AORTIC AND CARDIAC MINERALIZATION IN THE DOG

Aortic and cardiac mineralization was found in 21 of 3443 (0.61%) canine thoracic radiographs. In none of 786 feline thoracic radiographs reviewed were such lesions present. Mineralizations were superimposed on the ascending aorta (19 dogs) or on the caudal cardiac silhouette (2 dogs). In 2 of 4 dogs mineralization was identified echocardiographically dorsal to the aortic valve in close proximity to coronary arteries. Computed tomography confirmed mineralization of the aortic arch and root in 2 of 2 dogs. Necropsy and histopathologic examination in 1 dog revealed multiple nodular aortic tunica media calcifications with adjacent areas of degeneration. Lesions were significantly overrepresented in older dogs and in Rottweilers, and regarded as dystrophic calcification, caused either by age-related degenerative changes or chronic disease-related processes. There was no evidence of clinical significance attributed to the mineralization in any dog. Aortic and cardiac mineralization should be recognized as an incidental, non-significant finding in dogs of advanced age and differentiated from pleural and pulmonary structures.     

Familial aortic aneurysm in Leonberg dogs

A thoracic aortic aneurysm was diagnosed in a 6-month-old male Leonberg dog by use of radiography, transthoracic and transesophageal echocardiography, and magnetic resonance imaging. The aneurysm was associated with a twisted ascending aorta and dilatation of several other thoracic arteries (pulmonary trunk, brachiocephalic trunk, and left subclavian artery). Histologic examination of the aorta revealed cystic medial necrosis, with disruption of the elastic network, collagen fibers, and the muscle glycoprotein fibrillin-1. The dam and sire of the dog and 8 littermates were examined by use of transthoracic echocardiography. The sire and 1 male littermate also had an aneurysm of the ascending aorta. To the authors' knowledge, this is the first report of familial aortic aneurysm in dogs.     

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.     

Clinical and Pathological Features of Aortic Thromboembolism in 36 Dogs

Thirty-six dogs with aortic thromboembolism were identified in a retrospective study conducted using case material from the small animal necropsy service of the University of Pennsylvania, from 1977 through 1992. No age, breed, or sex predisposition was found. Thirty dogs presented with primary complaints referable to the aortic thromboembolus and the duration of signs varied from hours to months. In 16 dogs, the presence of the thromboembolus was confirmed antemortem by ultrasound or angiography. Coagulograms were performed in 11 animals, and were consistent with consumptive hemostatic disorders in 8. The aortic occlusions were determined to be emboli in 11 dogs, associated with cardiac disease (9 dogs) and neoplastic emboli (2 dogs). In 18 dogs, the aortic occlusions were determined to be caused by primary aortic thrombi. Nine of these dogs had renal disease and four dogs had severe atherosclerosis associated with thyroid disease. In seven dogs, it could not determined if the aortic occlusions were due to primary aortic thrombi or due to emboli. In 25 dogs, the aorta was the only vessel occluded; but in 11 dogs, thrombi were identified in vessels outside of the systemic arterial system. In 9 dogs, the pulmonary arteries contained thromboemboli; one dog had thrombi in the portal vein and pulmonary arteries, and one dog a cranial vena caval thrombus. Nine of 11 dogs with multiple vascular thrombi, as well as some of the dogs with primary aortic thrombi, may have had either a propensity for thrombosis (a hypercoagulable state) or an inability to lyse thrombi (a hypothrombolytic state).     

Relationship between pulmonary arterial pressure and pulmonary thromboembolism associated with dead worms in canine heartworm disease.

To examine effects of thromboemboli due to dead worms on pulmonary arterial pressure (PAP), 20 to 50 dead heartworms were inserted into the pulmonary arteries of 4 heartworm uninfected dogs (uninfected group) and 11 dogs infected with heartworms (infected group). In the uninfected group, the mean PAP rose 1 week after worm insertion (10.9 to 166. mmHg), but it recovered by the 4th week. Clinical signs, hemodynamics and blood gas findings also deteriorated at the 1st week, but recovered at the 4th week. Angiographic and pathological findings indicated that blood flow recovered through the spaces between thromboemboli and vessel walls at the 4th week. The infected dogs were divided into three groups. In the infected-I group (5 dogs), the intimal lesions of the pulmonary arteries were slight, and clinical and laboratory findings showed changes similar to those of the uninfected group. In the infected-II group (4 dogs), the pulmonary arterial lesions were severe and the mean PAP was higher (25.7 mmHg) than in the uninfected group before worm insertion. An increase in PAP (34.1 mmHg) and worsening of clinical and laboratory findings were noticed till the 4th week. Thromboemboli adhered extensively to the vessel walls. Two dogs in the infected-III group died of severe dyspnea on the 9th and 10th day, and the mean PAP rose remarkably at the 1st week (from 19.4 to 28.2 mmHg). Severe pulmonary parenchymal lesions with edema or perforation were observed. From the above results, it was clarified that effects of dead worms on PAP and clinical signs depended on the severity of pulmonary arterial lesions before worm insertion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Histologic examination of selected areas of canine pulmonary arteries

