Background: Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling and right ventricular (RV) dysfunction. ¹⁸F FDG PET/MRI may reveal metabolic altera-tions in the pulmonary parenchyma and vasculature. We investigated pulmonary FDG up-take in PAH versus healthy controls and its associations with hemodynamics, RV function, and clinical outcomes.
Methods: Twenty-eight stable PAH patients and 12 age-matched healthy controls underwent ¹⁸F-FDG PET/MRI. Standardized uptake values (SUV) were measured in lung parenchyma and proxi-mal pulmonary arteries. Hemodynamic parameters were obtained via right heart cath-eterization; RV–PA coupling was assessed as stroke volume/end-systolic volume (SV/ESV). Twen-ty PAH patients underwent follow-up imaging after targeted therapy. Clinical endpoints (CEP: death, hospitalization, disease progression) were analyzed by Kaplan–Meier and Cox regression.
Results: PAH patients showed markedly elevated lung parenchymal SUV (0.405 [0.338–0.533] vs. 0.225 [0.207–0.273], p< 0.001) and proximal PA SUV (3.46 [1.95–6.89] vs. 1.48 [1.15–1.65], p< 0.001). The two metrics were uncorrelated (r=+0.105, p=0.595). SUV PA Proximal correlated with mPAP (r=+0.551) and PVR (r=+0.517), while SUV Lung showed no hemodynamic correlations. After 24 months of therapy, RV–PA coupling im-proved significantly (p=0.037); lung SUV showed a non-significant trend toward reduction (Δ=−0.10, p=0.128). Sixteen CEPs occurred; impaired RV–PA coupling (HR=0.04, p=0.002), elevated mPAP (HR=1.08, p< 0.001), and reduced RVEF (HR=0.91, p< 0.001) were strong univaria-ble predictors. Neither SUV metric retained independent prognostic value in multivariable analysis.
Conclusions: Pulmonary parenchymal and proximal PA FDG uptake are markedly elevated inPAH. However, neither metric independently predicts hemodynamic severity or clinical outcomes, limiting their current role as reliable prognostic surrogates.