Key result
Higher TAPSE/sPAP in PAH linked to ~51% lower risk of mortality, transplant, or clinical worsening.
Why the study?
Although TAPSE/sPAP is a validated RV-PA coupling parameter in pulmonary arterial hypertension, its prognostic significance for clinical outcomes remains uncertain.
Does a higher TAPSE/sPAP ratio predict better clinical outcomes in patients with pulmonary arterial hypertension?
Meta-Analysis
Does a higher TAPSE/sPAP ratio predict better clinical outcomes in patients with pulmonary arterial hypertension?
TAPSE/sPAP is a strong prognostic marker in PAH, with higher values significantly associated with lower risks of mortality and clinical worsening.
Supports TAPSE/sPAP for PAH risk stratification; reinforces its prognostic value in meta-analysis.
OBJECTIVES: Tricuspid annular plane systolic excursion to systolic pulmonary artery pressure ratio (TAPSE/sPAP) is a simple and validated right ventricle-pulmonary artery (RV-PA) coupling parameter in pulmonary arterial hypertension (PAH). Its prognostic significance for clinical outcomes, however, remains uncertain. This study aimed to evaluate the association between TAPSE/sPAP and key clinical outcomes in PAH. METHODS: Medline, Embase, and Cochrane Library were searched from inception to 4 March 2025. Cohort studies evaluating associations between TAPSE/sPAP and clinical outcomes in PAH patients were included. Primary outcome was the composite endpoints of all-cause mortality, lung transplantation after re-evaluation, or clinical worsening. Secondary outcomes included individual components of the primary endpoint, time to clinical worsening (TTCW), and ratio of end-systolic elastance to arterial elastance (Ees/Ea). Hazard ratios (HR) with 95% confidence intervals (CIs) were pooled using a fixed-effect model. RESULTS: Fourteen studies were included. Higher baseline TAPSE/sPAP was significantly associated with a lower risk of composite endpoints (dichotomous HR = 0.49; continuous HR = 0.93), reduced all-cause mortality (dichotomous HR = 0.49; continuous HR = 0.94) and lower risk of clinical worsening (dichotomous HR = 0.36; continuous HR = 0.00). Follow-up TAPSE/sPAP was also inversely associated with the composite outcome (dichotomous HR = 0.43). No consistent association was observed between TAPSE/sPAP and Ees/Ea. CONCLUSION: TAPSE/sPAP is a strong prognostic marker in PAH, significantly associated with lower risk of composite endpoints, all-cause mortality, and clinical worsening. Follow-up TAPSE/sPAP also predicts outcomes, though its evidence for mortality and worsening remains limited and requires further study.
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Luo et al. (2026) conducted a meta-analysis in Pulmonary arterial hypertension. TAPSE/sPAP was evaluated on Composite endpoints of all-cause mortality, lung transplantation after re-evaluation, or clinical worsening (HR 0.49). Higher baseline TAPSE/sPAP in pulmonary arterial hypertension was associated with a lower risk of mortality, transplant, or clinical worsening (dichotomous HR 0.49; continuous HR 0.93).
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