BackgroundRight atrial area (RAA) is a prognostic factor in human patients with pulmonary arterial hypertension (PAH). Reference intervals for RAA have been described in healthy dogs.ObjectivesTo evaluate RAA indexed to the body surface area in dogs with PAH as an indicator of right atrial size, PAH severity and right‐sided congestive heart failure (R‐CHF).AnimalsA total of 119 client‐owned dogs, 48 dogs with PAH and 71 control dogs.MethodsProspective observational study. Pulmonary arterial hypertension was classified according to the tricuspid regurgitation pressure gradient (TRPG) as mild (36–50 mmHg), moderate (51–75 mmHg), or severe (>75 mmHg). The RAA index was calculated as the RAA divided by body surface area.ResultsThe RAA index was higher in dogs with moderate PAH (13.3 cm2/m2; range, 3.4–24.7 cm2/m2) and severe PAH (12.1 cm2/m2; range, 5.4–21.8 cm2/m2) than in those with mild PAH (6.7 cm2/m2; range, 4.8–10.7 cm2/m2) or in controls (7.3 cm2/m2; range, 4.2–10.2 cm2/m2; P < 0.001). The RAA index was higher (P < 0.0001) in dogs with R‐CHF (17.5 cm2/m2; range, 12.7–24.7 cm2/m2) compared to those without R‐CHF (7.6 cm2/m2; range, 4.4–19.4 cm2/m2). The most accurate cutoff value of the RAA index to identify R‐CHF was >12.3 cm2/m2 (sensitivity, 100%; specificity, 89.5%). In dogs with PAH, severity of tricuspid regurgitation (TR) was the only independent predictor of RAA index based on multivariate analysis (P < 0.02).Conclusions and Clinical ImportanceThe RAA index can be used to evaluate right atrial size in dogs and may be more effective than TRPG in predicting R‐CHF in dogs with PAH. The severity of TR is the main determinant of the RAA index in dogs with PAH.
The haemodynamic effects of oral prazosin and hydralazine were evaluated in patients with refractory heart failure and compared with those of intravenous nitroprusside in the same patients. Both oral agents were well tolerated and appeared to have beneficial haemodynamic effects. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin resulted in a more significant decline in left ventricular filling pressure and pulmonary vascular resistance than did hydralazine. Haemodynamic alterations induced by prazosin were similar to those induced by nitroprusside, which suggests a relatively balanced reduction of preload and afterload. With hydralazine, the increase in cardiac output without change in left ventricular filling pressure or pulmonary vascular resistance suggests minimal effect on preload but significant reduction in afterload.
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