Key result
PAC and RC-time, rather than PVR, most strongly predict RV-PA coupling.
Why the study?
PVR incompletely captures pulsatile afterload, leading to the hypothesis that PAC and RC-time better explain RV-PA coupling across PH subgroups and at Denver altitude.
Do pulmonary arterial compliance and RC-time provide superior explanation of RV-PA coupling compared with PVR alone across pulmonary hypertension phenotypes?
Observational (n=67)
Do pulmonary arterial compliance and RC-time provide superior explanation of RV-PA coupling compared with PVR alone across pulmonary hypertension phenotypes?
Effect estimate: β = +145.3 (PAC), β = -0.20 (log RC-time)
p-value: p=<0.001
Pulmonary arterial compliance, rather than resistance, is the dominant hemodynamic determinant of RV-PA coupling across pulmonary hypertension phenotypes.
PAC was associated with RV-PA coupling; leaves open whether modulating PAC improves outcomes in pulmonary hypertension.
Rationale Right ventricular–pulmonary artery (RV–PA) coupling integrates right-sided contractility with pulmonary vascular load and is a key determinant of prognosis in pulmonary hypertension (PH). Although pulmonary vascular resistance (PVR) remains the primary clinical descriptor of afterload, it incompletely captures the pulsatile component governed by pulmonary arterial compliance (PAC) and the resistance–compliance time constant (RC-time). We hypothesized that PAC and RC-time provide superior explanation of RV–PA coupling compared with PVR alone across all PH subgroups and at Denver altitude. Methods We retrospectively analyzed hemodynamic and echocardiographic data from 67 subjects who underwent clinically indicated right-heart catheterization with concurrent transthoracic echocardiography. RV–PA coupling was quantified as the ratio of tricuspid annular plane systolic excursion to pulmonary artery systolic pressure (TAPSE/PASP). Hemodynamic parameters included thermodilution PVR, PAC estimated as stroke volume divided by pulmonary arterial pulse pressure, and RC-time (PVR × PAC). Subjects meeting mPAP > 20 mmHg, PAWP ≤ 15 mmHg, and PVR > 2 WU were classified as precapillary PAH. Multivariable linear regression was performed with RV coupling as the dependent variable and PVR, PAC, and log-transformed RC-time as predictors, adjusted for age, sex, and PH subtype. Results Mean mPAP was 39 ± 9 mmHg, PAWP 10 ± 3 mmHg, and PVR 4.6 ± 2.1 WU. The overall model explained 74% of the variance in RV–PA coupling (R² = 0.738, p < 0.001). PAC showed a strong positive association with coupling (β = +145.3 ± 15.7, p < 0.001), whereas log RC-time was negatively associated (β = −0.20 ± 0.06, p < 0.01). PVR was not independently related to coupling (β = 0.001 ± 0.008, p = 0.86). The inclusion of PAC and RC-time markedly improved model fit compared with PVR alone (ΔR² + 0.31, p < 0.001). Conclusions Pulmonary arterial compliance, rather than resistance, is the dominant hemodynamic determinant of RV–PA coupling across PH phenotypes and holds true at Denver altitude. The RC-time captures complementary aspects of pulsatile afterload, but PVR alone fails to predict coupling efficiency. These findings highlight the importance of incorporating compliance-based indices into hemodynamic phenotyping and may refine prognostication and therapeutic stratification in PAH and related disorders. This abstract is funded by: Borstein Family Foundation, Reuben M. Cherniack Fellowship, Colorado Pulmonary Vascular Disease Award, NIH 7R01HL144727, VA Merit Review Award 2 I01 BX00204
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Massad et al. (2026) conducted an observational in Pulmonary hypertension (n=67). Pulmonary arterial compliance (PAC) and RC-time vs. Pulmonary vascular resistance (PVR) was evaluated on RV-PA coupling (TAPSE/PASP ratio) (β = +145.3 (PAC), β = -0.20 (log RC-time), p=<0.001). Pulmonary arterial compliance (β = +145.3, p<0.001) and RC-time (β = -0.20, p<0.01), rather than pulmonary vascular resistance, were the dominant hemodynamic determinants of RV-PA coupling.
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