is concluded that cardiac dilatation and hypertrophy occur consistently in chronically anemic neonatal pigs. These changes are independent of age or body weight of the animal.     

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.     

Changes over time in echocardiographic measurements in young Standardbred racehorses undergoing training and racing and association with racing performance

OBJECTIVE: To evaluate changes over time in echocardiographic measurements in young Standardbred racehorses undergoing training and racing and determine whether there was any relationship between cardiac dimensions and racing performance. DESIGN: Longitudinal observational study. ANIMALS: 103 horses. PROCEDURE: 2-dimensional and M-mode echocardiography was performed 4 times at 6-month intervals. RESULTS: Significant cardiac enlargement took place during the study period as indicated by increases in left ventricular internal diameter in diastole (LVIDd), estimated left ventricular muscle mass (LV mass), and mean wall thickness attributable to eccentric left ventricular hypertrophy. Estimated body weight was positively correlated with left ventricular size, and males had significantly larger LVIDd and LV mass than did females. Horses that were racing regularly had larger LVIDd and LV mass than did unraced horses. A significant relationship between left ventricular size and racing performance was observed. The relationship was strongest at the time of the fourth examination. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that age must be taken into account when interpreting results of echocardiography in young Standardbred racehorses because significant cardiac enlargement takes place with age and training. A larger heart was found in horses that were racing, and size of the heart was correlated with athletic performance of the horse.     

Hypertrophic cardiomyopathy in an aged dog

A 14-year-old female Yorkshire terrier was presented with the complaint of cardiac murmur and convulsive seizure. Thickened mitral valve, left atrial enlargement, excess motions of the left ventricular (LV) free wall and the ventricular septum, and tricuspid, mitral and aortic valve regurgitations were recognized on echocardiography. Follow-up echocardiography revealed the progression of concentric LV hypertrophy and LV outflow obstruction. Clinical symptoms associated with cardiac failure did not develop during the observation period. The pathological examination of the heart revealed that the dog had the morphological hallmarks of hypertrophic cardiomyopathy: massive ventricular hypertrophy, disorganization of cardiac muscle cells, interstitial myocardial fibrosis, and abnormal intramural coronary arteries.     

Capillaries of the myocardium of Lama (Lama glama)

The heart of 12 adult llamas, one female and 11 males, 2-7 years of age, was studied gross-anatomically (absolute and relative heart weight) and microscopic-anatomically (left and right ventricular wall, left auricle). Comparing the 9 younger animals (2-3 years old) with the 3 older llamas (5-7 years old) a significant increase of the absolute heart weight and of the number of capillaries per mm2 and a significant decrease of the intercapillary distance in the left ventricular wall was found. This results in an increase of capillarity in the studied heart regions (5.5% compared to 6.9%). The simultaneous increase of the capillary-to-myocyte-ratios from 0.9 to 1.1 shows a significant correlation to the cross-sectional area of the myocytes (r = 0.79) and an also significant but negative correlation to the number of myocytes per mm2 (r = -0.82). In both groups the cross-sectional area of the myocytes and their diameter differs significantly in the three regions of the heart (left ventricular wall--214 micron 2 resp. 17.5 microns; right ventricular wall--156 micron 2 resp. 15.5 microns; left auricle--96 micron 2 resp. 11.5 microns). It is to be supposed, that the morphological conditions of the cardiac vascular supply of llamas living in an altitude of 4000 m are improving with age.     

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.     

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.     

Persistent truncus arteriosus in a cat

A 5-month-old male domestic cat presented with a history of rapid, heavy breathing and cyanosis after exercise. Physical examination showed an abnormal respiratory pattern with an increased rate and stress-induced cyanosis. Auscultation revealed tachycardia and a grade 5/6 systolic murmur best heard over the left base. Radiographs showed evidence of right atrial and ventricular enlargement with distended pulmonary vessels and an enlarged ascending aorta. An echocardiographic examination revealed a dilated right atrium, eccentric right ventricular hypertrophy and an overriding aorta associated with a large ventricular septal defect (VSD). The pulmonary trunk could not be identified by echocardiography. Doppler and saline contrast studies showed large right-to-left shunting through the VSD. These findings were compatible with persistent truncus arteriosus, which was confirmed at necropsy.     

Arrhythmogenic right ventricular cardiomyopathy coincided with the cardiac fibrosis in the inner muscle layer of the left ventricular wall in a boxer dog

A 7-year-old female boxer dog died suddenly without any clinical signs. It was suspected that the dog had arrhythmogenic right ventricular cardiomyopathy (ARVC) due to ventricular premature complexes and ventricular tachycardia at 3 years of age. The final diagnosis of ARVC was confirmed by histological characteristics, such as loss of cardiocytes and fibrofatty replacement, occurring in the right and left ventricular walls. In the cardiocytes, non-lipid vacuoles were observed. Cardiac fibrosis and intimal thickening of the small arteries occurred without fatty replacement in the inner muscle layer including the papillary muscles of the left ventricular wall. This paper describes the pathomorphological details of an ARVC case with coincidental cardiac fibrosis in the inner muscle layer of the left ventricular wall.     

