Current Clinical Status of Vascular Non-Invasive Imaging Methodologies

Current Clinical Status of Vascular Non-Invasive Imaging Methodologies

Thanjavur Bragadeesh (University of Hull, UK) and Ann C. Tweddel (University of Hull, UK)
DOI: 10.4018/978-1-61350-095-8.ch018
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Abstract

Rupture of high risk atherosclerotic plaque is responsible for acute vascular events such as myocardial infarction and sudden cardiac death. Several non-invasive vascular imaging methods have been developed to identify and characterise atherosclerotic plaques at risk of rupture. In this chapter we will discuss the background, rationale, and current state of non-invasive vascular imaging.
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Introduction

Many risk factors and physiological responses contribute to the development of atherosclerotic plaques, a disease process that primarily affects large and medium sized arteries. Fatty streaks appear within the vascular intima early in adolescence and evolve over many decades into atherosclerotic plaques with the deposition of lipids, necrotic debris, migration of smooth muscle and inflammatory cells (Ross & Glomset, 1976a, 1976b; Stary, 1992, 2000). A fibrous cap produced by smooth muscle cells maintain the stability of the plaque and separates the thrombogenic core of the plaque from the blood stream. In the early stages of development the plaques do not obstruct the vessel lumen due to outward expansion of the vessel wall (positive remodeling) (Glagov, Weisenberg, Zarins, Stankunavicius, & Kolettis, 1987).

The stability of the fibrous cap and the entire plaque is regulated by the lymphocytes and macrophages cells within the plaque(Daugherty & Rateri, 2002). Lymphocytes and macrophages when activated secrete interferon, matrix degrading proteases and other cytokines that inhibit smooth muscle cells, reduce collagen production and effect thinning of the fibrous cap (Davies, 1996; Libby, Ridker, & Maseri, 2002; Packard & Libby, 2008; Virmani, Burke, Farb, & Kolodgie, 2006). Eventual erosion and/or rupture of the fibrous cap expose the necrotic core to the blood stream leading to thrombus formation and abrupt closure of the vessel lumen. Several postmortem studies have confirmed the presence of plaque erosion (Farb et al., 1996) and rupture (Burke et al., 1997)in patients who presented with acute vascular events. Other characteristic features such as increased neovascularisation and macrophage accumulation especially in the shoulder region of the plaque have also been noted in ruptured plaques(Moreno et al., 2004; Muller, Abela, Nesto, & Tofler, 1994). Plaque components and hallmarks of a rupture prone plaque are summarized in Table 1.

Table1.
Plaque components and factors that predispose to plaque rupture
               Plaque components     Atheromatous core – lipid, necrotic debris
     Extracellular matrix
     Calcium
     Fibrous cap
     Features of high risk plaque     Thin cap fibroatheroma
     Large lipid/necrotic core
     Active inflammation – plaque infiltration with macrophages and lymphocytes
     Outward positive remodeling
     Increased plaque microneovascularisation
     Plaque ulceration / Plaque fissure
     Spotty calcification
     Platelet aggregation and thrombus formation

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