Clinical Usefulness of Right Ventricular-Pulmonary Artery Coupling in Patients with Heart Failure

Abstract

Heart failure (HF) imposes a significant burden on public health, affecting over 56.19 million people worldwide. Right ventricular (RV) dysfunction may occur in HF patients due to various factors, including adverse interventricular interactions, ischemic heart disease, and HF-correlated pulmonary hypertension. Additionally, the deterioration of RV function plays a critical role in the progression of HF, regardless of left ventricular (LV) systolic function, suggesting an unfavorable outcome. Throughout the progression of HF and increasing afterload, the right ventricle undergoes adaptive remodeling to preserve adequate cardiac output. Right ventricular-pulmonary artery (RV-PA) coupling integrates the dynamic adaptation of RV systolic function to afterload and has been considered a stronger predictor of HF prognosis than other conventional parameters. Thus, accurate evaluations of RV-PA coupling are significant in the clinical diagnosis and management of HF patients, along with prognostic speculation. In this review, we summarize the basic principles and measurements of RV-PA coupling and focus on its clinical significance across each subtype of HF.

Keywords: heart failure; heart failure with preserved ejection fraction; right ventricular dysfunction; right ventricular-pulmonary artery coupling.

Figure 1

Progression from RV-PA coupling to uncoupling in the course of progressively increasing afterload and PVR caused by HF. (A) Normal RV-PA coupling. (B) With increasing RV afterload, RV adaptively remodels to maintain sufficient output, RV hypertrophy, diastolic dysfunction, and RV systolic function occur. (C) With progressively increasing afterload and PVR, RV dilates to maintain stroke volume, accompanied by tricuspid regurgitation, RA, IVC, and SVC dilation. RV systolic function and output are impaired when RV-PA uncoupling occurs. HF: heart failure; RV, right ventricle; RV-PA, right ventricular-pulmonary artery; IVC: inferior vena cava; PVR: pulmonary vascular resistance; SVC, superior vena cava.

Figure 2

Right ventricular pressure–volume loop from which effective arterial elastance (Ea) and end-systolic elastance (Ees) are derived. EDV: end-diastolic volume; EDPVR: end-diastolic pressure–volume relationship; ESP: end-systolic pressure; ESPVR: end-systolic pressure–volume relationship; ESV: end-systolic volume; V₀: hypothetical uncompressed ventricular volume.

Figure 3

Examples of measurements of right ventricular-pulmonary artery coupling in HFpEF (A–E) and HFrEF (F–J) patients using 2DE and speckle tracking echocardiography. (A,F) Measurements of TAPSE. (B,G) Measurement of S’. (C,H) Calculation of RVFAC. (D,I) Evaluation of RVFWS. (E,J) Estimation of PASP using peak tricuspid regurgitation velocity, RVSP, and inferior vena cava diameter. 2DE: two-dimensional echocardiography; FAC: functional area change; HFpEF: heart failure with preserved ejection fraction; HFrEF: heart failure with reduced ejection fraction; PASP: pulmonary arterial systolic pressure; RVFWS: free wall longitudinal strain; RVSP: right ventricular systolic pressure; S’: tricuspid annular systolic velocity; TAPSE: tricuspid annular plane systolic excursion.

Figure 4

Examples of assessments of SV/ESV using CMR and 3DE. (A,B) Measurement of EDV, ESV, and SV using CMR; (C) measurement of EDV, ESV and SV using 3DE. 3DE: three-dimensional echocardiography; CMR: cardiac magnetic resonance; EDV: end-diastolic volume; ESV: end-systolic volume; SV: stroke volume.