Right Ventricular Myocardial Adaptation Assessed by Two-Dimensional Speckle Tracking Echocardiography in Canine Models of Chronic Pulmonary Hypertension

Abstract

Background: Pulmonary hypertension (PH) is a life-threatening disease in dogs characterized by an increase in pulmonary arterial pressure (PAP) and/or pulmonary vascular resistance. Right ventricle adapts to its pressure overload through various right ventricular (RV) compensative mechanisms: adaptive and maladaptive remodeling. The former is characterized by concentric hypertrophy and increased compensatory myocardial contractility, whereas the latter is distinguished by eccentric hypertrophy associated with impaired myocardial function.Objectives: To evaluate the RV adaptation associated with the increase of PAP using two-dimensional speckle tracking echocardiography.Animals: Seven experimentally induced PH models.Methods: Dogs were anesthetized and then a pulmonary artery catheter was placed via the right jugular vein. Canine models of PH were induced by the repeated injection of microspheres through the catheter and monitored pulmonary artery pressure. Dogs were performed echocardiography and hemodynamic measurements in a conscious state when baseline and systolic PAP (sPAP) rose to 30, 40, 50 mmHg, and chronic phase. The chronic phase was defined that the sPAP was maintained at 50 mmHg or more for 4 weeks without injection of microspheres.Results: Pulmonary artery to aortic diameter ratio, RV area, end-diastolic RV wall thickness, and RV myocardial performance index were significantly increased in the chronic phase compared with that in the baseline. Tricuspid annular plane systolic excursion was significantly decreased in the chronic phase compared with that in the baseline. The RV longitudinal strain was significantly decreased in the sPAP30 phase, increased in the sPAP40 and sPAP50 phases, and decreased in the chronic phase.Conclusions: Changes in two-dimensional speckle tracking echocardiography-derived RV longitudinal strain might reflect the intrinsic RV myocardial contractility during the PH progression, which could not be detected by conventional echocardiographic parameters.

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

“…Although TR velocity showed the same tendency as PVRecho, a previous study has reported that systolic PAP estimated by TR velocity showed poor agreement with that measured by catheterization ( 31 ), and ACVIM consensus stated that PH diagnosis by TR velocity alone should be avoided ( 1 ). Furthermore, our previous study reported that RV compensated for mild pressure overload by hyperactivation and decompensated for moderate-to-severe and chronic pressure overload in dogs with experimentally induced PH ( 27 ), suggesting that the pseudo-normalization of RV systolic function cannot be avoided as PH progresses. Therefore, the overall assessment of RV performance and afterload, such as PVRecho and PVRecho2, might be more useful for the clinical assessment of PH rather than the assessment using TR velocity and/or RV performance variables alone.…”

“…In this study, an increased RVIDd index was also associated with the presence of R-CHF with high AUC, sensitivity, and specificity, as well as PVRecho2. We previously described RV maladaptation against RV afterload in dogs with chronic PH and that RV dysfunction would induce RV dilatation to maintain RV cardiac output ( 27 ). Dogs with R-CHF in this study also showed RV dysfunction based on a decrease in RV-SL and RV-SrL and increased RV afterload based on TR velocity.…”

“…All 2D-STE analyses were performed using the same offline workstation as that used for standard echocardiography. RV-SL and RV-SrL were obtained from the RV focus view using the left ventricular four-chamber algorithm ( 16 , 17 , 27 ). The region of interest for 2D-STE was determined by manually tracing the RV endocardial border.…”

“…RV-SL and RV-SrL were measured using only RV free wall analysis (3seg), performed by tracing from the level of the lateral tricuspid annulus to the RV apex (Figure 2A), and RV global analysis (6seg), performed by tracing from the lateral tricuspid annulus to the septal tricuspid annulus via the RV apex (i.e., both RV free wall and interventricular septum) (Figure 2B). RV-SL was reported as the absolute value of the negative peak obtained from the strain wave (16,17,27). The RV-SrL was obtained from the strain rate wave and was reported as the absolute value of the negative peak during systole (27)(28)(29).…”

“…RV-SL was reported as the absolute value of the negative peak obtained from the strain wave (16,17,27). The RV-SrL was obtained from the strain rate wave and was reported as the absolute value of the negative peak during systole (27)(28)(29).…”