ABSTRACT
Interstitial collagen confers stability and tensile strength to the fibrous cap in thin-cap fibroatheroma (TCFA). There appears to be a dynamic balance between collagen synthesis and breakdown in atherosclerotic plaques maintained by the inflammatory state of the lesion11. Macrophages, in response to stimulation by T cells, can produce matrix metalloproteinases (MMPs), which actively break down collagen and other extracellular matrix proteins in the fibrous cap, compromising its integrity12-15. There is extensive evidence linking macrophage infiltration with plaque instability16-18. Histologically, disrupted plaques demonstrate intense macrophage infiltration localized within the thin fibrous cap. Macrophages are more frequently demonstrated in coronary plaque obtained from patients with acute coronary syndromes (ACS) compared with patients with stable angina. Therefore, these cells are
Milestones in the development of cardiac OCT at MGH Reference
First systematic characterization of human atherosclerotic 7 plaque with OCT
Demonstration of the ability of OCT to detect and quantify the amount of macrophages in atherosclerotic 20 plaque
First in-animal application of OCT imaging of coronary arteries in vivo 30 First in-human application of OCT imaging of coronary arteries in vivo and comparison of OCT to 22
IVUS in imaging in vivo atherosclerotic plaque in humans First systematic published studies evaluating OCT during PCI in humans 23, 24 In vivo evaluation of plaque morphology and macrophage content in patients with various 25, 26
coronary syndromes
Table 14.1 Development of cardiac OCT at the Massachusetts General Hospital (MGH)
Figure 14.1 OCT images and corresponding histological analysis for fibrous (a), calcific (c) and lipid-rich (e) plaque types. In fibrous plaques the OCT signal (F) is observed to be strong and homogeneous. In comparison, both calcific (C) and lipidrich regions (arrows) appear as a signal-poor region within the vessel wall. Lipid-rich plaques have diffuse or poorly demarcated borders, whereas the borders of calcific nodules are sharply delineated. Images b, d and f depict corresponding histological preparations. (b, Movat pentachrome stain; d, hematoxylin-eosin stain; f, Masson trichrome stain; original magnification × 40). Scale bars, 500 µm. (From reference 31)
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Figure 14.2 (a) OCT image of a thin-cap fibroatheromawithcorrespondinghistology (b). (Movat’s pentachrome; magnification × 20). Bar, 250µm. Cap thickness was 44.1 µm by OCT and 40.4 µm by histology. (From reference 7)
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both an integral functional component and a marker of the inflammatory process that is fundamental to the atherosclerotic process in humans. The ability to identify macrophages in vivo would provide invaluable information in assessing the inflammatory state of a plaque and its vulnerability to rupture.
