Perspective:

The following are 10 points to remember about this update on acute coronary syndromes:

1. Acute coronary syndrome occurs as a result of myocardial ischemia, and its manifestations include acute myocardial infarction and unstable angina.

2. Culprit plaque morphology in these patients varies from thrombosis with or without coronary occlusion to sudden narrowing of the lumen from intraplaque hemorrhage.

3. The coronary artery plaque morphologies primarily responsible for thrombosis are plaque rupture and plaque erosion, with plaque rupture being the most common cause of acute myocardial infarction, especially in men. Autopsy data demonstrate that women <50 years of age more frequently have erosion, whereas in older women, the frequency of rupture increases with each decade.

4. Ruptured plaques are associated with positive (expansive) remodeling and characterized by a large necrotic core and a thin fibrous cap that is disrupted and infiltrated by foamy macrophages.

5. Plaque erosion lesions are often negatively remodeled with the plaque itself being rich in smooth muscle cells and proteoglycans with minimal to absence of inflammation.

6. Plaque hemorrhage may expand the plaque rapidly, leading to the development of unstable angina. Plaque hemorrhage may occur from plaque rupture (fissure) or from neovascularization (angiogenesis).

7. Clinical observations suggest that culprit lesions responsible for acute coronary syndromes generally are less calcified than plaques responsible for stable angina, indicating that calcium confers stability to plaques rather than the opposite.

8. Atherosclerosis is now recognized as an inflammatory disease, with macrophages and T-lymphocytes playing a dominant role. Recently, at least two subtypes of macrophages have been identified. M1 is a pro-inflammatory macrophage, whereas M2 seems to play a role in dampening inflammation and promoting tissue repair. A third type of macrophage, hemoglobin-associated macrophage or M (Hb), which is observed at the site of hemorrhage, also can be demonstrated in human atherosclerosis.

9. Thrombosis-prone (vulnerable) plaques are worth identifying in order to treat such lesions aggressively, but not necessarily invasively.

10. Finally, in order to further our understanding of the specific biological events that trigger plaque instability, as well as to monitor the effects of novel antiatherosclerotic therapies, newer imaging modalities in vivo are needed.