Qspace pro8/31/2023 ![]() However, new CMR contrast agents are often unsuccessful clinically because of increased complexity, costs, and side effects. ![]() Clinical applications of CMR are enhanced by novel contrast-agents that can enable molecular imaging of specific vessel wall components at a cellular level. Our goal of imaging atherosclerosis is the prediction of acute events and guidance for treatment by non-invasive cardiovascular magnetic resonance (CMR) for enhanced molecular and structural observations in vivo. High-resolution details of plaque structure and composition can be visualized by ex vivo 3D microscopic reconstruction techniques and histology, but these methods can distort both lipid and cellular organization. Imaging the multicellular constituents of the atherosclerotic plaque to comprehend the spatially distributed “system” of cellular and biological factors that promote plaque formation has long been considered a grand challenge. However, in the presence of accumulating lipids and unresolved inflammation, SMC transform to macrophage-like foam cells and migrate to the tunica intima, which impairs their architectural and mechanical properties and leads to plaque progression, destabilization, and vulnerability to rupture. SMC are plaque-stabilizing, in that they contribute to the formation of a fibrous cap overlying the necrotic core. Smooth muscle cells (SMC), normally present in the tunica media, contribute mechanical properties to the vessel wall through contraction and the production of extracellular matrix (ECM) proteins to maintain vascular tone, blood pressure, and blood flow. It is important to detect dangerous plaques and monitor treatments before the acute event of thrombosis, which requires detailed characterization of the vessel wall at the site of lipid deposition. Although this is an ex-vivo study, detection of micro and mesoscale level vascular destabilization as enabled by GQI with tractography could increase the accuracy of diagnosis and assessment of treatment outcomes in individuals with atherosclerosis.Ītherosclerosis is characterized by chronic, unresolved inflammation in the arterial wall, initiated by subendothelial deposition of lipids, primarily cholesterol esters (CE) from low-density lipoproteins, that accumulate and promote progression of the plaque to advanced atherosclerosis. This provides a detailed transmural map of normal and inflamed vessel walls in the setting of atherosclerosis that has not been previously achieved using traditional CMR techniques. GQI with tractography is a new method for atherosclerosis imaging that defines a pathological architectural signature for the atheromatous plaque composed of distributed SMC, ECM, inflammatory cells, and thrombus and lipid. Moreover, the locations of CE were differentiated from cellular constituents by their higher restrictive diffusion properties, which permitted chemical confirmation of CE by high field voxel-guided CMRS. ![]() GQI with tractography portrayed the locations of these components across the atherosclerotic vessel wall and differentiated multi-level organization of normal, pro-inflammatory cellular phenotypes, or thrombus. Our methods revealed new structural properties of advanced atherosclerosis incorporating SMC and lipid distributions. We compared rabbits with normal chow diet and cholesterol-fed rabbits with endothelial balloon injury, which accelerates atherosclerosis and produces advanced rupture-prone plaques, in a well-validated rabbit model of human atherosclerosis. We applied cardiovascular magnetic resonance spectroscopy (CMRS) and diffusion weighted CMR (DWI) with generalized Q-space imaging (GQI) analysis to architecturally define features of atheroma and correlated these to the microscopic distribution of vascular smooth muscle cells (SMC), immune cells, extracellular matrix (ECM) fibers, thrombus, and cholesteryl esters (CE). Current bioimaging techniques are unable to capture the pathognomonic distribution of cellular elements of the plaque and thus cannot accurately define its structural disorganization. Atherosclerosis often remains subclinical until extensive inflammatory injury promotes vulnerability of the atherosclerotic plaque to rupture with luminal thrombosis, which can cause the acute event of myocardial infarction or stroke. Atherosclerosis is an arterial vessel wall disease characterized by slow, progressive lipid accumulation, smooth muscle disorganization, and inflammatory infiltration.
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