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Chapter 33: Coronary Thrombosis: Local and Systemic Factors

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Initial atherosclerotic lesions result from the accumulation of inflammatory cells and lipids in which part or layer of the arterial wall?

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A. Arterial lumen

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B. Intima

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C. Media

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D. Adventitia

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E. All of the above

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The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 33) Atherosclerosis is a systemic disease involving the intima of large and medium-sized arteries that is characterized by intimal thickening caused by the accumulation of cells and lipids (option B).1 However, secondary changes may occur in the underlying media (option C) and adventitia (option D), particularly in advanced disease stages. The early atherosclerotic lesions might progress without compromising the lumen because of compensatory vascular enlargement (Glagovian remodeling) (option A).2 Importantly, the culprit lesions leading to acute coronary syndromes are usually mildly stenotic and therefore barely detected by angiography.3 These high-risk, rupture-prone lesions usually have a large lipid core, a thin fibrous cap, and a high density of inflammatory cells.

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Which of the following factors contributes to the attenuation of the proatherogenic state and lesion progression?

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A. Vascular cell adhesion molecule-1 (VCAM-1)

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B. Matrix metalloproteinases (MMPs)

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C. Elevated high-density lipoprotein (HDL)

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D. Lipids at injury site

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E. Interferon (IFN)-gamma

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The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 33) Inflammation is an important process that affects plaque progression, vulnerability, and subsequent thrombus formation. Inflammatory cells (monocyte/macrophages, T cells, and mast cells) present in the core and shoulder of atherosclerotic lesions release inflammatory cytokines and MMPs that affect each step of atherosclerosis from lesion formation, to progression, to disruption and ACS (option B). The circulating monocytes are recruited within the subendothelial space in response to the synthesis and exposure of adhesive proteins triggered by the early accumulation of lipids (option D). The internalized monocytes release inflammatory mediators, such as netrin-1 and VCAM-1, that are responsible for their retention in the lesions (option A). Mast cells are proinflammatory through the release of histamine, leukotrienes, interleukin (IL)-6, and interferon (IFN)-gamma (option E). Attenuation of the proatherogenic state occurs through HDL-raising and may facilitate the efflux of the wall macrophages (option C).

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Which of the following statements about the coagulation cascade is correct?

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A. Injury to vessel wall exposes subendothelial proteins such as collagen and von Willebrand factor (vWF) that can ...

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