Selected areas of pulmonary arteries from 18 healthy mixed-breed dogs were examined using histologic staining techniques. Smooth muscle cell, collagen, and elastin content of the tunica intima and tunica media were assessed. Fifteen dogs had abnormalities of tunica intima or tunica media in at least one arterial section examined. Of all arterial sections examined, 40% had histologic changes of the tunica intima or tunica media, and 42% of these vascular lesions were in the main pulmonary artery. The most commonly occurring pathologic change was loss of smooth muscle cells and elastin of the tunica media and replacement by collagen. This lesion is similar to cystic medionecrosis of the aorta. Seemingly, a high frequency of spontaneous vascular lesions exist in pulmonary arteries of young dogs.     

Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart and lungs

OBJECTIVE: To determine the prevalence and severity of pulmonary arterial lesions in cats seropositive for heartworms (Dirofilaria immitis) but lacking adult heartworms in the heart and lungs during necropsy. ANIMALS: 630 adult cats from an animal control shelter in Florida. PROCEDURE: Cats were tested for adult heartworms in the heart and pulmonary arteries and antibody against heartworms in the serum. Histologic examination was conducted on the right caudal lung lobe of 24 heartworm- and antibody-positive cats; 24 heartworm-negative and antibody-positive cats; and 24 heartworm-, antibody-, and antigen-negative cats. Wall areas of 10 small to medium-sized pulmonary arteries of each cat were measured and expressed as a proportion of total cross-sectional area. RESULTS: Heartworm infection or seropositive status was significantly and strongly associated with seventy of medial hypertrophy of pulmonary arterial walls. Heartworm- and antibody-positive cats and heartworm-negative and antibody-positive cats had a significant increase in wall thickness, compared with wall thickness for heartworm- and antibody-negative cats. Heartworm- and antibody-positive cats had the most severe hypertrophy. The proportion with occlusive medial hypertrophy was significantly higher in heartworm- and antibody-positive cats (19/24 [79%]) and heartworm-negative and antibody-positive cats (12/24 [50%]), compared with heartworm- and antibody-negative cats (3/24 [13%]). CONCLUSIONS AND CLINICAL RELEVANCE: Cats with serologic evidence of exposure to heartworms, including those without adult heartworms in the lungs and heart, have a greater prevalence of pulmonary arterial lesions than heartworm-negative cats without serologic evidence of exposure. Additional studies are needed to define the pathogenesis, specificity, and clinical importance of these lesions.     

Chronic myocardial infarction due to arteriosclerosis of coronary arteries followed by acute thromboembolism of caudal abdominal aorta in a cat

A 10-year-old cat with the paresis of hind limbs was initially diagnosed as a hypertrophic cardiomyopathy followed by acute thromboembolism of caudal abdominal aorta from the findings of the medical examinations. However, this case was proved to be an chronic myocardial infarction due to arteriosclerosis of coronary arteries by the pathologic diagnosis. In the left ventricular, the hypertrophy and the narrowing were slight, and a coagulative infarction was seen obviously. The intramural coronary arteriosclerosis showed thickening of the wall due to medial hyperplasia by fibrosis, and arterial stenosis. Myocardial infarction and arteriosclerosis are scarcely any reports of these lesions in cats. This case is valuable for an extremely rare case of myocardial infarction in the cat.     

