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CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
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Chapter Summary
This chapter describes plaque characteristics contributing to coronary thrombosis, provides mechanistic insights into lesion progression, and summarizes diagnostic imaging. At least half of both physiologically and anatomically significant lesions do not fair worse with modern medical therapy than with revascularization, and it is likely that the plaques of event-free patients are stable or have low wall shear stress. Recognition of high-risk plaques is prudent, and it is thus important for clinicians to understand the pathology of atherosclerotic disease of coronary arteries (see Fuster and Hurst’s Central Illustration). Plaque rupture is thought to be responsible for at least two-thirds of cases of coronary thrombosis and subsequent acute coronary events, including sudden death; plaque erosion accounts for most of the remaining cases of thrombosis, and calcified nodules contribute to less than 5% of adverse outcomes. The importance of progressively increasing necrotic core burden covered by thin and inflamed fibrous caps is highlighted. The rapid enlargement of plaques is attributed to repeated subclinical plaque rupture–thrombosis–healing cycles. On the other hand, fibroatheromatous, fibrous or fibrocalcific plaques in the absence of overlying thrombosis, and the presence of significant luminal obstruction form the basis of stable chest pain syndromes. Native coronary atherosclerosis develops over decades to result in clinical events and differs from clinical events associated with accelerated vein graft atherosclerosis or in-stent neoatherosclerosis.
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More than 50 years ago, when the risk factors for coronary artery disease had become established, injury to the arterial wall from the risk factors was proposed to be the basis of phenotypic alteration and proliferation of medial smooth muscle cell (SMC) resulting in their subendothelial migration and development of neointimal atherosclerotic lesions.1,2 Although SMC migration remains a major player in the pathogenesis of atherosclerosis, inflammatory cells and consequent local cytokine milieu were later found to be the primum movens for disease initiation, maturation, progression, and plaque rupture or even erosion.3–5 With the increasing understanding of pathogenesis of atherosclerosis, a pathological classification was developed to describe the evolution of disease.6–8 The classification captured pathological manifestations of early neointimal lesions and advanced plaques, and recognized that deep plaque fissures and ulcerations were responsible for development of luminal thrombosis and clinical manifestations of acute coronary syndrome. The lesions were classified by the American Heart Association (AHA) as (I) intimal thickening, (II) fatty streak formation, (III) pre-atheroma, (IV) atheroma with well-defined intimal cap, (V) fibroatheroma or atheroma with overlaid new fibrous connective tissue, and (VI) complicated lesions with surface defects, hemorrhage, thrombosis, calcification, or a combination of these characteristics.8 An appropriate emphasis on the recognition of precursor lesions that potentially gave rise to clinical events was subsequently incorporated in the clinicopathological correlative classification.9 Identification of important structural plaque characteristics conceivably ...