Associations Between Resolvin D1 and Culprit Plaque Morphologies: An Optical Coherence Tomography Study in Patients with ST-Segment Elevation Myocardial Infarction

Figures

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  Figure 1. Representative cross-sectional image of various pathological features of culprit plaques acquired through optical coherence tomography. (a) Plaque rupture, identified by disrupted fibrous cap (↑) and underlying cavity (*); (b) Plaque erosion, identified by intact fibrous cap overlayed with thrombus (↑); (c) Thin-cap fibroatheroma, identified by low backscattering area (necrotic core) covered by fibrous cap (↑) with thickness < 65 μm; (d) Calcification, identified by signal-poor or heterogeneous region (*) with a sharply delineated border; (e) Macrophage infiltration, identified by signal-rich, highly backscattering, confluent or punctate focal regions (↑); (f) Healed plaques, identified by one or more heterogeneous signal-rich layer (*) of different optical signal intensities located near by the luminal surface and clearly demarcated from the underlying tissue.

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  Figure 2. Study flow chart. OCT, optical coherence tomography; RvD1, resolvin D1.

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  Figure 3. Levels of RvD1 according to pathological features identified by OCT.

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  Figure 4. Graphical summary of interactions between defective efferocytosis, apoptosis and necrosis of Mφ, plaque damage, and production of RvD1. Phagocytosis of cholesterol particles lead to formation of foam cells in large amount, causing defective efferocytosis of these apoptotic Mφ, which result in the growth of necrotic core, and the later rupture or damage of atherosclerotic plaques. Meanwhile, efferocytes and apoptotic Mφ release RvD1, which is partially released to the circulation and results in an elevated level of circulating RvD1.