Finite element analysis of wall stress in the equine pulmonary artery

Reasons for performing study: Arterial calcification is found frequently in the pulmonary artery of racehorses, but the aetiology is unknown. Calcification might be associated with increased wall stress due to arterial geometry (shape) and exercise‐induced hypertension. Hypothesis: High wall stress levels are found in the regions associated with calcified lesion formation, exacerbated as transluminal pressure increases to levels associated with exercise. Methods: The pulmonary arteries of 5 horses, unaffected by calcification, were dissected and pressurised to resting and exercising physiological transluminal pressures and scanned with MRI. Arterial geometries were reconstructed to form 3D computer models and finite element analyses performed. Wall stress levels were measured in 4 regions of interest: the arterial trunk and bifurcation, the wall ipsilateral and contralateral to the bifurcation. Measurements were made for arterial transluminal pressures of 25, 50 and 100 mmHg. Results: High wall stress levels were consistently found at the pulmonary artery bifurcation and wall ipsilateral to the bifurcation, where calcified lesions typically form. Lower wall stress levels were found along the trunk and the wall contralateral to the bifurcation where lesions are less frequently found. Wall stress levels increased 5‐fold over a 4‐fold increase in pressure. The wall stress levels ranged 10 kPa in the wall of the branch contralateral to the bifurcation at 25 mmHg to 400 kPa in the bifurcation at 100 mmHg. Conclusions: Wall stress from arterial geometry and increased pulmonary artery transluminal pressure are factors that may be associated with calcification of the equine pulmonary artery. Potential relevance: Arterial calcification may increase the risk of arterial wall failure in racing horses.     

Rudimentary Coronary Artery in Syrian Hamsters (Mesocricetus auratus)

Congenital underdevelopment of one or more main branches of the coronary arteries has been reported in man, but not in non-human mammals. In man, this defective coronary artery arrangement may cause myocardial ischaemia and even sudden death . The main goal of this study was to describe the coronary artery distribution patterns associated with the presence of a markedly underdeveloped (rudimentary) coronary artery in Syrian hamsters. Moreover, an attempt was made to explain the morphogenesis of these patterns, according to current knowledge on coronary artery development. Eleven affected hamsters belonging to a laboratory inbred family were examined by means of internal casts of the heart, great arterial trunks and coronary arteries. The aortic valve was tricuspid (normal) in seven hamsters and bicuspid in the other four. A rudimentary coronary artery arose from the right side of the aortic valve in four specimens, from the left side of the aortic valve in a further three, and from the dorsal aortic sinus in the remaining four. In all cases, a second, well-developed coronary artery provided for all the coronary blood flow. Except for the existence of a rudimentary coronary artery, the present anomalous coronary artery distribution patterns are similar to coronary artery patterns reported in Syrian hamsters, dogs and humans in association with a solitary coronary ostium in aorta. We suggest that an unusual prolonged time interval in the development of the embryonic coronary stems might be a key factor in the formation of coronary arteries displaying significantly dissimilar developmental degrees.     

Improvement in pulmonary arterial lesions after heartworm removal using flexible alligator forceps

Improvement of pulmonary arterial lesions after heartworm removal using flexible alligator forceps was investigated by measuring pulmonary arterial pressure (PAP), and by angiographic and histopathological examinations in 11 dogs. PAP obtained immediately after worm removal corresponded well with angiographic abnormalities. In 2 dogs, high PAP immediately after worm removal fell gradually by 12 weeks, and obstructions on angiogram were resolved at 4 to 12 weeks. In 4 dogs, slightly high PAP fell to the normal range at 4 weeks, and angiographic abnormalities were considerably reduced at 4 to 12 weeks. In 5 dogs, PAP returned to normal range immediately after worm removal, and angiographic changes almost disappeared at 4 to 8 weeks. On biopsy immediately after worm removal, samples of the main pulmonary arteries showed severe intimal proliferations with villous or papillary protrusion into the lumen. Autopsy at 12 to 20 weeks indicated that the intimal protrusions were remarkably reduced as compared with the biopsy samples in all cases. However, villous intimal protrusions were seen in the caudal lobar arteries in cases with remaining alive worms. New vessels seemed to develop into thromboemboli with time. From these findings, it is clear that the pulmonary arterial lesions improved after heartworm removal, and the clinical signs disappeared following the improvement in hemodynamics. Aspirin therapy (5 mg/kg/day) for 4 weeks after worm removal in 5 dogs did not improve the intimal lesions as compared to 3 control dogs.     

Pulmonary arteriopathy and idiopathic pulmonary arterial hypertension in six dogs

