Validation of the Tricuspid Annular Plane Systolic Excursion/Systolic Pulmonary Artery Pressure Ratio for the Assessment of Right Ventricular-Arterial Coupling in Severe Pulmonary Hypertension

Abstract

Background: The ratios of tricuspid annular plane systolic excursion (TAPSE)/echocardiographically measured systolic pulmonary artery pressure (PASP), fractional area change/invasively measured mean pulmonary artery pressure, right ventricular (RV) area change/end-systolic area, TAPSE/pulmonary artery acceleration time, and stroke volume/end-systolic area have been proposed as surrogates of RV-arterial coupling. The relationship of these surrogates with the gold standard measure of RV-arterial coupling (invasive pressure-volume loop-derived end-systolic/arterial elastance [Ees/Ea] ratio) and RV diastolic stiffness (end-diastolic elastance) in pulmonary hypertension remains incompletely understood. We evaluated the relationship of these surrogates with invasive pressure-volume loop-derived Ees/Ea and end-diastolic elastance in pulmonary hypertension.

Methods: We performed right heart echocardiography and cardiac magnetic resonance imaging 1 day before invasive measurement of pulmonary hemodynamics and single-beat RV pressure-volume loops in 52 patients with pulmonary arterial hypertension or chronic thromboembolic pulmonary hypertension. The relationships of the proposed surrogates with Ees/Ea and end-diastolic elastance were evaluated by Spearman correlation, multivariate logistic regression, and receiver operating characteristic analyses. Associations with prognosis were evaluated by Kaplan-Meier analysis.

Results: TAPSE/PASP, fractional area change/mean pulmonary artery pressure, RV area change/end-systolic area, and stroke volume/end-systolic area but not TAPSE/pulmonary artery acceleration time were correlated with Ees/Ea and end-diastolic elastance. Of the surrogates, only TAPSE/PASP emerged as an independent predictor of Ees/Ea (multivariate odds ratio: 18.6; 95% CI, 0.8-96.1; P=0.08). In receiver operating characteristic analysis, a TAPSE/PASP cutoff of 0.31 mm/mm Hg (sensitivity: 87.5% and specificity: 75.9%) discriminated RV-arterial uncoupling (Ees/Ea <0.805). Patients with TAPSE/PASP <0.31 mm/mm Hg had a significantly worse prognosis than those with higher TAPSE/PASP.

Conclusions: Echocardiographically determined TAPSE/PASP is a straightforward noninvasive measure of RV-arterial coupling and is affected by RV diastolic stiffness in severe pulmonary hypertension.

Clinical trial registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT03403868.

Keywords: acceleration; echocardiography; hypertension; magnetic resonance imaging; pressure.

Figure 1.

Surrogates for right ventricle (RV)-arterial coupling and their association with single-beat end-systolic elastance (Ees)/arterial elastance (Ea) in patients with pulmonary hypertension. A, Surrogates were compared with data obtained from invasively measured single-beat pressure-volume loops in the study cohort. B, Tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (PASP), fractional area change (FAC)/mean pulmonary artery pressure (mPAP), RV area change/end-systolic area (ESA), and stroke volume (SV)/ESA (all measured by echocardiography except mPAP [right heart catheterization] and SV [cardiac magnetic resonance]) showed significant associations with invasively measured single-beat Ees/Ea. No association of Ees/Ea with TAPSE/pulmonary artery acceleration time (ρ=−0.016; P=0.926) and PASP/ESA (ρ=−0.015; P=0.924) was evident. Pmax indicates maximum pressure of an isovolumic beat.

Figure 2.

Association of surrogates for right ventricle (RV)-arterial coupling with RV single-beat arterial elastance (Ea) and end-diastolic elastance (Eed) in patients with pulmonary hypertension. A, Tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (PASP), (B) Fractional area change (FAC)/mean pulmonary artery pressure (mPAP), (C) RV area change/end-systolic area (ESA), and (D) stroke volume (SV)/ESA (all measured by echocardiography except mPAP [right heart catheterization] and SV [cardiac magnetic resonance]) showed significant associations with i, Ea and ii, Eed in the study cohort. Ea and Eed showed no significant association with TAPSE/pulmonary artery acceleration time (ρ=−0.072, P=0.631 and ρ=−0.051, P=0.734, respectively) and PASP/ESA (ρ=0.118, P=0.452 and ρ=0.085, P=0.589, respectively).

Figure 3.

Stratification of end-diastolic elastance (Eed) according to tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (PASP) tertile in patients with pulmonary hypertension. Eed showed significant differences across tertiles of the echocardiographic TAPSE/PASP ratio in the study cohort (Kruskal-Wallis test). Boxes show median and interquartile range; whiskers show minimum to maximum.

Figure 4.

Receiver operating characteristic curve analysis of tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (PASP), fractional area change (FAC)/mean pulmonary artery pressure (mPAP), and stroke volume (SV)/end-systolic area (ESA) for discriminating right ventricle (RV)-arterial uncoupling in patients with pulmonary hypertension. TAPSE, PASP, FAC, and ESA were assessed by echocardiography in the study cohort; mPAP was assessed by right heart catheterization; and SV by cardiac magnetic resonance. RV-arterial uncoupling was defined as single-beat end-systolic elastance (Ees)/arterial elastance (Ea) <0.805. Diagonal segments were produced by ties. AUC indicates area under the curve.

Figure 5.

Kaplan-Meier plots of outcomes in patients stratified by tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (PASP). Stratification by echocardiographic TAPSE/PASP (≥0.31 mm/mm Hg and <0.31 mm/mm Hg) revealed significant differences in A, clinical worsening in patients with pulmonary hypertension (study cohort; estimates of mean and median time to clinical worsening are shown in Table III in the Data Supplement), and (B) overall survival in patients with idiopathic pulmonary arterial hypertension (external validation cohort; subset of a previously published cohort).