Retrospective evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs

Pulmonary arterial hypertension (PH) is a pathologic condition in dogs characterized by abnormally high pressures in the pulmonary circulation and has been associated with a poor outcome. Sildenafil is a type V phosphodiesterase inhibitor that produces nitric oxide mediated vasodilatation. Sildenafil treatment decreases pulmonary arterial pressure and pulmonary vascular resistance in people with PH. The purpose of this study was to describe the clinical characteristics and outcome of dogs with PH treated with sildenafil. The cardiology database was searched for dogs with PH treated with sildenafil. PH was defined as systolic pulmonary arterial pressure (PAPs) > or = 25 mmHg at rest. Medical records were reviewed for the following information: signalment, duration and type of clinical signs before treatment, underlying disease, estimated or measured PAPs, dosage and dosing interval of sildenafil, and the effect of treatment on clinical signs and pulmonary arterial pressure and survival time. Thirteen affected dogs were identified. Clinical signs included collapse, syncope, respiratory distress, and cough. Duration of clinical signs before presentation ranged from 3 days to 5 months. An underlying cause was identified in 8 dogs. The median sildenafil dosage was 1.9 mg/kg. Ten dogs received concurrent medications. Median PAPs was 90 mmHg; 8 dogs were reevaluated after therapy, and the median decrease in PAPs was 16.5 mmHg. The median survival time of all dogs was 91 days. Sildenafil appeared to be well tolerated in dogs with PH and was associated with decreased PAPs and amelioration of clinical signs in most. Sildenafil represents a reasonable treatment option for dogs with pulmonary hypertension.     

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Acute necrotising pulmonary vasculitis and pulmonary hypertension in a juvenile dog

A five-month-old female Jack Russell terrier was presented for investigation of acute lethargy, anorexia, coughing, respiratory distress and weakness. Examination findings included cyanosis, a grade 3 of 6 systolic heart murmur and prolonged capillary refill time. Radiography and echocardiography revealed severe pulmonary hypertension, cor pulmonale and right-sided heart failure. Indirect measurement of the systolic pulmonary artery pressure estimated pressures over 100 mmHg. Despite treatment the patient died. Post-mortem examination did not identify a congenital cardiovascular anomaly. Histopathology confirmed acute necrotising pulmonary arteritis and immunohistochemistry failed to identify any immune complex or complement deposition.     

Eosinophilic pulmonary granulomatosis in a young dog with prolonged remission after treatment

A two‐year‐old Jack Russell terrier was presented for evaluation of chronic cough and exercise intolerance. Previous treatment with antibiotics and glucocorticoids had only partially ameliorated the clinical signs. During investigation, hypoxaemia, peripheral eosinophilia and an eosinophilic bronchoalveolar lavage fluid were noted. Thoracic radiographs revealed two ovoid clearly delineated soft‐tissue opacities, one in the caudal segment of the left cranial lung lobe (diameter 26 mm) and the other in the right cranial lung lobe (diameter 20 mm). These findings were verified by computed tomography, which identified an additional smaller lesion (diameter 16 mm) dorsally in the right caudal lobe. Ultrasound‐guided fine‐needle aspiration samples confirmed the diagnosis of eosinophilic pulmonary granulomatosis and treatment with prednisolone and azathioprine was initiated. Within 1 month, granulomas were no longer detectable radiographically. All medication was discontinued after 7 months and currently, after 2·5 years, the dog remains free of clinical signs. To the authors’ knowledge this is the first case report to describe prolonged remission from idiopathic canine eosinophilic pulmonary granulomatosis.     

Reversible pulmonary hypertension associated with lungworm infection in a young cat

Two ten-week-old kittens presented with dyspnea. Two weeks later dyspnea had worsened and both kittens had developed a heart murmur. One kitten died and necropsy showed severe granulomatous pneumonia and moderate bronchi(oli)tis and peribronchi(oli)tis caused by Aelurostrongylus abstrusus. The results from echocardiography, thoracic radiography and the other kitten's fecal examination were interpreted as severe parasitic pneumonia caused by A. abstrusus infection with pulmonary hypertension. Repeated administration of milbemycine-oxime and praziquantel resulted in cessation of larvae shedding and resolution of clinical, radiographic and echocardiographic signs of bronchopneumonia and pulmonary hypertension.     

A high fiber diet responsive case in a poodle dog with long-term plant eating behavior

An 11-year-old, castrated male Miniature Poodle dog was referred due to daily plant eating followed by vomiting for 7 years. Each time the dog went out for a walk, he had been munched grass, and then vomited. There were no abnormal findings on medical examinations. Through behavior examination and consultation, we diagnosed this dog as having a plant eating problem. Because we assumed that the dog had eaten plants to supply of dietary deficiency or relieve digestive problems, advised the owner to discontinue supplying previous diet and to feed high-fiber diet. On the follow up, the owner said that the dog had not eaten plants and vomited from 3 days after initial dietary change. The dog has not shown any clinical signs for 13 months. This clinical finding shows a possibility that deficient diet, especially fiber, relates to the plant eating behavior of a dog.     

