P195 - FLORBETABEN FOR IMAGING OF VASCULAR AMYLOID: EVALUATION OF AMYLOID INFLAMMASOME IMAGING IN CAROTID AND CORONARY ARTERIES IN PATIENTS WITH UNSTABLE ATHEROSCLEROSIS (FERMATA)
Medical Student University of Ottawa Windsor, Ontario, Canada
Background: Atherosclerosis is a major cause of cardiovascular morbidity and mortality, contributing to conditions such as myocardial infarction and stroke. Vulnerable plaques, characterized by a lipid-rich core and fibrous cap, can rupture, leading to thrombosis. Inflammation, driven by macrophages and the inflammasome, is a key factor in plaque destabilization. Despite advances, predicting which plaques are prone to rupture remains challenging. Imaging techniques may help identify high-risk plaques and improve patient outcomes. The primary objective of the FERMATA study is to determine whether [18F]-Florbetaben uptake differs between culprit and non-culprit coronary arteries in patients with recent acute coronary syndromes (ACS) or stroke/transient ischemic attack (TIA), to evaluate the potential of [18F]-Florbetaben PET/CT as a non-invasive marker of plaque inflammation and rupture risk
METHODS AND RESULTS: This single-center pilot study recruited eighteen patients within 30-120 days of STEMI, NSTEMI, or stroke/TIA, all with confirmed large-vessel atherosclerosis. Exclusions included cardioembolic stroke, severe left ventricular dysfunction (EF < 30%), and pregnancy. Participants underwent [18F]-Florbetaben PET/CT imaging, with CT angiography, to assess tracer uptake in culprit and non-culprit arteries. The tissue-to-blood ratio (TBR) was measured for each artery, and a two-sample independent t-test compared mean TBR values between culprit and non-culprit arteries. The study revealed a significant difference in mean TBR between culprit and non-culprit arteries (culprit artery: 1.60 ± 0.33; non-culprit artery: 1.40 ± 0.34; p = 0.049). The culprit artery demonstrated higher [18F]-Florbetaben uptake compared to both non-culprit arteries, suggesting that enhanced tracer uptake correlated with increased plaque burden and inflammation.
Conclusion: This pilot study is the first to explore the use of [18F]-Florbetaben PET/CT imaging to identify vulnerable plaques prone to rupture. Our findings suggest that [18F]-Florbetaben PET/CT may help identify high-risk plaques, supporting its potential role in atherosclerosis imaging. Future studies with larger cohorts are necessary to validate these findings, refine imaging thresholds, and determine the clinical implications for risk stratification and intervention planning. Identifying high-risk plaques through imaging could transform atherosclerosis management, allowing for improved risk stratification, targeted interventions, and better patient outcomes.