Arterial plaque stability

Arterial plaque stability refers to the structural and composition-based resistance of an atherosclerotic lesion to rupture and subsequent thrombosis. A stable plaque is typically characterized by a thick, collagen-rich fibrous cap and a small necrotic lipid core, whereas a vulnerable or unstable plaque features a thin fibrous cap, a large necrotic core, and high levels of inflammatory cell infiltration. Key molecular drivers of instability include matrix metalloproteinases (MMPs), which degrade the extracellular matrix, and proinflammatory cytokines that recruit macrophages and promote smooth muscle cell apoptosis. Therapeutic strategies aim to enhance stability by reducing the lipid burden, inhibiting proteolytic activity, and suppressing vascular inflammation. Drugs such as statins and PCSK9 inhibitors promote stability by decreasing the lipid core size and exerting pleiotropic anti-inflammatory effects that reinforce the fibrous cap.

Other names

Plaque stabilityPlaque vulnerabilityAtherosclerotic plaque stabilityPlaque rupture resistanceVulnerable plaque

Drugs stabilize arterial plaques by inhibiting HMG-CoA reductase (statins) or PCSK9 to reduce LDL-C and the volume of the necrotic core, and by suppressing inflammatory signaling (e.g., IL-1β, IL-6) to reduce the production of matrix-degrading enzymes like MMP-9, thereby strengthening the fibrous cap.