EN
Atherosclerosis almost never announces itself in time. It advances silently for decades, and what brings a person to the doctor is either a chance finding on an ultrasound or an event that has already happened — chest pain, cramping pain in the legs on walking, a stroke. So a conversation about “treating atherosclerosis” is in fact almost always a conversation about two things: how to assess the risk before the catastrophe, and what to do once plaques have been found.
What happens in the vessel
Cholesterol is deposited in the wall of an artery, chronic inflammation develops around it and a plaque forms. Two scenarios then become possible. The plaque gradually narrows the lumen, and the organ starts to receive too little blood under exertion: hence angina, or pain in the calves when walking. Or the cap of the plaque tears, a clot forms at that spot and the vessel closes suddenly — a heart attack or a stroke. The second scenario is more dangerous and less predictable, and that is exactly why treatment aims not only at widening what has narrowed but at making the plaque more stable.
First, an honest assessment of risk
A German assessment for suspected atherosclerosis usually starts not with expensive technology but with figures: a full lipid profile, glucose and HbA1c, blood pressure, kidney function, smoking, family history. All of it is fed into the European risk score SCORE2 (SCORE2-OP for people over 70), which estimates the probability of a cardiovascular event over the next ten years.
Lipoprotein(a) stands apart. Its level is genetically determined and barely changes over a lifetime, so measuring it once is enough. In the updated European lipid guideline of 2025, 50 mg/dl is named as the threshold above which Lp(a) counts as an additional risk factor. If the calculated risk falls in the middle and the decision is not obvious, imaging helps: ultrasound of the carotid and femoral arteries shows whether there are plaques at all, and a CT coronary calcium score shows how far the process has gone in the heart’s arteries. Beyond that, as indicated, come exercise testing, CT coronary angiography and, more rarely, invasive coronary angiography.
How it is treated
The basis is lowering LDL cholesterol, giving up smoking, controlling blood pressure and blood sugar, movement and diet. That sounds dull right up to the moment it becomes clear that the entire evidence base rests on those points.
The LDL targets in the 2025 European guideline are unchanged: the higher the risk, the lower the target, and below 55 mg/dl for the very-high-risk group. What is new is different: first, for a separate group at extreme risk (repeated vascular events despite maximal treatment, disease in several vascular territories) an even lower bar is allowed. Second, combining drugs is recommended earlier, rather than waiting to see that a statin alone was not enough. The range includes, besides statins and ezetimibe, PCSK9 inhibitors by injection, inclisiran given twice a year, and bempedoic acid for those who cannot tolerate statins.
Where the narrowing is already critical, an intervention is discussed: a stent, bypass surgery, or surgery or stenting of the carotid artery. An important detail for those travelling to Germany: since 1 October 2025, procedures for carotid stenosis have been on the German list of procedures for which a patient has a legal right to an independent second opinion at the insurer’s expense. That is a direct signal that the decision to operate is not regarded here as self-evident.
What is in the laboratories, and what that does not yet mean
Munich researchers at the LMU Institute for Cardiovascular Prevention have studied the inflammatory side of atherosclerosis for many years — in particular the CXCR4 receptor, which influences the strength of the vessel wall, and the mechanisms by which immune cells rid themselves of excess cholesterol. The work is interesting and continues: in 2023 the group showed in mice that acting on the regulation of CXCR4 reduces damage to the vessels.
But no medicine has come of it yet: these are preclinical models, and the road to use in people is long. Closer to practice is another line — drugs that lower Lp(a); the first large trial of their effect on heart attacks and strokes is finishing, and results are expected shortly. Until they are published, lowering Lp(a) remains an experimental approach, and one has to work with what is already proven.
This material is for information only and does not replace a consultation with a doctor. Targets, the treatment regimen and whether an intervention is needed are determined only after an examination in person.