Unusual congenital pulmonary anomaly with presumed left lung hypoplasia in a young dog

A seven‐month‐old, entire, male miniature schnauzer dog was referred with acute vomiting, inappetence and depression primarily as a result of a gastric foreign body (pine cones). During investigations, thoracic radiographs revealed increased volume of the right lung lobes, deviated cardiomediastinal structures and elevation of the heart from the sternum. Thoracic computed tomography revealed left cranial lung lobe hypoplasia and extension of the right cranial lung parenchyma across the midline to the left hemithorax. Branches of the right pulmonary vessels and bronchi also crossed the midline and extended to the left caudal lung lobe. These findings suggested that the right and left lungs were fused. In humans this finding is consistent with horseshoe lung, which is an uncommon congenital malformation. To the authors’ knowledge, this case represents the first report of such a pulmonary anomaly in a dog.     

Clinical and pathological characterisation of primary pulmonary hypertension in a dog

Primary pulmonary hypertension was diagnosed in an eight-year-old labrador retriever on the basis of echocardiographic findings of severe right ventricular eccentric hypertrophy, abnormally high systolic and diastolic pulmonary arterial pressures calculated by applying the modified Bernoulli equation to the tricuspid and pulmonary insufficiency peak velocities, and the absence of any underlying disease known to cause secondary pulmonary hypertension. The clinical abnormalities developed gradually, from exercise intolerance starting early in life to terminal right-sided congestive heart failure. Consistent histopathological findings were severe intimal and medial thickening of small arteries and arterioles that led to vascular obliteration.     

Severe pulmonary arterial hypertension due to Angiostrongylosus vasorum in a dog

A dog was presented with a history of dyspnea, coughing, and ascites. Angiostrongylosis and severe pulmonary arterial hypertension (PAH) were found, as well as a marked discordance between the electrical and mechanical events of the heart. Pulmonary arterial hypertension related to Angiostrongylus vasorum has rarely been reported.     

A vitamin e response in a young dog

Extract

This subject will be covered in three sections, first, a brief history of how the idea of using trained dogs to help the blind was conceived, then the present-day methods of training guide dogs, and, finally, how the blind person is trained with their guide dog to work together as a team.     

Reversible pulmonary hypertension presenting simultaneously with an atrial septal defect and angiostrongylosis in a dog

A one-year-old female neutered beagle was presented with marked abdominal effusion. Echocardiography showed marked dilatation of the right cardiac chambers, an atrial septal defect and severe tricuspid insufficiency. Systolic pulmonary arterial pressure (sPAP), evaluated by continuous wave Doppler echocardiography, was very high (80 mmHg), with a right to left interatrial shunt. The radiographic images were compatible with widespread pneumonitis. Numerous larvae of Angiostrongylus vasorum were visible on direct faecal examination. The animal was given fenbendazole for 15 days, combined with diuretics, an antibiotic and a vasodilator. Two weeks later, the dog showed a marked improvement. The treatment, except the anthelmintic, was continued for seven weeks and then stopped. At that stage, Doppler echocardiography revealed that the sPAP had returned to normal (20 mmHg) and the interatrial shunt had reversed (left to right). Eighteen months later, clinical and Doppler echocardiographic examinations were normal.     

Chylothorax in a dog with pulmonary lymphangiosarcoma

Lymphangiosarcoma of the pulmonary pleura was found to be the cause of persistent chylothorax in an eight-year-old, intact male golden retriever. After a two-month course of medical management, a lymphangiogram and thoracic duct ligation were performed with the objective of decreasing further effusion. At surgery, gross lung pathology was biopsied and yielded a histopathological diagnosis of pulmonary pleural lymphangiosarcoma. A relatively rare tumor, lymphangiosarcoma of the pulmonary pleura has not previously been documented as a source of chylothorax in the dog.     

Sildenafil citrate therapy in 22 dogs with pulmonary hypertension

BACKGROUND: Pulmonary hypertension (PH) is a disease condition characterized by abnormally increased pulmonary artery pressures and often is associated with a poor prognosis. Sildenafil is a phosphodiesterase inhibitor that causes pulmonary arterial vasodilation and reduction in pulmonary artery pressures. HYPOTHESIS: Treatment with sildenafil will improve echocardiographic determinants of PH in dogs, while also improving quality of life and survival. ANIMALS: Twenty-two dogs with clinical and echocardiographic evidence of pulmonary hypertension. METHODS: A retrospective study evaluating the effects of sildenafil on physical examination, ECG and radiographic findings, blood pressure and echocardiographic findings of PH, clinical score, and outcome was completed. PH was defined as a peak tricuspid regurgitation flow velocity > or = 2.8 m/s or a peak pulmonic insufficiency flow velocity > or = 2.2 m/s. RESULTS: Sixteen of 22 dogs with PH were elderly females of small body size. Their clinical score was significantly improved (P = .0003) with sildenafil treatment, but physical examination findings remained unchanged. Heart rate, respiratory rate, vertebral heart size, ECG heart rate, and systolic blood pressure did not change significantly with sildenafil treatment (P > .05). Peak tricuspid regurgitation flow velocities did not change significantly with the treatment of sildenafil, but selected systolic time intervals were significantly improved. Survival times for all dogs ranged from 8 to > 734 days. CONCLUSIONS AND CLINICAL IMPORTANCE: Sildenafil did not significantly lower the degree of measurable PH in dogs. Clinical improvement and increased quality of life was seen with sildenafil treatment, despite lack of significant change in other variables.