Cardiomyopathy in α-Kinase 3 (ALPK3)-Deficient Mice

Cardiomyopathy developed in mice deficient for α-kinase 3 (ALPK3), a nuclear kinase previously implicated in the differentiation of cardiomyocytes. Alpk3 (-/-) mice were produced according to normal Mendelian ratios and appeared normal except for a nonprogressive cardiomyopathy that had features of both hypertrophic and dilated forms of cardiomyopathy. Cardiac hypertrophy in Alpk3 (-/-) mice was characterized by increased thickness of both left and right ventricular (LV and RV) walls and by markedly increased heart weight and increased heart weight/body weight and heart weight/tibia length ratios. Magnetic resonance imaging studies confirmed the increased thickness in both septal and LV free walls at end-diastole, although there was no significant change in LV wall thickness at end-systole. Myocardial hypertrophy was the predominant feature in Alpk3 (-/-) mice, but several changes more typically associated with dilated cardiomyopathy included a marked increase in end-diastolic and end-systolic LV volume, as well as reduced cardiac output, stroke volume, and ejection fractions, suggesting LV chamber dilation. Magnetic resonance imaging showed a 50% reduction in both septal and free wall LV contractility in Alpk3 (-/-) mice. Interstitial fibrosis and inflammation were notably absent in Alpk3 (-/-) mice; however, light and electron microscopy revealed altered cardiomyocyte architecture, characterized by reduced numbers of abnormal intercalated discs being associated with mild disarray of myofibrils. These lesions could account for the impaired contractility of the myofibrillar apparatus and contribute to the pathogenesis of cardiomyopathy in Alpk3 (-/-) mice.     

Epigallocatechin-3 gallate prevents cardiac hypertrophy induced by pressure overload in rats

Pressure overload diseases, such as valvular stenosis and systemic hypertension, manifest morphologically in patients as cardiac concentric hypertrophy. Prevention of cardiac remodeling due to increased pressure overload is important to reduce morbidity and mortality. Epigallocatechin-3 gallate (EGCG) is a major bioactive polyphenol present in green tea which has been found to be a nitric oxide-mediated vasorelaxant and to be cardioprotective in myocardial ischemia-reperfusion injury. Therefore, we investigated whether EGCG supplementation could reduce in vivo pressure overload-mediated cardiac hypertrophy. Cardiac hypertrophy was induced by suprarenal transverse abdominal aortic constriction (AC) in rats. Three weeks after AC surgery, heart to body weight ratio increased in the AC group by 34% compared to the sham group. EGCG administration suppressed the load-induced increase in heart weight by 69%. Attenuation of cardiac hypertrophy by EGCG was associated with attenuation of the increase in myocyte cell size and fibrosis induced by aortic constriction. Despite abolition of hypertrophy by EGCG, transstenotic pressure gradients did not change. Echocardiogram revealed that increased left ventricular systolic dimensions and deteriorated systolic function were relieved by EGCG. These results suggest that EGCG prevents the development of left ventricular concentric hypertrophy by pressure overload and may be a useful therapeutic modality to prevent cardiac remodeling in patients with pressure overload myocardial diseases.     

Blood volume increase in salt-induced pulmonary hypertension, heart failure and ascites in broiler and White Leghorn chickens.

In this study we tested the hypothesis that excess dietary salt produces an expansion of extracellular fluid volume which may be associated with pulmonary hypertension-induced right ventricular failure in chickens with rapid growth rates. One-week-old broiler and White Leghorn chickens were given 0.5% salt in their drinking water for three weeks. Saline water had a minimal effect on White Leghorns. The hypothesis appears to be correct since salt-treatment in broilers resulted in up to 30% expansion in blood volume and there was 50% mortality from pulmonary hypertension-induced right ventricular failure and ascites. There was marked (up to 88% in some broilers) right ventricular hypertrophy, an indicator of pulmonary hypertension. There was less left ventricular hypertrophy as shown by an increase in the ratio of the right to total ventricle weight. There was up to 32% decrease in growth rate. There was renal hypertrophy in the salt-treated birds as shown by a higher kidney to body weight ratio.     

