
© Freepik
September 30, 2025
Dr. Andrea Gartenbach
Every two minutes, a person in Europe dies from a cardiovascular disease. Usually without any warning. Heart attack or stroke is often the first visible manifestation of a quietly progressing medical history. The problem: Our traditional preventive system detects risks only when it's actually already too late.
Legal preventive care focuses on blood pressure and total cholesterol, with men over 65 also getting an aortic screening. But this falls short. Total cholesterol, for example, doesn't indicate how many risky particles are circulating in the blood, promoting deposits in vessels, known as atherogenic particles. And even ultrasound examinations of large vessels only show changes once the disease is advanced. Particularly critical: The coronary arteries, which are the most vulnerable and where the risk is highest, remain invisible in this routine.
This inadequate diagnostics not only affects members of the statutory health insurance. Many private health insurances now also align their coverage with the guidelines of statutory preventive care. As a result, essential preventive diagnostics are often not covered there either. Instead of enabling progress, prevention is based on outdated standards.
Speaking of outdated:
Cholesterol is not an enemy but a vital building block. It stabilizes cell membranes and serves as a precursor for vitamin D, bile acids, and hormones like cortisol, testosterone, or estradiol. About 80 percent is produced by the liver itself; only a small part comes from diet. Therefore, the risk is determined not by the sheer amount, but by the transport form and the combination with genetic, metabolic, and inflammatory factors.
Modern prevention must consider many levels, including biomarkers that are now readily available.
Permanently elevated blood pressure acts like constant waves on the delicate inner lining of the vessels, the endothelium. Tiny injuries occur, platelets settle, fats accumulate. This creates the basis for dangerous plaques.
This is about the transport forms of cholesterol and fats in the blood:
ApoB is the central marker for the number of atherogenic particles. The more particles, the greater the risk of deposits.
Complete lipid paneli.e. LDL, HDL and Triglyceride including subfractionation of lipids into particle number, size, and density.
Lipoprotein(a), or Lp(a) for short, is a special form of LDL cholesterol to which an additional protein is attached. This not only promotes deposits but also inflammation and blood clots. Guidelines recommend a one-time measurement of Lp(a) in all adults. For women, it is advisable to check the value additionally before and after menopause, as the cardiovascular risk increases significantly during this phase of life. It is a strong genetic risk factor.
ApoE genotype influences how our body processes fats. Some variants are associated with an increased risk of arteriosclerosis or Alzheimer's.
The endothelium is the thin cell layer lining all blood vessels, like a protective film. It regulates many important processes: blood flow, substance exchange, blood clotting, and inflammatory responses. When the endothelium is damaged, deposits can form, the first step towards arteriosclerosis.
Certain blood values indicate the state of this layer:
hsCRP indicates silent, systemic inflammation that weakens vessels and promotes plaque formation.
Lp-PLA2 indicates whether inflammation is already active directly in the vessel wall.
Homocysteine, a degradation product of protein metabolism, makes the vessels more vulnerable and also signals that methylation, an important regulatory process for detoxification and gene regulation, is not running optimally.
Sugar and fat metabolism also play a key role:
Fasting glucose and insulin show how well the body regulates blood sugar.
The HOMA indexcalculated from sugar and insulin levels, indicates early insulin resistance, one of the key drivers of vascular damage.
Adipokines like leptin and adiponectin are messengers from fatty tissue. They reveal whether fat cells act pro-inflammatory or regulate healthily.
Micronutrients that serve as cofactors, such as the omega-3 index, show how many of the anti-inflammatory omega-3 fatty acids EPA and DHA are found in cell membranes.
Markers of oxidative and nitrosative stress such as 8-OHdG, MDA-LDL and nitrotyrosine are functionally complementary laboratory values.
8-OHdG- DNA damage by free oxygen radicals
MDA-LDL- oxidized LDL particles, indication of lipid-based oxidative stress
Nitrotyrosine- occurs when reactive nitrogen compounds (peroxynitrite) damage cells – an early warning sign of endothelial stress.
NT-proBNP A marker to detect early onset heart failure.
The Heart rate variability (HRV) provides insight into how flexibly the heart adapts to stress and recovery. Persistently low values indicate stress on the nervous system.
A Polysomnography is a special sleep measurement that detects breathing pauses (sleep apnea). These are often overlooked risk factors for the heart and vessels.
However, blood values do not reflect the complete reality. What matters is what actually happens in the vessels.
CAC score measures via CT how much the coronary arteries are already calcified and is an established indicator of individual risk.
CT coronary angiography not only makes calcifications visible, but also soft, unstable plaques that are particularly dangerous.
AI-supported tools like Cleerly from the USA can distinguish between hard and soft plaques even more precisely, allowing for a differentiated risk assessment.
Of course, CT procedures mean radiation exposure (and with angiography, additionally contrast agents). But especially in prevention, targeted use for risk stratification is indispensable – to detect unstable plaques in time before they become a clinical problem.
Cardiovascular diseases do not develop overnight. They are the result of decades-long, silent processes. Yet our current preventive system often detects them only when it's too late. We therefore need a new standard: ApoB or Non-HDL-C as superior markers of particle number instead of just LDL-C, an Lp(a) screening at least once in a lifetime for all adults, inflammation, metabolic, and stress markers as an early warning system, and modern imaging that makes the actual risk visible.
The tools are there. Now politics and health insurers must have the courage to use them consistently.