Abstract
Atherosclerosis is responsible for the majority of heart attacks and is characterized by several modifications of the arterial wall including an inflammatory reaction. The silent course of atherosclerosis has made it necessary to develop predictors of disease complications before symptomatic lesions occur. Vulnerable to rupture atherosclerotic plaques are the target for molecular imaging. To this aim, different radiopharmaceuticals for PET/CT have emerged for the identification of high-risk plaques, with high specificity for the identification of the cellular components and pathophysiological status of plaques. By targeting specific receptors on activated macrophages in high-risk plaques, radiolabelled somatostatin analogues such as 68Ga-DOTA-TOC, TATE,0 or NOC have shown high relevance to detect vulnerable, atherosclerotic plaques. This PET radiopharmaceutical has been tested in several pre-clinical and clinical studies, as reviewed here, showing an important correlation with other risk factors.
Highlights
Cardiovascular atherosclerotic disease is a systemic condition that affects major arteries of the body, being the most common cause of death in the western world and expected to reach 22.2 million people by 2030 [1]
The physiopathology of atherosclerosis is characterized by the presence of complex events, where an inflammatory cascade is triggered by the deposit of low-density lipoproteins (LDL) at sites of endothelial injury, and by the posterior recruiting of macrophages, which catch the oxidized LDL remnants [4]
Conducted a prospective study to validate the use of 68 Ga-DOTA-TATE as a vascular inflammation imaging agent (VISION STUDY); they confirmed that high-target SSTR2 gene expression occurs exclusively among activated proinflammatory M1 macrophages in atherosclerosis and demonstrated the presence of SSTR-2 receptors from patients with coronary vascular disease
Summary
Cardiovascular atherosclerotic disease is a systemic condition that affects major arteries of the body, being the most common cause of death in the western world and expected to reach 22.2 million people by 2030 [1]. Despite the widespread use of 18 F-FDG in cardiovascular disease, the non-specific uptake of the radiopharmaceutical is the most important drawback for imaging atherosclerosis [5] To overcome these limitations, new probes have been studied that allow for the identification of vulnerable plaques with better specificity, with potential for localization and for the identification of the cellular components and pathophysiological status of the plaque. The rationale for PET-based molecular imaging in this scenario is to better understand the pathogenic mechanisms underlying atherosclerosis to use the information to evaluate treatment efficacy as well as to identify those patients with the highest risk of events related to plaque rupture [13]. This review describes state-of-the-art imaging, with radiolabelled somatostatin analogues, and the processes associated with plaque rupture
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