Article Figures & Data
Figures
- FIGURE 1.
Multimodal characterization of myocardial fibrosis in AS patients before TAVR. Shown are 2 cases with high and low myocardial 68Ga-FAPI signal, as indicated by representative midventricular short-axis PET/CT image (column 2) and parametric polar maps of 68Ga-FAPI uptake (column 3; polar maps are 2-dimensional display of 3-dimensional LV activity with apex in center, base in periphery, anterior wall on top, inferior wall on bottom, septum on left, and lateral wall on right). High 68Ga-FAPI signal was associated with mild elevation of native T1 from CMR (column 1) and mild reduction of global longitudinal strain at TTE (column 4). Yet, neither CMR T1 nor TTE global longitudinal strain show similarly clear distinction between patients when compared with 68Ga-FAPI signal. GLS = global longitudinal strain.
- FIGURE 2.
Regression plot for myocardial volume of elevated 68Ga-FAPI signal (FAP volume) and LV function parameters derived from CMR: end-systolic volume (A), end-diastolic volume (B), LV mass (C), and LVEF (D). EDV = end-diastolic volume.
- FIGURE 3.
Regression plot for myocardial volume of elevated 68Ga-FAPI signal (FAP volume) and LV function parameters derived from TTE: LVEF before TAVR (A), LVEF after TAVR (B), mean transaortic gradient (C), and global longitudinal strain (D). GLS = global longitudinal strain.
- FIGURE 4.
Segmental analysis: SUVmean of 68Ga-FAPI ligand at PET was significantly higher in basal than midventricular and distal myocardial segments.
- FIGURE 5.
Classification of segments into 68Ga-FAPI–upregulated (FAPI+) and 68Ga-FAPI–negative segments (FAPI−) when compared with blood pool background signal, illustrated by patient example (polar map). Native T1 relaxation time was significantly longer in 68Ga-FAPI–positive segments. More LGE was found in 68Ga-FAPI–positive segments, and global longitudinal strain was significantly impaired in 68Ga-FAPI–positive segments. Yet, agreement between 68Ga-FAPI, T1, and longitudinal strain elevation was only partial. FAPI+ = 68Ga-FAPI–upregulated; FAPI− = 68Ga-FAPI–negative; LS = longitudinal strain.
- FIGURE 6.
Regression plot for in-hospital LVEF improvement in percentage and myocardial volume of elevated 68Ga-FAPI signal (FAP volume) (A), preprocedural levels of N-terminal prohormone of brain natriuretic peptide (B), and preprocedural global longitudinal strain (%) (C). GLS = global longitudinal strain; NT-proBNP = N-terminal prohormone of brain natriuretic peptide.
Tables
All AS patients
(n = 23)Sex-matched AS
patients (n = 18)Oncologic sex-matched
controls (n = 9)P Age-and sex-matched
AS patients (n = 5)Oncologic age-and
sex-matched controls
