Atherosclerosis is one of the most important and yet most underestimated diseases of our time. It develops completely unnoticed over years and decades, causes no pain, and often only shows symptoms when significant damage has already occurred – in the worst case, in the form of a heart attack or stroke. This gradual calcification and narrowing of the arteries is the leading cause of cardiovascular diseases, which are the most frequent cause of death worldwide. Yet, in many cases, atherosclerosis is preventable or at least slowable.

What happens in atherosclerosis

The term atherosclerosis is derived from the Greek words 'athero' meaning porridge and 'sklerosis' meaning hardening – a fitting description of the disease process. Deposits called plaques, consisting of fats, cholesterol, calcium, and other substances, form in the walls of the arteries. These plaques grow over time and narrow the vessel lumen, reducing blood flow. Even more dangerous, however, is the risk of a plaque rupturing. A blood clot then forms at the ruptured site, which can suddenly and completely block the artery. If this happens in a coronary artery, a heart attack results. If it occurs in an artery supplying the brain, a stroke results. In the leg arteries, it leads to peripheral arterial disease, commonly known as intermittent claudication.

More than just 'calcification'

For a long time, atherosclerosis was simply viewed as calcification or blockage of the arteries due to too much fat in the blood. Today, we know that it is a complex inflammatory process. Its development typically begins with damage to the innermost layer of the blood vessels, the endothelium. This damage can be caused by high blood pressure, smoking, elevated blood sugar levels, or other factors. Through the damaged endothelium, LDL cholesterol particles can penetrate the vessel wall. There, they are oxidized and trigger an inflammatory response. Immune cells migrate in and attempt to absorb the oxidized LDL, but in doing so, they themselves become so-called foam cells, which remain in the vessel wall. This process continues, the plaques grow, and over time, calcium is deposited, leading to hardening. This guide explains how you can assess your personal atherosclerosis risk, understand modern risk markers such as ApoB and Lp(a), and protect your vascular health through targeted measures.

Atherosclerosis doesn't develop by chance. It's promoted by a combination of various factors, some of which are modifiable and others not. Understanding these risk factors is the first step toward prevention. You can't change some factors, but you can minimize the modifiable risks and thus significantly reduce your overall risk.

Risk factors that cannot be influenced

Age is the strongest non-modifiable risk factor. With each passing year, the risk of atherosclerosis increases because cumulative damage to the blood vessel walls intensifies. Gender also plays a role: men, on average, develop the disease about ten years earlier than women, which is partly attributed to the protective effect of estrogen before menopause. After menopause, however, the risk becomes more similar. Genetic predisposition influences both lipid metabolism and vascular sensitivity and susceptibility to inflammation. If heart attacks or strokes have occurred in your family at a young age, especially among male relatives under 55 or female relatives under 65, you may have an increased genetic risk.

Modifiable risk factors

The good news is that the most important risk factors are modifiable. High blood pressure damages the vessel walls through constantly elevated pressure and promotes the penetration of LDL cholesterol. Blood pressure below 130/80 mmHg is now considered optimal. Elevated LDL cholesterol is the main driver of plaque formation – the more LDL particles circulate in the blood, the more can penetrate the vessel walls. Smoking is one of the most potent preventable risk factors. It directly damages the endothelium, promotes inflammation, increases the tendency for thrombosis, and lowers protective HDL cholesterol. Diabetes mellitus massively accelerates atherosclerosis, as elevated blood sugar levels damage the vessels and exacerbate inflammatory processes. Obesity, especially visceral abdominal fat, promotes inflammation and is associated with insulin resistance, high blood pressure, and unfavorable blood lipids. Lack of exercise is an independent risk factor, regardless of weight. Stress and psychological factors such as depression can also contribute to atherosclerosis through various mechanisms.

Risk factors accumulate

An important concept is that risk factors don't act in isolation, but rather reinforce each other. Someone who smokes, is overweight, has high blood pressure and high cholesterol, and carries a significantly higher risk than someone with only one of these factors. Conversely, this also means that improving multiple factors yields a disproportionately large benefit. Even if you have a genetic predisposition, you can significantly reduce your risk through a healthy lifestyle.

In recent years, a paradigm shift has taken place in cardiology. Instead of focusing solely on classic LDL cholesterol, another marker is coming into focus: apolipoprotein B, or ApoB for short. Many experts consider ApoB to be the best single marker for assessing the risk of atherosclerosis – better than LDL cholesterol, better than total cholesterol, and better than the ratio of different cholesterol fractions.

What is ApoB and why is it important?

