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.

Highlights

  • Pulmonary hypertension (PH), a life-threatening disease in dogs, is characterized by increased pulmonary arterial pressure (PAP, normal range: systolic PAP; 15–25 mmHg, mean PAP; 10–15 mmHg, and diastolic PAP; 5–10 mmHg) and/or pulmonary vascular resistance [1, 2]

  • The dogs were administered repeated microsphere infusions for 2.2 ± 1.0, 6.9 ± 3.8, 14.9 ± 5.7, and 50.9 ± 13.1 weeks to meet the definition of sPAP30, sPAP40, sPAP50, and chronic, respectively

  • two-dimensional speckle tracking echocardiography (2D-STE)-derived right ventricular (RV) systolic function was temporarily decreased due to the acute rise in PAP; it improved with RV hypertrophy; this may be a sign of RV adaptive remodeling

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Summary

Introduction

Pulmonary hypertension (PH), a life-threatening disease in dogs, is characterized by increased pulmonary arterial pressure (PAP, normal range: systolic PAP; 15–25 mmHg, mean PAP; 10–15 mmHg, and diastolic PAP; 5–10 mmHg) and/or pulmonary vascular resistance [1, 2]. To compensate for low cardiac output due to increased PAP, the right ventricle responds through two compensatory mechanisms: adaptive and maladaptive remodeling [6,7,8,9] 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. 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

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