Background And Purpose: High-risk atherosclerosis is an underlying cause of cardiovascular events, yet identifying the specific patient population at immediate risk is still challenging. Here, we used a rabbit model of atherosclerotic plaque rupture and human carotid endarterectomy specimens to describe the potential of molecular fibrin imaging as a tool to identify thrombotic plaques.

Methods: Atherosclerotic plaques in rabbits were induced using a high-cholesterol diet and aortic balloon injury (N=13). Pharmacological triggering was used in a group of rabbits (n=9) to induce plaque disruption. Animals were grouped into thrombotic and nonthrombotic plaque groups based on gross pathology (gold standard). All animals were injected with a novel fibrin-specific probe Ga-CM246 followed by positron emission tomography (PET)/magnetic resonance imaging 90 minutes later. Ga-CM246 was quantified on the PET images using tissue-to-background (back muscle) ratios and standardized uptake value.

Results: Both tissue-to-background (back muscle) ratios and standardized uptake value were significantly higher in the thrombotic versus nonthrombotic group (<0.05). Ex vivo PET and autoradiography of the abdominal aorta correlated positively with in vivo PET measurements. Plaque disruption identified by Ga-CM246 PET agreed with gross pathology assessment (85%). In ex vivo surgical specimens obtained from patients undergoing elective carotid endarterectomy (N=12), Ga-CM246 showed significantly higher binding to carotid plaques compared to a D-cysteine nonbinding control probe.

Conclusions: We demonstrated that molecular fibrin PET imaging using Ga-CM246 could be a useful tool to diagnose experimental and clinical atherothrombosis. Based on our initial results using human carotid plaque specimens, in vivo molecular imaging studies are warranted to test Ga-CM246 PET as a tool to stratify risk in atherosclerotic patients.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8792326PMC
http://dx.doi.org/10.1161/STROKEAHA.121.035638DOI Listing

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