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The Pathophysiology of Myocardial Infarction: From Coronary Occlusion to Clinical Consequence

1Coronary Supply and the Myocardial Oxygen Balance2Atherosclerotic Plaque Rupture and Coronary Thrombosis3Ischemia: Metabolic and Functional Consequences of Oxygen Deprivation4From Reversible Injury to Irreversible Cell Death5Inflammation, Healing, and Infarct Remodeling6Clinical Manifestations: ECG, Biomarkers, and Pump Dysfunction
Atherosclerotic Plaque Rupture and Coronary Thrombosis

Inside the Vulnerable Plaque

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Look at the cross-section of the artery. The lumen is the open channel where blood flows, and the plaque is the mass bulging into it. The pale outer rim is the fibrous cap, a collagen and smooth-muscle barrier. Beneath it sits the yellow lipid-rich necrotic core, packed with cholesterol crystals and dead cell debris. The dark cluster at the cap's edge is where macrophages concentrate and release enzymes that digest collagen. A vulnerable plaque has a thin cap and a large core, so the barrier is weak. In rupture, the cap tears and blood touches the core directly. In erosion, the cap stays mostly intact but its surface lining is stripped away, exposing collagen underneath. Either way, the result is the same: thrombogenic material is now in contact with flowing blood.
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An atherosclerotic plaque is a focal thickening of the arterial intima built from a lipid-rich necrotic core, foam cells and inflammatory cells, and a fibrous cap. The necrotic core contains extracellular lipid, cholesterol crystals, and debris from dead macrophages. The fibrous cap is a layer of smooth-muscle cells and collagen that separates the core from the lumen; its thickness and collagen content determine whether the plaque stays intact.

A plaque is called vulnerable when its cap is thin, its lipid core is large, and macrophages and other inflammatory cells are concentrated at the cap's shoulder. These cells release enzymes such as matrix metalloproteinases that degrade collagen, weakening the cap. Two mechanisms can then expose the core to blood: rupture, in which the cap tears and blood contacts the core directly, and erosion, in which the cap remains largely intact but its endothelial surface is denuded or apoptotic, exposing underlying collagen and matrix. Rupture is the more common cause of complete occlusion; erosion is more frequent in younger patients and in women. Once the thrombogenic core or subendothelial matrix is exposed, circulating platelets and coagulation factors can begin to build a thrombus.

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