Pulmonary arteriopathy (PA) is the pathologic hallmark in human medicine of diffuse constrictive (medial and intimal remodeling) or multifocal complex (plexiform and dilatative lesions) arterial lesions, or both, that lead to irreversible obliteration of the arterial lumen. Clinically, PA leads to pulmonary arterial hypertension (PAH), of which idiopathic (IPAH) is one of the 5 subsets, and ultimately, to right-sided heart failure (RHF). Clinical and pathologic findings from 6 dogs with diagnosis of IPAH and PA were reviewed. These dogs were of various pure (5/6, 83%) and mixed (1/6, 17%) breeding, 5 months to 9 years (mean 5.2 years) old, and predominantly female (4/6, 67%) and reproductively intact (4/6, 67%). Doppler echocardiography (n = 5) indicated increased pulmonary arterial pressures during systole (70-135 mm Hg, mean 98 mm Hg) and diastole (35-80 mm Hg, mean 58 mm Hg). All 6 dogs had right ventricular pressure overload, right ventricular eccentric hypertrophy, and RHF. Histologic examination confirmed the clinical diagnosis of IPAH in all dogs, revealing PA characterized by 1 of the 4 main human histologic subsets: 1) isolated medial hypertrophy (1/6, 17%); 2) medial hypertrophy-intimal thickening without the plexiform lesion (1/6, 17%); 3) medial hypertrophy-intimal thickening concurrent with the plexiform lesion, which often was regionally clustered and situated near branching points of the respiratory artery, the poststenotic dilatation lesion, and vasculitis (4/6, 66%); and 4) isolated arteritis (1/6, 17%). Ancillary lesions similar to those in humans also complicated the PA (5/6, 83%). The complex lesions and ancillary exudative alveolitis seemed to be important indicators of severe, likely rapidly progressive and fatal, IPAH.     

Pathological findings in dogs naturally infected with Angiostrongylus vasorum in Newfoundland and Labrador, Canada.

Fifty-six dogs from St. John's, Newfoundland, Canada, were evaluated for Angiostrongylus vasorum infection. Small numbers of nematodes were found within pulmonary arteries of 6 dogs. Larvae were identified in fecal samples in 2 of 6 dogs. All 6 dogs had multifocal granulomatous pneumonia and sometimes foci of chronic thrombosis, which varied from very mild to severe. One dog had extensive pulmonary lesions resulting in cor pulmonale. Right heart failure was characterized by right ventricular hypertrophy, hepatic congestion, ascites, and hydrothorax. Microscopically, in most cases, eggs, larvae, and sometimes intravascular adults, were present within lung tissue sections. Small foci of granulomatous inflammation with and without larvae were present in kidney and brain in 4 dogs. An additional dog, diagnosed antemortem with angiostrongylosis via fecal examination, was also examined. Pathological findings consisted of severe pyogranulomatous interstitial pneumonia with myriad eggs, larvae, and numerous intravascular pulmonary adult nematodes with extensive arterial thrombosis. Five hundred and seventy-two adult worms were removed from pulmonary arteries. Foci of granulomatous inflammation, often associated with larvae and/or eggs, were present in tracheobronchial lymph nodes, adrenal gland, brain, and kidneys. Severe seizuring noted antemortem was attributed to several large, discrete areas of acute hemorrhagic infarction within the cerebrum and cerebellum. Natural A. vasorum infection in domestic dogs in eastern Newfoundland causes lung pathology of variable severity, which in some cases, may progress to cor pulmonale and which may be associated with extrapulmonary lesions and clinical signs.     

Relationship between pulmonary arterial pressure and lesions in the pulmonary arteries and parenchyma, and cardiac valves in canine dirofilariasis.

The relationship between pulmonary hypertension and lesions was examined in 41 dogs infested naturally with heartworms, which consisted of 28 cases with pulmonary heartworm disease and 13 cases with caval syndrome. Pulmonary arterial pressure (PAP) was measured before and 1 or 7 days after heartworm removal with a flexible alligator forceps. In these dogs, lesions were examined after the last measurement of PAP. The mean PAP was 28.2 +/- 16.0 mmHg (10.9 to 81.4 mmHg in range) at post-removal phase. Pulmonary arterial intimal lesions, pulmonary thromboemboli, pneumonic lesions, tricuspid valvular lesions and mitral valvular lesions were macroscopically recognized in 95, 59, 39, 54 and 56% of cases, respectively. These lesions were classified by severity and the relationship with PAP was examined by the multiple correlation analysis. The multiple coefficient correlation was found the highest between PAP and thromboemboli, followed by mitral valvular lesion, tricuspid valvular lesion, and pneumonic lesion. There was no significant correlation between PAP and intimal lesions. The coefficient of determination showed the highest value in thromboemboli when one variable was used, and increased only very slightly when a variable of thromboemboli was added to those of other lesions. The cases with high PAP had fresh thromboemboli in large pulmonary arteries. From these evidences, it was concluded that thromboemboli following natural death of heartworm was the most important factor causing an increase in PAP and developing clinical signs in canine heartworm disease.     

Bromodeoxyuridine labeling and DNA content of pulmonary arterial medial cells from hypoxia-exposed and nonexposed healthy calves.

