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Simple Summary: Pulmonary hypertension is a fatal comorbidity in dogs with left-sided heart disease. Various oral pulmonary vasodilators have been effective in treating canine pulmonary hypertension; however, no studies have compared their hemodynamic effects. This study compared the hemodynamic effects of selected pulmonary vasodilators (15 µg/kg beraprost, 1.0 mg/kg sildenafil, and their combination) in canine models of mitral regurgitation (the most common cardiac disease in dogs). Significant improvements in pulmonary hypertension were observed with all study drugs. Pulmonary vasodilating effects differed among the study's drugs. Sildenafil showed a more potent pulmonary vasodilating effect than beraprost; however, sildenafil significantly worsened the left-heart loading condition. Although beraprost showed a weaker pulmonary vasodilating effect than sildenafil, no significant worsening in the left-heart loading condition was observed. Combination therapy resulted in the strongest pulmonary and systemic vasodilating effects without worsening the left-heart loading condition. This study demonstrated the differences between beraprost and sildenafil in pulmonary and systemic vasodilating effects. Sildenafil involved the risk of worsening the left-heart load, although it was effective in treating pulmonary hypertension. Combination therapy with beraprost and sildenafil synergistically dilated the pulmonary and systemic vessels, indicating a more potent treatment option. Previous reports have shown that various oral pulmonary vasodilators are effective against canine pulmonary hypertension (PH). However, no studies have compared their hemodynamic effects. We aimed to compare the hemodynamic effects of 15 µg/kg beraprost sodium, 1.0 mg/kg sildenafil, and their combination, in dogs with experimentally induced mitral regurgitation. This experimental crossover study evaluated the hemodynamic and functional effects of oral pulmonary vasodilators by application of right-sided heart catheterization and echocardiography. Beraprost significantly decreased pulmonary and systemic vascular resistance. Additionally, beraprost increased right-ventricular stroke volume and left-ventricular cardiac output without worsening left-heart size and left-atrial pressure. The pulmonary vasodilatory effects of sildenafil were stronger, and its systemic vasodilatory effects were weaker than those of beraprost. However, sildenafil significantly increased the left-ventricular volume, left-atrial pressure indicator, and right-ventricular cardiac output. Combination therapy resulted in the strongest pulmonary and systemic vasodilating effects without worsening the left-heart size and left-atrial pressure indicators. Both beraprost and sildenafil were effective against canine PH; however, sildenafil was associated with the risk of worsening left-heart loading. Combination therapy with beraprost and sildenafil synergistically dilated pulmonary and systemic vessels, indicating a more potent treatment option for severe PH cases. [ABSTRACT FROM AUTHOR]

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]

Simple Summary: Pulmonary hypertension is a life-threatening complication in dogs with cardiopulmonary disease. Epoprostenol, a prostacyclin analog, is an intravenous pulmonary vasodilator used for treating pulmonary hypertension in humans; however, it has not been used in veterinary medicine. This study aimed to investigate the effects of epoprostenol on cardiac function and hemodynamics in canine models of chronic pulmonary hypertension. Six laboratory-owned dogs with chronic embolic pulmonary hypertension were anesthetized and underwent right heart catheterization and echocardiography before and after administering epoprostenol, dobutamine, dopamine, and pimobendan. In this study, high doses of epoprostenol significantly decreased pulmonary and systemic vascular resistance and increased left and right ventricular function. In contrast, dobutamine and dopamine significantly increased pulmonary arterial pressure and left and right ventricular function. Pimobendan significantly increased left and right ventricular function without increasing pulmonary arterial pressure. Our results indicate that high doses of epoprostenol might help effectively treat canine pulmonary hypertension through pulmonic and systemic vasodilating effects. Catecholamines improve left and right ventricular function; however, they might worsen the pathophysiology of pulmonary hypertension. Pimobendan also improved left and right ventricular function without worsening pulmonary hypertension pathophysiology; however, a stronger vasodilating effect was observed with epoprostenol. Pulmonary hypertension (PH) is a life-threatening complication in dogs with cardiopulmonary disease. Epoprostenol is an intravenous pulmonary vasodilator used to treat PH in humans; however, its efficacy in dogs remains unknown. We investigated the cardiovascular effects of epoprostenol and several cardiac agents for acute heart failure in canine models of chronic PH. Six dogs with chronic PH were anesthetized and underwent right heart catheterization and echocardiography before and after infusion of epoprostenol, dobutamine, dopamine and pimobendane. (The drug administration order was the same for all dogs). High-dose epoprostenol (15–20 ng/kg/min) tended to decrease pulmonary arterial pressure (PAP) while significantly decreasing pulmonary and systemic vascular resistance and increasing left and right ventricular (LV and RV, respectively) function. Pimobendan significantly increased LV and RV functions without increasing PAP. Conversely, dobutamine and dopamine significantly increased LV and RV function as well as PAP. This study revealed the efficacy of epoprostenol in treating canine PH through its pulmonary and systemic vasodilating effects. Although catecholamines improve LV and RV function, they might worsen PH pathophysiology, and careful monitoring may be necessary when using these drugs. Pimobendan improved LV and RV function without increasing PAP; however, a stronger vasodilating effect was observed with epoprostenol. [ABSTRACT FROM AUTHOR]

