Applying the ordinal model of atherosclerosis to imaging science: a brief review

Abstract

Atherogenesis has been well demonstrated to proceed in an ordinal fashion. Imaging technologies have advanced substantially in recent decades, enabling early detection of atherosclerosis. Some modalities, such as coronary CT, have seen broad clinical adaptation. In contrast, others, such as flow-mediated dilatation, remain predominantly research-based. Optimal and appropriate usage of these technologies remains an area of active investigation. We hypothesise that investigators ought to consider which stage of atherosclerosis is under investigation when choosing imaging modalities. Additionally, when assessing the efficacy of a particular treatment, some imaging modalities may be more appropriate than others. We review the most important available imaging modalities and suggest stages at which each may or may not be well used. Conceptual application of the classic stages of atherosclerosis model to the variety of modern imaging modalities available will result in more effective investigation and treatment of cardiovascular disease.

A new approach to the diagnosis and treatment of atherosclerosis: the era of the liposome

“…Early endothelial dysfunction can be diagnosed using functional measurements, such as peripheral artery tonometry, flow-mediated dilatation, and pulse wave velocity, and can be visualized using PET and CT. More advanced lesions with lipid accumulation can be observed using coronary intravascular ultrasound, MRI, and coronary CT angiography. Advanced plaques can be seen using electron-beam-CT [61] ( Figure 6).…”

Oscillatory fluid-induced mechanobiology in heart valves with parallels to the vasculature

“…They can occlude blood supply to the distal bed, and plaque rupture can activate thrombus deposition that further interrupts blood flow. Plaque deposition begins with endothelial dysfunction and unusual smooth muscle cell behavior due to environmental cues (13), in which loss of smooth muscle cell contractility leads to cell migration, plaque formation, and vascular calcification (14).…”

Targeting P-Selectin Adhesion Molecule in Molecular Imaging: P-Selectin Expression as a Valuable Imaging Biomarker of Inflammation in Cardiovascular Disease

“…Trauma, inflammation, and many other factors can trigger or alter the course of the disease (17). A recent review discusses a new perspective on the importance of applying selective imaging strategies in evaluating characteristic stages of atherogenesis and outlines the current clinical imaging modalities that may be appropriate at each stage (18). Available detection methods for evaluating early stages, however, lack the necessary accuracy to assess the molecular processes of plaque formation, vulnerability, and rupture (17,18).…”

“…The initial step of atherosclerosis-endothelial activation along the vessel wall-is followed by increased expression of adhesive molecules for leukocyte recruitment in areas of injury from lipid accumulation or hypertensive force (18,19). Leukocytes undergo intravasation into the inner layer of the vessel alongside myocytes for tissue repair, leading to monocytederived foam cells within the plaque and a fibrous cap, respectively.…”

“…Nonetheless, clinical nuclear agents currently used for inflammation imaging, such as 18 F-FDG, which accumulates in tissues with increased cellular glycolytic activity, are limited in scope by high background levels or nonspecific uptake that can complicate analysis and interpretation (4,5). With more recent preclinical advances, new contrast agents developed for MRI and ultrasound are emerging as strong contenders to image at the molecular level for diagnosing and monitoring inflammation (6,7).…”