Vascular medial thickening is a prominent finding in people and animals with refractory neonatal pulmonary hypertension. Smooth muscle cells are capable of 2 distinct growth responses in vivo: hypertrophy or hyperplasia. Hypertrophic smooth muscle cells may undergo DNA synthesis without cell division, leading to a polyploid state. To better understand the nature of smooth muscle cell growth in healthy and pulmonary hypertensive neonatal calves, we measured incorporation of the thymidine analog bromodeoxyuridine (BrdUrd) and total DNA content in medial cells from control (pulmonary arterial pressure = 32 +/- 2 mm of Hg) and hypobaric hypoxia-exposed (pulmonary arterial pressure = 120 +/- 7 mm of Hg) calves. Labeling of medial cells with BrdUrd measured by flow cytometry was increased (P < 0.02) in pulmonary arteries of hypoxia-exposed calves (n = 5), compared with control calves (n = 5). Immunohistochemical localization of BrdUrd indicated that BrdUrd labeling of large elastic pulmonary arteries from hypoxia-exposed calves was increased almost exclusively in the outer half of the medial wall. Increased BrdUrd labeling of muscular pulmonary arteries from hypoxia exposed calves was observed in the arterial media and adventitia, and tended to exit in clusters. Analysis of DNA content by flow cytometry indicated a decrease (P < 0.05) in percentage of tetraploid medial cells in pulmonary arteries from hypoxia-exposed calves, compared with control calves. Bivariate analysis for BrdUrd labeling and DNA content of cells from the pulmonary arteries of hypoxia-exposed calves indicated a subpopulation of diploid cells with positive BrdUrd labeling, suggestive of DNA synthesis and subsequent cell division.(ABSTRACT TRUNCATED AT 250 WORDS)     

Method of selective and non-selective angiocardiography for the horse

A practical and safe method of angiocardiography for the horse is described. The technique involved the rapid injection of 50 to 150 ml contrast agent via catheters in the right and left heart, pulmonary artery and aorta. The examination was carried out with the horse in the standing position or under general anaesthesia. Angiocardiograms were performed on 10 normal horses and satisfactory pictures of the right and left ventricles, pulmonary arteries, aorta and coronary circulation were obtained. The technique was also used in a foal with severe congenital heart disease. The most practical methods of recording the images in the standing position were cinefilm or video taperecording. In the recumbent position both cinefilm and radiographs were taken. No damage to the heart was inflicted by the catheters and only a few ventricular premature contractions (less than five) were produced by the pressure of injection. No signs of toxicity were recorded using repeated injections of contrast material (ie, less than 600 ml).     

MINERALIZED ARTERIOSCLEROSIS IN A CAT

In radiographs of a domestic short haired cat of unknown age, mineralization was identified in the pulmonary parenchyma, peripheral pulmonary vessels, the aortic outflow tract, aortic valve, celiac artery, cranial mesenteric artery, and the internal and external iliac arteries. The diffuse arterial mineralization was characterized histopathologically as arteriosclerosis. This is the first report of mineralized arteriosclerosis in a cat with corresponding radiographic signs. The arteriosclerosis is thought to be due to systemic hypertension but a definitive cause for the profound mineralization was not found. Causes of soft tissue mineralization are reviewed.     

大黄醇提液抗家兔实验性动脉粥样硬化作用的病理形态学研究

将30只雄性健康新西兰白兔随机分为5组,每组6只。对照组给予基础饲料;模型组给予高脂饲料;三个大黄组给予高脂饲料同时分别用不同药量的大黄醇提液灌胃。于第10周末处死家兔,观察、测量和比较主动脉弓、胸主动脉、腹主动脉和髂动脉分支处血管脂质斑块的病理变化,计算斑块面积占胸主动脉的百分比;光镜下观察心脏冠状血管的病理改变,并计算冠状小动脉粥样硬化的发生率,研究大黄醇提液抑制家兔动脉粥样硬化形成的作用。结果显示：大黄醇提液能一定程度上抑制家兔主动脉及腹主动脉AS形成,减少AS斑块面积,降低动脉分支处AS的发生率,减轻心脏冠状动脉AS的病变。     

The prevalence, gross lesions and histopathology of aortic onchocerciasis in Nigerian cattle

The incidence of aortic onchocerciasis due to Onchocerca armillata among slaughtered cattle in Ibadan, Nigeria, was about 2 per cent between 1979 and 1980. The average number of nodules per thoracic aorta was 7 and the mean size of each nodule was 9.7 +/- 2.6 mm. About 54 per cent of the nodules examined were calcified, and nodular calcification appeared to be related to the degree of infection or reinfection with the parasite. The histopathology of the aortic lesions is described.