How to Incorporate Tricuspid Regurgitation in Right Ventricular-Pulmonary Arterial Coupling

Adaptation of the right ventricle (RV) to a progressively increasing afterload is one of the hallmarks of pulmonary arterial hypertension (PAH). Pressure-volume loop analysis provides measures of load-independent RV contractility, i.e. end-systolic elastance, and pulmonary vascular properties, i.e. effective arterial elastance (E ). However, PAH induced-RV overload potentially results in tricuspid regurgitation (TR). TR makes RV eject to both PA and right atrium; thereby a ratio of RV end-systolic pressure (P ) to RV stroke volume (SV) could not correctly define E . To overcome this limitation, we introduced a two-parallel compliance model, i.e. E =1/(1/E +1/E ), while effective pulmonary arterial elastance (E =P /PASV) represents pulmonary vascular properties, effective tricuspid regurgitant elastance represents TR. We conducted animal experiments to validate this framework. First, we performed SV analysis with a pressure-volume catheter in the RV and a flow probe at the aorta in rats with and without pressure-overloaded RV to determine the effect of inferior vena cava (IVC) occlusion on TR. A discordance between the two techniques was found in rats with pressure-overloaded RV, not in Sham. This discordance diminished after IVC occlusion, suggesting that TR in pressure-overloaded RV was diminished by IVC occlusion. Next, we performed pressure-volume loop analysis in rats with pressure-overloaded RVs, calibrating RV volume by cardiac magnetic resonance. We found that IVC occlusion increased E , suggesting that a reduction of TR increased E . Using the proposed framework, E was indistinguishably to E post-IVC occlusion. We conclude that the proposed framework helps better understanding of the pathophysiology of PAH and associated right heart failure.