Echocardiography-derived effective pulmonary arterial elastance predicts mortality after transcatheter aortic valve replacement

Background

Right ventricular–pulmonary arterial (RV–PA) uncoupling influences outcomes after transcatheter aortic valve replacement (TAVR). Effective pulmonary arterial elastance (EPA), calculated non-invasively as right ventricular systolic pressure divided by stroke volume (RVSP/SV), integrates pressure and flow to quantify total right ventricular afterload. Its prognostic significance after TAVR remains uncertain.

Purpose

To determine whether echocardiography-derived EPA predicts mortality after TAVR and whether it provides incremental prognostic information beyond conventional RV–PA coupling metrics.

Methods

Consecutive adults undergoing first TAVR for severe aortic stenosis between 2010 and 2023 were retrospectively analyzed. EPA was derived from transthoracic echocardiography at baseline and 1 month. Patients were categorized by EPA quartiles (<0.35, 0.35–<0.45, 0.45–<0.60, ≥0.60 mmHg/mL) and by baseline-to-1-month trajectories (persistent low, improved, worsened, persistent high). The primary endpoint was all-cause mortality. Associations were evaluated using Kaplan–Meier analysis and multivariable Cox regression adjusting for age, sex, Charlson Comorbidity Index, left ventricular ejection fraction and aortic valve area. Incremental prognostic value was assessed using hierarchical modelling with Harrell’s C-index and likelihood ratio testing.

Results

Among 2,273 patients (mean age 80 ± 8 years; 57% men), median EPA was 0.45 (IQR 0.35-0.60) mmHg/mL. Higher EPA identified a high-risk phenotype characterized by lower stroke volume index, higher pulmonary pressures and adverse remodeling. During median follow-up of 3.5 years, 984 deaths occurred.

At baseline, the highest EPA quartile was independently associated with increased mortality (adjusted hazard ratio (HR) 2.15, 95% confidence interval (CI) 1.75–2.65). At 1 month, the highest quartile demonstrated even greater risk (adjusted HR 2.71, 95% CI 2.18–3.37).

Trajectory analysis (n=1,500) showed persistently high EPA (30%) and worsened EPA (9%) conferred the greatest mortality risk (adjusted HR 2.00, 95% CI 1.64–2.44 and HR 1.93, 95% CI 1.48–2.51, respectively).

In hierarchical analyses performed in the TAPSE-complete (n=898) and S′-complete (n=1,628) cohorts, EPA improved model performance beyond clinical variables (ΔLR χ²=23.96 and 42.01; both p<0.001; C-index +0.042 and +0.028), whereas adding TAPSE/RVSP or S′/RVSP after EPA yielded negligible discrimination gain (ΔC=+0.001; p=0.002 and 0.44).

Conclusions

Echocardiography-derived EPA independently predicts mortality after TAVR and provides prognostic information beyond conventional RV–PA coupling metrics. Persistent or worsening EPA identifies a high-risk phenotype, supporting EPA as a practical pressure–flow marker for risk stratification in severe aortic stenosis.Association between EPA and mortalityIncremental prognostic value of EPA