Association between pulmonary arterial compliance and ventricular–arterial interaction in pulmonary hypertension

Background

Pulmonary artery compliance (PAC), defined as stroke volume divided by pulmonary arterial pulse pressure, reflects the pulsatile component of right ventricular (RV) afterload and has been associated with adverse outcomes in pulmonary hypertension (PH). Although commonly regarded as a marker of pulmonary vascular stiffness, PAC incorporates flow-dependent components and may represent a more integrated hemodynamic parameter. The extent to which PAC reflects resistive load versus RV–pulmonary arterial (RV–PA) coupling remains incompletely defined.

Purpose

To investigate the association between PAC and RV–PA coupling, assessed by the TAPSE/SPAP ratio, and to determine whether this relationship is independent of pulmonary vascular resistance and filling pressures in patients with PH.

Methods

In this cross-sectional study, 138 consecutive patients with confirmed PH were enrolled. PAC was calculated as stroke volume divided by pulmonary artery pulse pressure (mL/mmHg). RV–PA coupling was estimated non-invasively using TAPSE/SPAP. Pulmonary vascular resistance (PVR), right atrial pressure (RAP), and pulmonary capillary wedge pressure (PCWP) were obtained from right heart catheterization. Pearson correlation and partial correlation analyses were performed. Multivariable linear regression analysis was conducted with PAC as the dependent variable, including TAPSE/SPAP, PVR, RAP, and PCWP as covariates. Collinearity diagnostics were assessed.

Results

PAC demonstrated a moderate positive correlation with TAPSE/SPAP (r = 0.55, p < 0.001) and a moderate inverse correlation with PVR (r = –0.43, p < 0.001). The association between PAC and TAPSE/SPAP remained significant after adjustment for PVR (partial r = 0.46, p < 0.001).

In multivariable analysis, TAPSE/SPAP (β = 0.425, p < 0.001) and PVR (β = –0.296, p < 0.001) were independently associated with PAC, whereas RAP (p = 0.656) and PCWP (p = 0.230) were not. The overall model was statistically significant (R² = 0.375, p < 0.001), accounting for 37.5% of the variance in PAC, with no evidence of relevant multicollinearity.

Conclusion

In patients with PH, PAC was independently associated with both PVR and RV–PA coupling. Notably, the standardized association with TAPSE/SPAP was numerically stronger than that observed for PVR, suggesting that ventricular–arterial interaction may contribute to PAC to a greater extent than resistive load alone. These findings support the concept that PAC represents an integrated hemodynamic parameter reflecting both vascular and ventricular components in PH.For image description, please refer to the figure legend and surrounding text.Figure 1For image description, please refer to the figure legend and surrounding text.