To understand why ApoB is so significant, one must know how cholesterol is transported in the blood. Cholesterol is fat-soluble and cannot float freely in the water-based blood. It is therefore packaged in small transport particles called lipoproteins. LDL, VLDL, and other atherogenic lipoproteins have one thing in common: each of these particles carries exactly one molecule of apolipoprotein B on its surface. ApoB is, so to speak, the identifier that allows these particles to bind to receptors. When we measure ApoB, we are essentially counting the number of all atherogenic lipoprotein particles in the blood. And this number of particles appears to be crucial for the risk of atherosclerosis—possibly more important than the amount of cholesterol they contain.

ApoB versus LDL cholesterol

The classic LDL cholesterol measurement used in standard blood tests indicates the amount of cholesterol in LDL particles. The problem is that LDL particles can vary in size and carry different amounts of cholesterol. In some people, the LDL particles are small and dense, while in others they are large and fluffy. Two people can have the same LDL cholesterol level but a completely different number of LDL particles. The person with the small, dense particles has more particles, and therefore more ApoB, and thus carries a higher risk – even though their LDL cholesterol level is identical. This discrepancy is particularly relevant in people with metabolic disorders such as diabetes, metabolic syndrome, or insulin resistance. In these cases, LDL cholesterol is often only moderately elevated, while ApoB can be significantly elevated because of the many small, dense LDL particles present. The classic LDL cholesterol measurement underestimates the risk in these situations.

Target values ​​and practical significance

Current guidelines are beginning to give greater consideration to ApoB. An ApoB level below 90 mg/dL is considered optimal for individuals without increased risk, below 80 mg/dL for those with increased risk, and below 65 mg/dL for those with very high risk, such as after a heart attack. It is important to understand that ApoB does not replace LDL cholesterol but complements it. If both values ​​are similarly elevated, there is no contradiction. The situation becomes interesting when they diverge. Normal LDL cholesterol with elevated ApoB is a warning sign of an underestimated risk. Elevated LDL cholesterol with normal ApoB may be less threatening than the LDL value alone suggests. Measuring ApoB is a simple blood test and is increasingly being incorporated into cardiovascular check-ups.

While most cardiovascular risk factors are modifiable through lifestyle, there is one important factor that is almost entirely genetically determined: lipoprotein(a), abbreviated Lp(a). This marker is even less well-known than ApoB, although elevated levels represent a significant risk. The insidious thing is that many people don't know they have elevated Lp(a) levels because these are not routinely measured.

What is Lp(a)?

Lipoprotein(a) is a lipoprotein particle structurally similar to LDL. It consists of an LDL-like core and an additional protein called apolipoprotein(a) bound to apolipoprotein B. The Lp(a) concentration in the blood is over 90 percent genetically determined and remains relatively constant throughout life. You are born with a certain Lp(a) level, and this hardly changes through diet or exercise. Approximately 20 to 25 percent of the population has elevated Lp(a) levels, which are associated with an increased risk of heart attack, stroke, and aortic valve calcification.

Why Lp(a) is dangerous

Lp(a) promotes atherosclerosis in several ways. Like LDL, it can penetrate the vessel wall and contribute to plaque formation. Additionally, it has prothrombotic properties, meaning it promotes blood clotting and thus increases the risk of clot formation. Apolipoprotein(a) has a structural similarity to plasminogen, a protein involved in dissolving blood clots. Lp(a) can compete with plasminogen and thus inhibit the natural clot dissolution process. Lp(a) is particularly relevant in people who suffer heart attacks despite seemingly optimal risk factors. For example, in families where heart attacks occur frequently at a relatively young age, even though all members are non-smokers, eat a healthy diet, and do not have high blood pressure, elevated Lp(a) levels could play a role.

Measure and trade

Since Lp(a) levels are genetically determined and relatively constant throughout life, a single measurement is usually sufficient. Measurement is recommended in cases of a family history of early cardiovascular disease, after a personal heart attack or stroke at a young age, and when other risk factors are optimal but an elevated risk still exists. An Lp(a) level above 50 mg/dl or 125 nmol/l is generally considered elevated, although these units vary depending on the laboratory and are not directly convertible. Currently, there are no approved medications that effectively lower Lp(a) – statins and other lipid-lowering drugs are ineffective. However, promising RNA therapies are in clinical development. In the meantime, an elevated Lp(a) level means that other risk factors should be optimized even more rigorously. LDL cholesterol should be kept particularly low, blood pressure and blood sugar levels should be optimally controlled, and smoking should be strictly avoided.

