Atherosclerosis Plaque Imaging and Characterization Using Magnetic Resonance Imaging

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US Cardiology 2006;2005:2(1):1-5

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Atherosclerosis and its thrombotic complications are the first cause of mortality and morbidity in industrialized countries. Furthermore, despite pharmacological intervention and lifestyle changes, cardiovascular disease (CVD) continues to be the principal cause of death in the US.1 Despite great advances in the understanding of the initiation and progression of atherosclerosis and its risk factors, to make a strong clinical impact, patients who have lesions that are vulnerable to rupture and thrombosis must be focussed on.

Atherosclerosis is a systemic disease that mainly affects medium- and large-sized arteries, is characterized by a thickening of the arterial intima, and is typically composed of a lipid core with an overlying fibrous cap. Angiography remains the gold standard for diagnosis and quantification of atherosclerotic plaques resulting in flow-limiting arterial stenoses, but only offers an indirect view of atherosclerosis burden. Positive remodeling of the arterial wall, a process in which the vessel dilates to limit the narrowing of the lumen in the presence of atherosclerotic plaques, leads to a clear underestimation of the true extension of atherosclerosis disease with angiography. Moreover, studies have shown that plaque vulnerability is related to plaque composition rather than to the degree of stenosis.2

Atherosclerosis Plaque Composition and Feature of Plaque Vulnerability

The main components of atherosclerotic plaques are:

  • fibrous elements such as connective tissue, extra-cellular matrix, including collagen, proteoglycans, and fibronectin elastic fibers;
  • lipids such as crystalline cholesterol, cholesteryl esters, and phospholipids;
  • smooth muscle cells, which are intimately associated with atherosclerotic plaque; and
  • inflammatory cells, such as monocyte-derived macrophages and T-lymphocytes, which contribute to the inflammatory pathogenesis of atherosclerosis.

The occurrence of these components in varying proportions in different plaques gives rise to a spectrum of lesions with varying stabilities,3 depending on the arterial region in which it is located (i.e. coronary arteries, carotids, or aorta). Acute coronary syndromes and stroke are mainly caused by the endothelial disruption of atherosclerotic plaques (superficial intimal erosion or fibrous cap rupture), triggering the formation of an intra-luminal thrombus. These atherosclerotic plaques are typically described as containing a large lipid core representing more than half of the plaque volume, a thin fibrous cap (less than 65╬╝m) and a heavy infiltrate of inflammatory cells (macrophages and lymphocytes).

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