ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs

Abstract

Pulmonary hypertension (PH), defined by increased pressure within the pulmonary vasculature, is a hemodynamic and pathophysiologic state present in a wide variety of cardiovascular, respiratory, and systemic diseases. The purpose of this consensus statement is to provide a multidisciplinary approach to guidelines for the diagnosis, classification, treatment, and monitoring of PH in dogs. Comprehensive evaluation including consideration of signalment, clinical signs, echocardiographic parameters, and results of other diagnostic tests supports the diagnosis of PH and allows identification of associated underlying conditions. Dogs with PH can be classified into the following 6 groups: group 1, pulmonary arterial hypertension; group 2, left heart disease; group 3, respiratory disease/hypoxia; group 4, pulmonary emboli/pulmonary thrombi/pulmonary thromboemboli; group 5, parasitic disease (Dirofilaria and Angiostrongylus); and group 6, disorders that are multifactorial or with unclear mechanisms. The approach to treatment of PH focuses on strategies to decrease the risk of progression, complications, or both, recommendations to target underlying diseases or factors contributing to PH, and PH‐specific treatments. Dogs with PH should be monitored for improvement, static condition, or progression, and any identified underlying disorder should be addressed and monitored simultaneously.

Pulmonary hypertension secondary to chronic mitral valve disease in dogs: prevalence and echocardiographic aspects

“…The right ventricle (RV) presents a spatial conformation that complicates echocardiographic evaluation (Boon 2006, Almeida-Filho 2007, however, in order to evaluate of RV systolic function in dogs with pulmonary hypertension has been used as indicator the RV end-diastolic área (RVEDA) as a 2-dimensional indicator of RV size, and the tricuspid annular plane systolic excursion (TAPSE), the fractional area change (FAC) and pulmonary artery distensibility dndex (Borgarelli et at. 2015, Visser et al 2016, Vezzosi et al 2018, Reinero et al 2020. In this study, when the RV remained smaller than the LV it was considered a slight increase; when the area of the RV was similar in size to the LV it was considered a moderate increase; and when the area of the RV was larger than that of the LV it was considered a significant increase (Almeida-Filho 2007).…”

“…When this condition becomes chronic, it may lead to an increase in arterial pressure with a potential effect on the right heart (Boon 2006, Chiavegato et al 2009, Borgarelli et at. 2015, Reinero et al 2020.…”

“…In this study, we identified an optimal correlation between the estimated pressure in the PA and the parameters of the E/A ratio (r=0.3324; p=0.0115) and the Ao/LA ratio (r= -0.3273; p=0.0129), which are related to the progression of mitral valve disease (Schober et al 2006, Chiavegato et al 2009, Borgarelli et at. 2015, Reinero et al 2020. This observation is critical because it indicates that an increase in the E/A ratio and reduction in the Ao/LA ratio in successive echocardiograms can serve as positive predictive factors for the development of PAH (Chiavegato et al 2009).…”

“…In mitral regurgitation caused by degenerative valve disease, chronic elevation of the left atrial pressure with subsequent pulmonary venous hypertension is considered one of the major causes of PAH (Pyle et al 2004, Stepien 2009, Reinero et al 2020. The increased preload is the main factor responsible for the retrograde congestion, making the blood initially accumulate in the pulmonary veins, the lungs, the pulmonary arteries and the right heart chambers, which may lead to findings such as tricuspid insufficiency and pulmonary hypertension in the most severe cases of mitral regurgitation (Stepien 2009).…”

Spontaneous tricuspid valve chordal rupture in a dog with severe, irreversible pulmonary hypertension caused by Angiostrongylus vasorum infection

“…The underlying mechanism of pulmonary hypertension is increased vascular resistance caused by the combination of vascular luminal obstruction and perivascular inflammation [3]. Pulmonary hypertension caused by this parasite can be partially or fully reversible, or irreversible [2,3,26,29]. The underlying mechanism why the pulmonary hypertension in certain dogs persists despite eradication of the French heartworm infection remains to be determined.…”