ApoB and Lp(a) are important, but not the only markers for atherosclerosis risk. A comprehensive picture of vascular health emerges from the combination of various parameters. Each individual marker illuminates a different aspect of the complex disease process, and only in combination do they form a complete risk profile.

The classic lipid profile

The standard lipid profile includes total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. LDL cholesterol remains an important marker, although ApoB may be more informative. An LDL below 100 mg/dL is considered optimal for most people, below 70 mg/dL for high-risk patients, and below 55 mg/dL after a heart attack. HDL cholesterol was long considered "good" cholesterol, protecting against atherosclerosis. Today, we know that the relationships are more complex. Low HDL is a risk marker, but artificially raising HDL with medication has not shown any benefit in studies. An HDL above 40 mg/dL in men and above 50 mg/dL in women is desirable. Triglycerides are a measure of the neutral fats in the blood. Elevated triglycerides are associated with increased risk, especially when combined with low HDL and small, dense LDL particles – a pattern typical of insulin resistance. Fasting triglycerides below 150 mg/dL are considered normal.

Inflammatory markers

Since atherosclerosis is fundamentally an inflammatory process, inflammatory markers can provide additional information. High-sensitivity C-reactive protein, or hsCRP, is the most extensively studied cardiovascular inflammatory marker. An hsCRP level below 1 mg/L indicates low cardiovascular risk, between 1 and 3 mg/L moderate risk, and above 3 mg/L elevated cardiovascular risk. It is important to note that hsCRP is influenced by many factors, such as acute infections or chronic inflammation from other causes. A single elevated value should therefore be monitored. Other inflammatory markers, such as interleukin-6 or fibrinogen, are being investigated in research but have not yet been firmly established in routine diagnostics.

Blood sugar and insulin resistance

Elevated blood glucose levels and insulin resistance are strong drivers of atherosclerosis. Fasting blood glucose should be below 100 mg/dL to avoid an increased risk. HbA1c, which reflects the average blood glucose level over the past two to three months, should be below 5.7 percent. Values ​​between 5.7 and 6.4 percent are classified as prediabetes and already indicate an increased cardiovascular risk. Fasting insulin and the HOMA index can detect insulin resistance before blood glucose levels rise, allowing for even earlier intervention.

Nutrition is one of the most important modifiable factors for vascular health. It works on several levels: it directly influences blood lipid levels, blood pressure, blood sugar, body weight, and systemic inflammatory activity. A vascular-friendly diet doesn't have to be complicated or restrictive – it's about long-term habits, not short-term diets.

The basic principles

The strongest scientific evidence for a heart-protective diet supports the Mediterranean diet. It is rich in vegetables, fruits, legumes, nuts, whole grains, and olive oil, contains moderate amounts of fish and poultry, and is low in red meat, processed foods, and sugar. The PREDIMED study showed that a Mediterranean diet with added olive oil or nuts can reduce the risk of heart attack and stroke by about 30 percent—an effect comparable to that of medication. High-fiber foods deserve special mention. Soluble fiber from oats, barley, legumes, and fruits binds cholesterol in the intestines and reduces its absorption. Three grams of beta-glucan from oats daily, contained in approximately 75 grams of rolled oats, can lower LDL cholesterol by five to ten percent.

A differentiated view of fats

The recommendation to reduce fat intake in general is outdated. The type of fat is crucial. Saturated fatty acids, primarily from animal products and coconut oil, raise LDL cholesterol. A moderate shift towards unsaturated fats is advisable. Trans fats from industrially hydrogenated fats are particularly harmful and should be avoided as much as possible – they are found in some baked goods, fried foods, and processed snacks. Monounsaturated fatty acids from olive oil, rapeseed oil, avocados, and nuts are beneficial for blood vessels. Omega-3 fatty acids from oily fish such as salmon, mackerel, and herring have anti-inflammatory properties and can lower triglycerides. Two servings of oily fish per week are recommended.

What you should reduce

Sugar and refined carbohydrates raise triglyceride levels, promote insulin resistance, and contribute to weight gain. Average sugar consumption far exceeds the WHO-recommended maximum of 25 grams per day. Highly processed foods often contain high amounts of salt, sugar, unhealthy fats, and additives—their regular consumption is associated with increased cardiovascular risk. Excessive salt consumption raises blood pressure. The recommended upper limit is six grams of salt per day, with the majority of salt consumed coming not from the salt shaker but from processed foods, bread, cheese, and ready-made meals. Alcohol should be consumed only in moderation, if at all. The earlier assumption that moderate alcohol protects the heart is increasingly being questioned.