with AHT (n = 5)P Variable Mean ± SD Range Mean ± SD Range Mean ± SD Range Mean ± SD Range Mean ± SD Range Area of FAP upregulation (% of LV) 32.0 ± 29.1 0–91 29.6 ± 30.6 0–91 4.44 ± 7.83 0–24 0.004 43.4 ± 20.6 17–68 9.40 ± 11.2 0–27 0.012 SUVmean (of total LV) 2.50 ± 0.43 1.88–3.51 2.58 ± 0.42 1.93–3.51 1.89 ± 0.46 1.44–2.63 <0.001 2.28 ± 0.45 1.81–2.93 1.47 ± 0.34 1.12–1.91 0.014 FAP volume (cm3) 42.2 ± 35.6 1.54–137.8 37.9 ± 35.4 1.54–137.8 2.90 ± 6.67 0.01–20.62 <0.001 43.1 ± 20.4 23.2–75.9 7.42 ± 8.56 0.71–18.3 0.007 Myocardial SUV–to–blood pool ratio 1.87 ± 0.5 1.20–3.15 1.81 ± 0.53 1.09–2.78 1.30 ± 0.56 0.74–2.57 0.030 1.86 ± 0.25 1.44–2.12 1.47 ± 0.34 1.18–1.99 0.003 Organ 68Ga-FAPI signal (SUVpeak) Myocardium 3.35 ± 0.91 1.87–5.42 3.46 ± 0.96 1.87–5.42 3.46 ± 0.96 1.21–3.86 <0.001 3.44 ± 0.67 2.48–4.21 1.62 ± 0.25 1.41–1.93 <0.001 Spleen 1.39 ± 0.38 0.79–2.12 1.41 ± 0.38 0.79–2.12 1.13 ± 0.25 0.83–1.51 0.052 1.35 ± 0.34 1.05–1.91 1.01 ± 0.04 0.99–1.06 0.147 Liver 1.33 ± 0.35 0.81–2.64 1.36 ± 0.38 0.81–2.31 1.29 ± 0.67 0.80–3.49 0.731 1.35 ± 0.41 0.99–1.88 1.41 ± 0.49 0.92–2.12 0.817 Bone marrow 0.90 ± 0.25 1.05–4.05 0.92 ± 0.26 0.43–1.29 0.99 ± 0.27 0.60–1.35 0.540 1.05 ± 0.29 0.74–1.90 0.78 ± 0.18 0.50–1.00 0.122 Lung 0.58 ± 0.21 0.23–1.13 0.63 ± 0.20 0.35–1.13 0.52 ± 0.33 0.30–1.39 0.326 0.66 ± 0.22 0.54–0.99 0.56 ± 0.17 0.40–0.74 0.417 Blood pool (left atrium) 1.89 ± 0.30 1.48–2.84 1.94 ± 0.31 1.48–2.84 1.43 ± 0.24 1.20–1.90 <0.001 1.71 ± 0.29 1.64–2.38 1.24 ± 0.52 1.41–1.80 0.082 AHT = arterial hypertension.
Variable All patients All patients indexed (mL/m2) Global function (n = 22) EDV (mL) 118.6 ± 26.7 (83–191) 66.5 ± 12.9 (45.0–102.0) ESV (mL) 43.5 ± 13.8 (29–84) 24.3 ± 6.8 (15.0–43.0) SV (mL) 75.2 ± 14.8 (53–119) 42.1 ± 7.0 (30.0–64.0) LVM (g) 116.2 ± 21.3 (77–157) 66.3 ± 11.9 (40.0–86.0) LVEF (%) 63.8 ± 4.4 (53–72) Global mapping (n = 20) T1 global native (ms) 977.2 ± 25.8 (939–1,049) T1 global contrast (ms) 448.8 ± 48.8 (363–539) ECV global (%) 28.0 ± 3.9 (22–38) ECV = extracellular volume fraction; EDV = end-diastolic volume; ESV = end-systolic volume; SV = stroke volume; LVM = LV mass.
Data are mean ± SD and range.
Variable Data LVEF (%, 2-dimensional) 60.1 ± 5.9 (44–70) LVEF (%, 2-dimensional) after TAVR 61.8 ± 3.7 (57–72) Transaortic gradient (mm Hg, maximum) 79.0 ± 13.6 (54–110) Transaortic gradient (mm Hg, mean) 50.4 ± 8.1 (38–70) Aortic regurgitation 7 (30.4) AVA (cm2) 0.68 ± 0.18 (0.37–0.95) THV SAPIEN (Edwards Lifesciences) 14 (60.9) THV CoreValve (Medtronic) 9 (39.1) Device success 23 (100) New permanent pacemaker 1 (4.3) AVA = aortic valve area; THV = transcatheter heart valve.
Qualitative data are number and percentage (n = 23); continuous data are mean ± SD and range.
Supplemental Data
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