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Background: Pulmonary hypertension (PH) secondary to respiratory disease is caused by pulmonary vascular remodeling and hypoxia. Severe PH can induce various clinical signs, including syncope and right‐sided heart failure. Hypothesis/Objectives: To investigate the echocardiographic characteristics in dogs with PH secondary to respiratory diseases. Animals: Thirty‐one dogs with respiratory diseases with or without PH and 15 healthy dogs. Methods: Prospective cross‐sectional study. Dogs were classified according to respiratory disease (obstructive airway/lung disease [OALD] or restrictive lung disease [RLD]) and PH‐relevant signs. The association between echocardiographic variables and PH (classified by respiratory disease and PH‐relevant signs) was investigated. Results: Twenty‐one dogs were diagnosed with PH; of these, 11 showed PH‐related signs (OALD, n = 2; RLD, n = 9), 14 had right ventricular hypertrophy, and 19 had pulmonary arterial enlargement. Right ventricular dysfunction and dilatation were observed only in dogs with PH‐related signs (n = 10). Left and right ventricular stroke volumes were significantly lower in dogs with PH (median [interquartile range]: 17.2 [12.4‐20.8] and 16.8 [15.3‐29.5] mL/m2, respectively). Dogs with RLD had higher echocardiography‐estimated pulmonary vascular resistance than those with OALD (median [interquartile range]: 3.1 [1.9‐3.3] and 1.6 [1.3‐2.2], respectively). Conclusions and Clinical Importance: Pulmonary arterial enlargement was the most common echocardiographic finding in dogs with PH secondary to respiratory diseases. Right ventricular dysfunction, dilatation, and decreased left and right ventricular stroke volume were significantly associated with the PH‐related signs, indicating that comprehensive echocardiography is recommended in dogs with respiratory disease. Restricted lung disease might induce more severe PH than OALD. [ABSTRACT FROM AUTHOR]

An 8‐year‐old Leonberger receiving immunosuppressive treatment with clinical signs of acute dyspnea, cyanosis, and difficulty standing was referred to our institution (Day 1). Treatment including oxygen, clopidogrel, and low‐molecular‐weight heparin was initiated for suspected pulmonary thrombosis. However, exertional dyspnea persisted until Day 10, and increased tricuspid regurgitation velocity, pulmonary vascular resistance, and McConnell's signs also were observed. Thus, beraprost sodium was administered PO on Day 11 to treat suspected pulmonary hypertension. On Day 13, contrast‐enhanced computed tomography identified extensive contrast defects in the pulmonary arteries, and IV monteplase was administered on Days 14 and 18, with marked improvement in respiratory status and exertional dyspnea on Day 20. Right ventricular function and McConnell signs also improved, and tricuspid regurgitation velocity and pulmonary vascular resistance decreased. On Day 250, echocardiography indicated further improvement in pulmonary hypertension pathophysiology. The patient was still progressing well with antithrombotic and pulmonary vasodilator treatment 400 days later. [ABSTRACT FROM AUTHOR]