Simple Summary: Dilated cardiomyopathy is a cardiac disorder most commonly observed in specific dog breeds and is characterized by diffuse left ventricular systolic dysfunction and left ventricular enlargement. Recent studies have reported a potential connection between diet and dilated cardiomyopathy, and some studies have shown a positive effect of diet change on cardiac function and prognosis in dogs with diet-related dilated cardiomyopathy. However, these reports were from large-breed dogs and did not include detailed assessments of myocardial function, such as two-dimensional speckle-tracking echocardiography. We report an overview of our experience in a small-breed dog with a clinical diagnosis of dilated cardiomyopathy, in which dietary modification resulted in improved cardiac enlargement and myocardial dysfunction evaluated by two-dimensional speckle-tracking echocardiography. We suggest that it is necessary to suspect a dietary association with dilated cardiomyopathy, even in small-breed dogs. Furthermore, the prognosis for diet-related dilated cardiomyopathy in small-breed dogs may also be as good as in previous reports of large-breed dogs when changing to appropriate diets. An 11-year-old intact female Papillion weighing 2.1 kg was referred to our institution with the main complaint of shallow, rapid breathing. At the first visit (day 0), although clinical signs improved due to the use of medication from the primary hospital, transthoracic radiography and echocardiography revealed left heart enlargement and left ventricular dysfunction. A clinical diagnosis of dilated cardiomyopathy (DCM) was made and oral administration of pimobendan, temocapril, and taurine was initiated. However, on day 10, the respiratory status worsened and furosemide was prescribed. On day 54, no significant improvement in heart size was observed. Additionally, the diet that this patient received met the recommendation for diet-related DCM by the U.S. Food and Drug Administration, and the patient's diet was changed from a grain-free diet to a grain-containing diet. On day 1191, the patient's respiratory status was stable and no clinical signs were observed. Transthoracic radiography and echocardiography revealed an improvement in left heart size. Additionally, improvements in the left and right ventricular myocardial strains were observed after changing the diet. We suggest that it may be necessary to suspect a dietary association with dilated cardiomyopathy, and a good prognosis might be expected by dietary modification, even in small-breed dogs. [ABSTRACT FROM AUTHOR]

Real-time three-dimensional echocardiography (RT3DE) enables a noninvasive assessment of right ventricular (RV) morphology. However, no study has evaluated the relationship between RV function obtained by RT3DE and RV pressure-volume loops. This hypothesis-driven, experimental study aimed to assess the utility of RT3DE in the evaluation of RV morphology and function. Ten anesthetized beagle dogs sequentially underwent dobutamine infusion, acute infusion of lactated Ringer's solution, and furosemide administration to alter RV contractility and loading conditions. RV pressure-volume loop-derived hemodynamic measurements and echocardiography, including two-dimensional speckle-tracking echocardiography and RT3DE, were performed in each study protocol. Bland–Altman analysis showed strong agreement in RV volume, ejection fraction, and stroke volume obtained by right heart catheterization and RT3DE. Multiple regression analyses revealed that the peak myocardial velocity of the lateral tricuspid annulus (RV s') and global RV longitudinal strain rate were significantly associated with end-systolic elastance (adjusted r2 = 0.66, p < 0.001). RV s', RV free wall longitudinal strain, and RT3DE-derived stroke volume/end-systolic RV volume ratio were associated with RV pressure-volume loops-derived end-systolic/arterial elastance ratio (adjusted r2 = 0.34, p < 0.001). RT3DE could detect the changes in catheterization-derived RV volume with a strong agreement and might be useful in estimating RV-pulmonary arterial coupling. [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]