维拉帕米对腹水综合征患鸡右心室重塑过程中增殖细胞核抗原变化的影响

右心肥大衰竭是导致腹水综合征(Ascites syndrome,AS)患鸡发病的重要因素。增殖细胞核抗原(Prolifera-ting cell nuclear antigen,PCNA)是细胞周期早期G1和S期的标记物,为同源三聚体,参与DNA的复制和修复。本试验观察了低温诱发AS过程中肉鸡右心组织PCNA表达的动态变化及其维拉帕米对其的影响。结果显示:在29、36、43、50日龄时,与对照组肉鸡相比,低温组肉鸡右心室心肌细胞增殖指数和成纤维细胞增殖指数极显著增高(P0.01);与低温组肉鸡相比,维拉帕米组肉鸡右心室心肌细胞和成纤维细胞增殖指数显著或极显著降低(P0.05或P0.01)。结果表明,环境低温可在一定程度上促进肉鸡右心室心肌细胞和成纤维细胞增殖。维拉帕米可抑制心肌细胞和成纤维细胞过度增殖,从而可能防止右心肥大的发生。     

Mitral valve dysplasia in a cat causing reversible left ventricular hypertrophy and dynamic outflow tract obstruction

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.     

Pathophysiologic mechanism of cardiac dysfunction in experimentally induced heartworm caval syndrome in dogs: an echocardiographic study

In dogs with experimentally induced heartworm infection, the onset of caval syndrome (CS) was characterized by a murmur, loudest over the tricuspid valve, and a large worm mass in the right ventricular lumen detectable during diastole by use of M-mode echocardiography. Two-dimensional echocardiography indicated that the worm mass was located in the right atrium and venae cavae and was "flowing" into the right ventricle during rapid diastolic filling. Paradoxical septal motion and vigorous right ventricular cranial wall motion also were observed. Other echocardiographic changes included decreased size of the left atrium and ventricle, aortic root, and ratio of left-to-right ventricular diastolic luminal diameter, compared with values obtained 6 months after experimentally induced heartworm infection. Right ventricular end diastolic diameter increased considerably. Most echocardiographic indices of left ventricular function (fractional shortening, velocity of circumferential fiber shortening, ejection fraction, and preejection period) were not altered appreciably, but estimates of cardiac index and stroke volume were markedly decreased. Electrocardiography revealed ventricular and supraventricular premature complexes in 7 of the 8 dogs studied, evidence of right ventricular enlargement in 6 of the 8 dogs studied, and increased mean heart rate, compared with that measured 6 months after inoculation of infective larvae, before the onset of CS. Cardiac catheterization was performed in 3 days at the onset of CS. Severe pulmonary arterial and right ventricular hypertension and decreased cardiac index (compared with values obtained before inoculation) were observed. Evidence of right ventricular inflow obstruction was not detected. Mean aortic blood pressure decreased with the onset of CS, but right ventricular end diastolic pressure increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Unexpected death in an adult dog with anomalous origin of the left coronary artery from the pulmonary trunk

A two-year-old female miniature poodle died unexpectedly while romping with its owner. Anomalous origin of the left coronary artery from the left pulmonic sinus was discovered at necropsy. Histologically, the right ventricle was unremarkable, but multifocal to coalescing necrosis and fibrosis occurred in the myocardium and endocardium of the left ventricle. Medial hypertrophy of small muscular pulmonary arteries was observed in the lung. The cardiac lesions were similar to those of children with anomalous origin of the left coronary artery from the pulmonary trunk. Pulmonary hypertension, which is suggested by the pulmonary arterial medial hypertrophy, could have increased left ventricular myocardial perfusion and delayed the ischemic myocardial damage that resulted in the death of this dog.     

Right to left patent ductus arteriosus,acute bronchointerstitial pneumonia,pulmonary hypertension and cor pulmonale in a foal

Patent ductus arteriosus (PDA) is a rare congenital cardiac defect in foals causing left to right shunting from the aorta to pulmonary artery. In extremely rare conditions, complications with pulmonary hypertension can result in right to left shunting (Eisenmenger's physiology); however, reversed or right to left shunting has not yet been precisely described in PDA-affected equids. This report describes a unique and unusual case of right to left PDA associated with acute respiratory distress syndrome in a 20-day-old male foal. A holosystolic murmur over the tricuspid valve area and adventitious pulmonary sounds respectively on cardiac and thoracic auscultations, caudodorsally interstitial and bronchointerstitial pulmonary opacities on thoracic radiography, right atrial and ventricular dilatations with paradoxical ventricular septal motion, increased ratio of pulmonary artery internal diameter to the aorta and tricuspid valve regurgitation on echocardiography were detected. Post-mortem and histopathological examinations revealed consolidated, dark red and diffusely enlarged lungs with granular appearance, marked enlargement of the right atrium and ventricle, pulmonary artery thickening and enlargement, patency of the ductus arteriosus, hyaline membrane formation, type II pneumocyte proliferation, hypertrophy and thickening of the pulmonary arteries medial layers and right ventricular myocardial cells distortion and hypertrophy. The findings suggest a right to left shunting through the persistent patency of the ductus arteriosus, pulmonary hypertension and cor pulmonale. We proposed pulmonary hypertension associated with bronchointerstitial pneumonia as a cause of this unusual case of PDA with reversed shunt direction.