Imaging aortic wall inflammation

Abstract

Inflammation affects the aortic wall through complex pathways that alter its biomechanical structure and cellular composition. Inflammatory processes that predominantly affect the intima cause occlusive disease whereas medial inflammation and degeneration cause aneurysm formation.Aortic inflammatory pathways share common metabolic features that can be localized by smart contrast agents and radiolabelled positron emission tomography (PET) tracers. 18F-Fluorodeoxyglucose (18F-FDG) is a non-specific marker of metabolism and has been widely used to study aortic inflammation in various diseased aortic states. Although useful in detecting disease, 18F-FDG has yet to demonstrate a reliable link between vessel wall disease and clinical progression.18F-Sodium fluoride (18F-NaF) is a promising biological tracer that detects microcalcification related to active disease and cellular necrosis within the vessel wall. 18F-NaF shows a high affinity to bind to diseased arterial tissue irrespective of the underlying inflammatory process. In abdominal aortic aneurysms, 18F-NaF PET/CT predicts increased rates of growth and important clinical end-points, such as rupture or the requirement for repair.Much work remains to be done to bridge the gap between detecting aortic inflammation in at-risk individuals and predicting adverse clinical events. Novel radiotracers may hold the key to improve our understanding of vessel wall biology and how this relates to patients. Combined with established clinical and morphological assessment techniques, PET imaging promises to improve disease detection and clinical risk stratification.

In the wall lies the truth: a systematic review of diagnostic markers in intracranial aneurysms

“…Apparently, inflammatory processes responsible for progression of atherosclerosis largely overlap with those underlying IA formation (2). At the same time, because of different triggers and target layers in the arterial wall, vascular inflammation leads to distinct consequences during IA and atherosclerosis formation (weakening of the vessel wall with further dilatation and rupture or progressive luminal stenosis and occlusion, respectively) (20).…”

Molecular Imaging of Thoracic Aortic Aneurysm Inflammation: A Review of Clinical and Experimental Studies

“…е -ПЭТ с 18 F-ФДГ, аксиальная плоскость. Визуализируется высокоинтенсивное поглощение РФП в проекции восходящей аорты (указано звездочкой).. меченного 68 Ga, и имеющего высокое сродство к рецепторам соматостатина 2 (SST2) [29]. В исследовании Tarkin J.M.…”

“…Наиболее подходящими в этом плане являются методы молекулярной визуализации, способные идентифицировать воспалительный процесс на разных его этапах, используя трэйсеры, ориентированные на конкретное патобиологическое звено [28]. В свете выше указанных фактов, методы молекулярной диагностики могут успешно использоваться для визуализации клеточной инфильтрации, апоптоза, ремоделирования аортальной стенки [29].…”

Imaging cellular activity and proliferation in the aortic wall

“…3 This is accompanied by inflammatory infiltration of the aortic wall by helper-T cells and macrophages. Cytokines released within the aortic media cause vascular smooth muscle cells to undergo phenotypical change, 4 losing their ability to replenish the extracellular matrix and instead exhibiting a pro-calcific phenotype. 5 Vascular injury therefore results in a self-propagating microenvironment where calcium and phosphate precipitate to form hydroxyapatite crystals and foci of micro-and then macro-scopic calcium deposits.…”

“…5 Vascular injury therefore results in a self-propagating microenvironment where calcium and phosphate precipitate to form hydroxyapatite crystals and foci of micro-and then macro-scopic calcium deposits. 4 Advances in biological radiotracer development and positron emission tomography (PET) potentially allow us to study these pathological processes in the aortic wall ( Table 1). The most widely used cardiovascular PET radiotracer is 18 F-Fluorodeoxyglucose ( 18 F-FDG), although longitudinal clinical studies have failed to consistently demonstrate the predictive value of this tracer in abdominal aortic aneurysm disease.…”