The role of intracoronary imaging in acute coronary syndromes: OCT in focus

Figures

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  Figure 1.. Histomorphological characteristics of plaque erosion and plaque rupture. Cross-sectional images of 2 culprit coronary plaques obtained from the patients with acute coronary syndromes (A,B); the boxed areas in the top panels are magnified in the bottom panels for better histological characterization. The sections are stained with Movat’s pentachrome. (A) The eroded plaque shows subcritical stenosis, an unremarkable necrotic core, and overlying thrombus on an intact fibrous cap. The cap is rich in smooth muscle cells and proteoglycans, and there is minimal inflammation at the base of the thrombus. The plaque does not show any positive remodeling. (B) Conversely, a positively remodeled, critically occlusive atherosclerotic plaque with a cholesterol crystal–rich large necrotic core (NC) covered by a very thin and inflamed fibrous cap, which is disrupted (area between the yellow arrowheads). Smooth muscle cells are visible in the medial layer and thin fibrous cap and minimally present at the base of the neointima. A large thrombogenic necrotic core is in communication with the vessel lumen with an occlusive thrombus.13

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  Figure 2.. Physical principle of operating OCT imaging.

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  Figure 3.. Lipid atherosclerotic plaque. Lipid plaques appear as poor signal regions with ill-defined borders (star), in contrast to the healthy region (box) composed of signal rich, signal poor and signal rich layers representing intima, media and adventitia respectively.

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  Figure 4.. Fibrous atherosclerotic plaque. Fibrous plaques appear as homogenous high signal regions (pathological intimal thickening) displacing media externally.

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  Figure 5.. Calcific atherosclerotic plaques. Calcific plaques appear as signal poor regions with sharply defined borders (arrows).

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  Figure 6.. Measuring fibrous cap thickness. After magnifying the small box, the remnant of the ruptured fibrous cap was measured and was 52 micrometers.

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  Figure 7.. Plaque rupture. Serial cuts in a pullback in LAD showing discontinuity of the plaque cap with subsequent formation of a cavity.

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  Figure 8.. Plaque erosion. Serial cuts in a pullback in proximal RCA showing thrombus formed at site of plaque erosion with eroded intima yet intact fibrous cap.

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  Figure 9.. White thrombus (in “A”), and red thrombus (in “B”). White thrombus is typically characterized by high signal low backscattering (A), while red thrombus (B), is characterized by lower signal with high backscattering.

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  Figure 10.. Thin cap fibro-atheroma. The right panel is magnification of the square in the left panel (as shown in thumbnail). A plaque with large ill-defined lipid pool and thin fibrous cap (measuring 58 µm). The arrow points to accumulation of macrophages (the bright line) beneath the thin cap.

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  Figure 11.. Neovascularization of atherosclerotic plaque (arrows).

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  Figure 12.. OCT depicting different mechanisms of stent thrombosis. Acute stent thrombosis with underlying stent edge dissection (A); Subacute stent thrombosis with underlying major malopposition (B); Late stent thrombosis and underlying isolated uncovered struts(C); neoatherosclerotic plaque in a case of very late stent thrombosis (D); Rupture of a neoatherosclerotic lesion (E and F); underexpanded stent with measurements of stent area and reference luminal area (H). Souteyrand et al.55