Vulnerable atherosclerotic plaque (VP)

Vulnerable atherosclerotic plaques, often identified as thin-cap fibroatheromas (TCFA), are unstable arterial lesions characterized by a large necrotic lipid core and a thin, collagen-poor fibrous cap (Virmani et al., 2000, Arterioscler Thromb Vasc Biol). These lesions are highly susceptible to spontaneous rupture or erosion, which triggers the formation of an occlusive thrombus, leading to acute cardiovascular events such as myocardial infarction or ischemic stroke (Naghavi et al., 2003, Circulation). The pathophysiology involves intense local inflammation, driven by macrophage infiltration and the secretion of matrix metalloproteinases (MMPs) that degrade the structural integrity of the fibrous cap (Libby, 2001, Nature). While the plaque itself is a complex tissue structure rather than a single molecular target, it is the primary focus of plaque-stabilizing therapies. Modern treatments aim to reduce the lipid core size and strengthen the fibrous cap using high-intensity statins and PCSK9 inhibitors, while emerging therapies like Canakinumab target specific inflammatory pathways to prevent clinical rupture (Ridker et al., 2017, NEJM).

Other names

Thin-cap fibroatheromaTCFAUnstable plaqueHigh-risk plaqueRupture-prone plaque

Pharmacological management focuses on plaque stabilization through intensive lipid-lowering via HMG-CoA reductase inhibition or PCSK9 inhibition, which reduces the lipid core volume (Nicholls et al., 2016, JAMA). Additionally, anti-inflammatory agents reduce the activity of matrix-degrading enzymes, while antiplatelet therapy prevents the thrombotic consequences of plaque rupture (Libby et al., 2019, J Am Coll Cardiol).