Atherosklerose — Cardiovascular Risk Panel

Targeted cardiovascular risk assessment combining a full lipid panel with high-sensitivity CRP, homocysteine, and lipoprotein(a) — the four pillars of modern atherosclerosis risk stratification beyond standard cholesterol testing.

The Atherosklerose panel goes beyond a standard lipid screen by including the three most validated non-lipid cardiovascular risk markers. Standard lipid panels miss approximately 50% of cardiovascular events — many patients who suffer heart attacks have normal LDL cholesterol. This panel addresses that gap. The lipid component includes total cholesterol, HDL, LDL, and triglycerides. HDL-to-total-cholesterol ratio and triglyceride-to-HDL ratio are increasingly recognised as more predictive of cardiovascular events than any single lipid parameter. Triglycerides above 150 mg/dL in the context of low HDL suggest insulin resistance and atherogenic small dense LDL particles. High-sensitivity CRP (hs-CRP) measures low-grade systemic inflammation, which is now understood as a central driver of atherosclerosis rather than merely a bystander. The JUPITER trial demonstrated that statin therapy reduces cardiovascular events in patients with elevated hs-CRP even when LDL cholesterol is normal, establishing inflammation as an independent treatment target. Values below 1.0 mg/L indicate low cardiovascular risk, 1.0-3.0 moderate risk, and above 3.0 high risk — though values above 10 suggest acute inflammation or infection rather than cardiovascular risk. Homocysteine is an amino acid intermediate in methionine metabolism. Elevated levels (above 15 micromol/L) are associated with a 2-3 fold increase in cardiovascular risk, independent of traditional risk factors. Homocysteine elevation often reflects inadequate B-vitamin status (folate, B12, B6) and responds well to supplementation in most cases. The MTHFR C677T polymorphism, carried by 10-15% of Europeans in homozygous form, impairs folate metabolism and predisposes to hyperhomocysteinaemia. Lipoprotein(a) is a genetically determined cardiovascular risk factor that is elevated in approximately one in five Europeans. Unlike LDL, Lp(a) does not respond to diet or statin therapy. Its measurement is recommended at least once in a lifetime by the European Atherosclerosis Society, as elevated Lp(a) influences the intensity of treatment for other modifiable risk factors. Values above 50 mg/dL confer significant additional cardiovascular risk.