Pulmonary Vascular Resistance Estimated by Echocardiography in Dogs With Myxomatous Mitral Valve Disease and Pulmonary Hypertension Probability

Abstract

Post-capillary pulmonary hypertension (PH) is a life-threatening complication in dogs with myxomatous mitral valve disease (MMVD). An increase in pulmonary vascular resistance (PVR) is associated with post-capillary PH progression. In humans, PVR estimated by echocardiography (PVRecho) enables the non-invasive assessment of PVR in patients with PH. This study aimed to evaluate the clinical utility of PVRecho in dogs with MMVD, PH probability, and right-sided congestive heart failure (R-CHF). Dogs with MMVD and detectable tricuspid valve regurgitation were included in the study. Dogs were classified into three PH probability groups (low/intermediate/high) and according to the presence or absence of R-CHF. All dogs underwent echocardiographic measurements for right ventricular (RV) morphology and function. PVRecho was calculated by two methods using tricuspid valve regurgitation velocity and velocity–time integral of the pulmonary artery flow (PVRecho and PVRecho2). RV size indicators were significantly higher with a higher probability of PH. RV strain and velocity–time integral of the pulmonary artery flow in the high probability group were significantly lower than those in the other groups. Tricuspid valve regurgitation velocity, PVRecho, and PVRecho2 were significantly higher with an increase in PH probability. Logistic regression analysis revealed a significant association between the presence of R-CHF and increased PVRecho2 and end-diastolic RV internal dimension normalized by body weight. PVRecho and PVRecho2 showed significant differences among the PH probability groups. These non-invasive variables may be useful for the diagnosis and stratification of PH and the determination of the presence of R-CHF in dogs with MMVD.

Utility of Real-Time Three-Dimensional Echocardiography for the Assessment of Right Ventricular Morphology and Function in Large Animal Models

“…If CV ≥ 10.0 and ICC ≤ 0.7, the data should be judged by a third blinded independent observer. For the other echocardiographic variables than RT3DE, the laboratory intra- and interobserver measurement variabilities have already been reported in our previous studies [ 11 , 17 , 18 ].…”

“…Global RV analysis (6seg) was also performed by tracing from the lateral tricuspid annulus to the septal tricuspid annulus (including the interventricular septum) via the RV apex. The RV-SL was recorded as the absolute value of the negative peak of the strain wave [ 10 , 11 , 12 , 17 , 18 ]. The RV-SrL was recorded as the absolute value of the negative peak of the strain rate wave during systole [ 10 , 12 ].…”

Animal models of pulmonary hypertension due to left heart disease

“…Although an attempt to apply an animal model of volume loading‐induced heart failure 72 to the study of PH‐LHD has been proposed, its incompatibility with the pathological process of the disease does not yet allow its mainstreaming. Considering PH‐LHD caused by myxomatous mitral valve disease occurring in dogs, 73 its predominant echocardiography findings do not support its establishment as a stable model. Although metabolomics has been employed to in vivo models of PH challenged by monocrotaline, hypoxia, or SU5416/hypoxia at the tissue or cellular level or in vitro models (such as pulmonary arterial smooth muscle cells under the stimulus of hypoxia), 74–78 to date, the metabolic reprogramming of animal models mimicking PH‐LHD remains unveiled.…”

“…In preclinical studies of PH-LHD, none of the current available animal models, including aortic banding, left coronary artery ligation, and the recent combination of metabolic syndrome with aortic banding or vascular endothelial growth factor receptor blocker (Figure 2), can fully characterize PH-LHD and simulate the development of the disease. Although an attempt to apply an animal model of volume loading-induced heart failure 72 to the study of PH-LHD has been proposed, its incompatibility with the pathological process of the disease does not yet allow its mainstreaming.Considering PH-LHD caused by myxomatous mitral valve disease occurring in dogs,73 its predominant echocardiography findings do not support its establishment as a stable model. Although metabolomics has been employed to in vivo models of PH challenged by monocrotaline, hypoxia, or SU5416/hypoxia at the tissue or cellular level or in vitro models (such as pulmonary arterial smooth muscle cells under the stimulus of hypoxia),[74][75][76][77][78] to date, the metabolic reprogramming of animal models mimicking PH-LHD remains unveiled.…”

Investigation of Beraprost Sodium on Cardiac Function and Hemodynamics in Canine Models of Chronic Pulmonary Hypertension

“…SVI was calculated by dividing systolic systemic arterial pressure obtained from the oscillometric method by LV stroke volume normalized by the body surface area (LV SV). PVI was calculated by dividing invasive systolic PAP by RV stroke volume normalized by body surface area (RV SV) ( 35 ). LV SV and RV SV were measured using the cross-sectional area method as described previously ( 36 ).…”