Stable versus unstable atherosclerosis: Clinical aspects,☆☆,

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Plaque vulnerability

The risk of plaque disruption depends more on plaque type than on plaque size; lipid-rich and soft plaques are more vulnerable and prone to rupture than are collagen-rich and hard plaques.3 Furthermore, they are highly thrombogenic after disruption because of high content of tissue factor.4 Pathoanatomic studies have identified 3 major determinants of a plaque’s vulnerability to rupture (Figure 1): (1) the size of the lipid-rich core; (2) inflammation with plaque degradation; and (3) lack of

Plaque disruption

Rupture of vulnerable plaques occurs frequently. Autopsy data indicate that 9% of healthy persons harbor disrupted plaques (without superimposed thrombosis) in their coronary arteries, which increases to 22% in persons with diabetes or hypertension.35 In fatal coronary artery disease, more than one disrupted plaque, with or without superimposed thrombosis, usually is present in the coronary arteries.13, 36

Disruption of the plaque surface occurs most often where the cap is thinnest and most

Plaque thrombosis

The most feared consequence of coronary plaque disruption is thrombotic occlusion of the artery. Approximately 75% of thrombi responsible for acute coronary syndromes are precipitated by plaque disruption, whereby the highly thrombogenic gruel is exposed to the flowing blood. In the remaining 25%, superficial plaque erosion without frank disruption (ie, no deep injury) is usually present.2 Most disrupted plaques are resealed by a small mural thrombus, and only sometimes does a major luminal

Clinical manifestations

Plaque disruption itself is asymptomatic, and the associated rapid plaque growth is usually clinically silent. However, rupture-related hemorrhage into the plaque, luminal thrombosis, and/or vasospasm may cause sudden flow obstruction, giving rise to an acute coronary syndrome. The culprit lesion is frequently “dynamic,” causing intermittent flow obstruction, and the clinical presentation and the outcome depend on the severity and duration of myocardial ischemia.1, 40 A nonocclusive or

Conclusions

For event-free survival in patients with coronary atherosclerosis, we must focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. There appear to be 3 major determinants of a plaque’s vulnerability to rupture: (1) the size of the lipid-rich core, (2) inflammation with plaque degradation, and (3) lack of SMCs with impaired healing. Lipid accumulation, macrophage infiltration, and lack of SMCs destabilize plaques,

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    Reprint requests: Prof Erling Falk, Department of Cardiology, Research Unit, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark. E-mail: [email protected]

    ☆☆

    Am Heart J 1999;138:S421-S425.

    0002-8703/99/$8.00 + 0   4/0/101757

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