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Background <p>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 [<sup>68</sup>Ga]Ga-FAPI PET imaging biomarker that reflects AS burden and predicts outcomes after TAVI.</p> Methods <p>Nineteen patients with severe symptomatic AS underwent [<sup>68</sup>Ga]Ga-FAPI-04 PET/CT at 60, 70, and 120&#xa0;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<sub>mean</sub>, blood-pool SUV<sub>mean</sub>, 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 (<i>n</i> = 11) were assessed using a predefined composite clinical response.</p> Results <p>Blood-pool SUV<sub>mean</sub> declined from 60 to 120&#xa0;min, whereas myocardial SUV<sub>mean</sub> 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 <i>p</i> = 0.596). By contrast, myocardial SUV<sub>mean</sub> fell from 3.8 ± 0.7 (60&#xa0;min) to 2.1 ± 0.9 (120&#xa0;min; <i>p</i> &lt; 0.001). TBR(EFM) correlated with NT-proBNP at all time-points (60&#xa0;min <i>r</i> = 0.65, <i>p</i> = 0.007; 120&#xa0;min <i>r</i> = 0.72, <i>p</i> = 0.003), whereas SUV<sub>mean</sub> did not (60&#xa0;min <i>p</i> = 0.576; 120&#xa0;min <i>p</i> = 0.109). Baseline TBR(EFM) was significantly lower in one-year responders than non-responders (1.7 ± 0.2 vs. 2.9 ± 0.9; <i>p</i> = 0.013), with separation present at each time point (<i>p</i> &lt; 0.05). Higher baseline TBR(EFM) associated with lower reductions in NT-proBNP at one year (<i>p</i> &lt; 0.05).</p> Conclusions <p>Myocardial [<sup>68</sup>Ga]Ga-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 [<sup>68</sup>Ga]Ga-FAPI assessment. These hypothesis-generating findings require validation in larger, multicenter cohorts.</p> Graphical abstract <p></p>

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Time-robust myocardial [68Ga]Ga-FAPI PET biomarker reflects aortic stenosis severity and predicts post-TAVI outcomes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月16日

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  • Song Xue,
  • Qianling Ye,
  • Aleksa Lazarević,
  • Kevin Hamzaraj,
  • Patrick Binder,
  • Christian Nitsche,
  • Attila Kiss,
  • Bruno K Podesser,
  • Marcus Hacker,
  • Xiang Li,
  • Raffaella Calabretta

摘要

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 [68Ga]Ga-FAPI PET imaging biomarker that reflects AS burden and predicts outcomes after TAVI.

Methods

Nineteen patients with severe symptomatic AS underwent [68Ga]Ga-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 SUVmean, blood-pool SUVmean, 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 SUVmean declined from 60 to 120 min, whereas myocardial SUVmean 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 SUVmean 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 SUVmean 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 [68Ga]Ga-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 [68Ga]Ga-FAPI assessment. These hypothesis-generating findings require validation in larger, multicenter cohorts.

Graphical abstract