How we think about cardiovascular risk has changed a lot. We used to focus on total cholesterol and later LDL cholesterol (LDL-C) as the main villains. Now, the picture is more precise: risk is driven by how many atherogenic particles are circulating, which genetically “high-risk” particles are present, and how much inflammation is active in the vessel wall. At the heart of this newer view is a practical triad of biomarkers: apolipoprotein B-100 (ApoB), which counts the number of atherogenic lipoprotein particles; lipoprotein(a) [Lp(a)], a mostly inherited LDL-like particle with added thrombotic risk; and high-sensitivity C-reactive protein (hsCRP), a marker that tracks systemic and vascular inflammation.