Key result
The apparent futility of PAPi in aortic stenosis may stem from unaccounted pulmonary artery compliance heterogeneity and reliance on indirect Fick-derived cardiac output with an error of ~15%.
Re-evaluating PAPi in aortic stenosis patients with low stroke volume index and accounting for pulmonary artery compliance may reveal its true prognostic value.
Grouping PAPi by quartiles (Q1 ≤ 2.67) may mask its utility in advanced disease. In TAVR cohorts with lower stroke volume index (SVI),6 PAPi <2.0 predicted adverse outcomes. Critically, your Q1 group had only mildly reduced SVI (35 vs. 38 mL/m2), potentially including ‘pseudo-low PAPi’ patients (high PAC compensating for borderline SVI). Re-testing PAPi in the subset with SVI < 30 mL/m2 (n ≈ 60 by your data) might reveal its predictive value. PAC calculation relied on indirect Fick-derived cardiac output (error ~15%).7 This could attenuate true SVI-PAC correlations—a limitation acknowledged but not quantified in your discussion. Critically, pulmonary capillary wedge pressure (PCWP) directly modulates PAC's haemodynamic interpretation,8 yet its interaction with PAPi was unexplored. Future studies could integrate: Synchronized echocardiography (TAPSE/PASP ratio for RV-PA coupling). CT-based pulmonary artery volumetry5 to distinguish adaptive versus maladaptive remodelling. PAPi's apparent futility may stem from unaccounted PAC heterogeneity and suboptimal risk stratification. Validating PAC thresholds and high-risk phenotypes will refine prognostication in AS.
No takes yet. Share an insight, caveat, or question.
Hu et al. (2025) conducted a letter in Aortic Stenosis. Pulmonary Artery Pulsatility Index (PAPi) was evaluated. The apparent futility of PAPi in aortic stenosis may stem from unaccounted pulmonary artery compliance heterogeneity and reliance on indirect Fick-derived cardiac output with an error of ~15%.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: