Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 56

A vulnerable plaque is characterized by a lipid-rich necrotic core that is surrounded by a thin fibrous cap and infiltrated by inflammatory cells, especially metalloproteinase-rich macrophages (called thin-cap fibroatheroma). The thin cap ruptures, especially at the shoulders/margins of the plaque where the stress is highest, and leads to thrombus formation. Plaque rupture is, thus, characterized by a ruptured cap and a thrombus in continuity with a necrotic core. The ruptured cap is identified as a flap on IVUS or OCT. Most plaque ruptures are non-occlusive and silent, contributing to a stair-step progression of coronary stenosis. Stable CAD stenoses are frequently multiple layers of healed plaque ruptures. On IVUS, heavy atherosclerosis and compensatory vessel expansion (positive remodeling) often indicate prior episodes of plaque rupture and a vessel that has expanded to its limit, risking a more symptomatic rupture (the plaque is running out of energy supply).

Plaque erosion, on the other hand, is characterized by thrombus formation over a thick cap that has not ruptured (no communication with the necrotic core), or over a fibrointimal plaque rich in smooth muscle cells without a necrotic core (fibrotic plaque).^175-177 Plaque erosion is responsible for ~25% of MIs, more so in women, especially young female smokers (< 50 years old). Compared with plaque rupture, plaque erosion occurs, on average, on less stenotic lesions.

Plaque rupture leads to the complex eccentric morphology and overhanging borders on angiography. Conversely, plaque erosion has an uncomplicated angiographic morphology with smooth borders.