Fibroblast activation protein imaging in reperfused ST-elevation myocardial infarction: comparison with cardiac magnetic resonance imaging

Abstract

The goals were to explore the correlation of 18 F-labeled broblast activation protein inhibitor (FAPI) and cardiovascular magnetic resonance (CMR) parameters in ST-elevation myocardial infarction (STEMI) patients with successful primary percutaneous coronary intervention (PPCI) and to investigate the value of FAPI imaging in predicting cardiac functional recovery. MethodsFourteen rst-time STEMI patients (11 men, mean age: 62 ± 11 years) after PPCI were prospectively recruited. All patients underwent baseline FAPI imaging ( 6± 2 days post-MI) and CMR (8 ± 2 days post-MI). Ten patients had convalescent CMR (84 ± 4 days post-MI). Myocardial FAPI activity was analyzed on extent (the percentage of FAPI uptake volume over the left ventricular volume, FAPI%), intensity (target-to-background uptake ratio, TBRmax), and amount (FAPI%×TBRmax). Serum biomarkers during the acute phase, late gadolinium enhancement (LGE), T2-weighted imaging (T2WI), extracellular volume (ECV), microvascular obstruction (MVO), and cardiac function from CMR imaging were analyzed. ResultsLocalized but inhomogeneous FAPI uptake was observed, which was larger than the edematous and infarcted myocardium. The MVO area showed lower FAPI uptake compared with the surrounding myocardium. FAPI activity was associated with myocardial injury biomarkers, T2WI, LGE, and ECV at both per-patient and per-segment levels (all p < 0.05). Among the CMR parameters, T2WI had the greatest correlation coe cient with both FAPI% and FAPI%×TBRmax. Baseline TBRmax was correlated with convalescent left ventricular ejection fraction (LVEF)(r = −0.73, p = 0.02). ConclusionFAPI imaging detects more involved myocardium than CMR in reperfused STEMI, and was associated with myocardial damage and convalescent LVEF.

A clinical study on relationship between visualization of cardiac fibroblast activation protein activity by Al18F-NOTA-FAPI-04 positron emission tomography and cardiovascular disease

“…There may be a simultaneous dysregulation of metabolic and hypertrophic pathways in the human heart responsible for the increase in FAPI uptake. Previous studies demonstrated circulating FAP and TGF-β1 levels significantly declined (31). The inconsistency between tissue-level and circulating-level biomarkers raises the possibility that peripheral biomarkers may not be reliable indicators of tissue status (39).…”

“…Cardiac FAP activation has been reported in a variety of pathological conditions (3,(28)(29)(30). Myocardial fibrosis after myocardial infarction has been reported in several studies (5,9,11,31). Radiotracer delivery may be inadequate in infarcted areas, explaining this pattern of tracer uptake.…”

Fibroblast activation protein imaging in atrial fibrillation: a proof-of-concept study

“…Recently, radiolabeled fibroblast activation protein inhibitor (FAPI)-targeting tracers have been developed to detect activated fibroblasts [4]. Both our research and that of other groups have demonstrated that FAPI imaging is feasible for the assessment of pathological fibroblast activation in ventricles [5,6]. If this technique is also feasible in the atriums, the initial reversible phase of atrial fibrosis could be detected, thus guiding treatments aimed at reversing the pathological fibrotic process.…”

Detection of myocardial fibrosis: Where we stand

“…Accumulating studies of nuclear medicine have paid great attention to fibrosis-specific molecular imaging. Several imaging methods, such as collagelin labeling (e.g., using 99 mTc-labeled collagelin), activated fibroblast and myofibroblast labeling (e.g., using 68 Ga-labeled or 18 F-labeled fibroblast activation protein inhibitor) techniques, have emerged (6,77,78). Though promising, more studies are required to validate its detection accuracy in humans.…”