Baseline myocardial [68Ga]Ga-FAPI TBR(EFM) was significantly lower in patients who showed clinical improvement at 1 year post-TAVI (1.7 ± 0.2) compared to non-responders (2.9 ± 0.9) with p=0.013.
Observational (n=19)
Open-label
No
Does myocardial [68Ga]Ga-FAPI PET TBR(EFM) correlate with NT-proBNP and predict 1-year clinical response in patients with severe symptomatic aortic stenosis undergoing TAVI?
Myocardial [68Ga]Ga-FAPI PET using a blood-pool-normalized ratio (TBR) at 60 minutes provides a stable biomarker of active fibroblast signaling that correlates with hemodynamic stress and predicts 1-year clinical response after TAVI.
Effect estimate: p=0.013 (Mann-Whitney test) for difference in baseline myocardial TBR(EFM) between responders and non-responders
Absolute Event Rate: 1.7% vs 2.9%
p-value: p=0.013
Abstract Background Aortic stenosis (AS) induces myocardial remodeling and fibroblast activation, yet modifiable biomarkers capable of capturing active fibrogenesis and predicting post-transcatheter aortic valve implantation (TAVI) recovery are currently scarce. Fibroblast activation protein (FAP)–targeted PET serves as a noninvasive tool to visualize activated fibroblasts in vivo. We evaluated a time-robust, blood-pool–normalized myocardial 68 GaGa-FAPI PET imaging biomarker that reflects AS burden and predicts outcomes after TAVI. Methods Nineteen patients with severe symptomatic AS underwent 68 GaGa-FAPI-04 PET/CT at 60, 70, and 120 min. Using an in-house semi-automatic pipeline, the left ventricular (LV) myocardium was segmented, and regions of elevated fibroblast activity (EFM) were delineated using a blood-pool–anchored, time-point–specific threshold. We quantified myocardial SUV mean , blood-pool SUV mean , and a normalized myocardium-to-blood index, TBR(EFM), and assessed associations with N-terminal pro-brain natriuretic peptide (NT-proBNP) and left-ventricular ejection fraction (LVEF). One-year outcomes ( n = 11) were assessed using a predefined composite clinical response. Results Blood-pool SUV mean declined from 60 to 120 min, whereas myocardial SUV mean decreased less, yielding stable TBR(EFM) across time points (60/70/120 min: 2.2 ± 0.8, 2.1 ± 0.9, 2.3 ± 0.9; ANOVA p = 0.596). By contrast, myocardial SUV mean fell from 3.8 ± 0.7 (60 min) to 2.1 ± 0.9 (120 min; p < 0.001). TBR(EFM) correlated with NT-proBNP at all time-points (60 min r = 0.65, p = 0.007; 120 min r = 0.72, p = 0.003), whereas SUV mean did not (60 min p = 0.576; 120 min p = 0.109). Baseline TBR(EFM) was significantly lower in one-year responders than non-responders (1.7 ± 0.2 vs. 2.9 ± 0.9; p = 0.013), with separation present at each time point ( p < 0.05). Higher baseline TBR(EFM) associated with lower reductions in NT-proBNP at one year ( p < 0.05). Conclusions Myocardial 68 GaGa-FAPI TBR may provide a time-robust index of active fibroblast signaling that relates to myocardial hemodynamic stress and stratifies one-year clinical response after TAVI. A single 60-minute acquisition with TBR quantification may be sufficient for myocardial 68 GaGa-FAPI assessment. These hypothesis-generating findings require validation in larger, multicenter cohorts. Graphical abstract
Xue et al. (Mon,) conducted a observational in Patients with severe symptomatic aortic stenosis undergoing transcatheter aortic valve implantation (TAVI) (n=19). [68Ga]Ga-FAPI-04 PET/CT imaging vs. null was evaluated on Composite clinical response at 1 year after TAVI defined as improvement in at least two clinical domains among NT-proBNP decrease ≥30%, NYHA functional class improvement ≥1 class, hsCRP decrease ≥15% if elevated, patient-reported dyspnea improvement, or LVEF increase ≥5% if baseline < 60% (p=0.013 (Mann-Whitney test) for difference in baseline myocardial TBR(EFM) between responders and non-responders, p=0.013). Baseline myocardial [68Ga]Ga-FAPI TBR(EFM) was significantly lower in patients who showed clinical improvement at 1 year post-TAVI (1.7 ± 0.2) compared to non-responders (2.9 ± 0.9) with p=0.013.