Besides diet, other lifestyle factors play a central role in vascular health. Regular physical activity, not smoking, stress management, and sufficient sleep are not lifestyle recommendations for a clear conscience, but effective medical interventions with proven effects on atherosclerosis and cardiovascular events.

Movement as medicine

Regular physical activity improves virtually every cardiovascular risk factor. It lowers blood pressure, raises HDL cholesterol, reduces triglycerides, improves insulin sensitivity, aids weight management, and reduces inflammatory markers. Furthermore, it improves endothelial function—the ability of blood vessels to dilate when needed. Recommendations include at least 150 minutes of moderate activity per week, such as brisk walking, cycling, or swimming, or 75 minutes of vigorous activity, such as jogging. Strength training on two days per week is also recommended. More important than precisely meeting these guidelines is consistency: any movement is better than none, and small changes add up. Those who have been inactive will experience the greatest health benefits from even beginning moderate activity.

Quitting smoking – the biggest single win

Smoking is the preventable risk factor with the greatest impact on atherosclerosis. It directly damages the endothelium, promotes inflammation, increases blood clotting and LDL oxidation, lowers HDL cholesterol, and raises blood pressure. The risk of heart attack is two to four times higher in smokers. The good news: Recovery begins immediately after quitting smoking. Within two to five years of quitting, cardiovascular risk approaches that of a non-smoker. It's never too late to quit, and it's worthwhile at any age. Anyone who has difficulty quitting should seek professional help—nicotine replacement therapy, medication, and behavioral therapy can significantly increase the success rate.

Sleep and stress

Sleep deprivation and chronic stress are often underestimated as risk factors. Short sleep, defined as less than six hours per night, is associated with elevated blood pressure, inflammatory markers, insulin resistance, and an increased risk of heart attack. Sleep apnea, characterized by pauses in breathing during the night, is also a cardiovascular risk factor in its own right and should be treated. Chronic stress activates the sympathetic nervous system and increases cortisol, blood pressure, and inflammatory markers. Techniques such as meditation, yoga, progressive muscle relaxation, or simply taking regular breaks can help. Social isolation and depression are also associated with increased cardiovascular risk and deserve attention.

If lifestyle changes alone are insufficient to adequately reduce cardiovascular risk, medication comes into play. The decision to use medication always involves weighing the individual risk against the benefits and potential side effects of the drugs. In high-risk cases, medication can be life-saving.

Statins – The Gold Standard

Statins are the best-studied and most effective medications for reducing cardiovascular risk. They inhibit an enzyme in the liver involved in cholesterol synthesis, thus lowering LDL cholesterol by 30 to 50 percent, depending on the specific drug and dosage. In addition, statins have so-called pleiotropic effects: they stabilize plaques, reduce inflammation, and improve endothelial function. Numerous large studies have shown that statins reduce heart attacks, strokes, and cardiovascular mortality. Their effectiveness increases with the baseline risk. Statins are essential for individuals who have already suffered a heart attack. For primary prevention, meaning individuals without a previous event, the decision depends on the overall risk. Side effects such as muscle pain can occur, but are often mild and can be managed by changing the medication or adjusting the dosage.

Other lipid-lowering drugs

If statins alone are insufficient or not tolerated, other options are available. Ezetimibe inhibits cholesterol absorption in the intestine and can lower LDL by a further 15 to 20 percent. The combination of a statin and ezetimibe is often beneficial. PCSK9 inhibitors are modern, highly effective antibodies that can lower LDL by 50 to 60 percent. They are administered as a subcutaneous injection and are used in cases of very high risk or familial hypercholesterolemia. Bempedoic acid is a newer oral medication that can offer an alternative for patients with statin intolerance. Fibrates primarily lower triglycerides and are indicated in cases of severely elevated triglycerides.

Other medications

Blood pressure-lowering medications are essential for managing hypertension – the choice is made individually depending on comorbidities and tolerability. Low-dose aspirin for blood thinning is no longer generally recommended for primary prevention, as the risk of bleeding can outweigh the benefits. However, antiplatelet therapy is standard after a heart attack or stroke. For people with diabetes, newer antidiabetic drugs such as SGLT2 inhibitors and GLP-1 agonists play an important role, as they reduce cardiovascular risk regardless of blood glucose levels.

The insidious nature of atherosclerosis lies in its silent nature. The plaques grow for years and decades without causing any symptoms. By the time the disease finally manifests itself through a heart attack or stroke, significant damage has already been done. This is why preventive risk assessment is so important – it allows for timely intervention, long before an event occurs.

Which tests are useful?

A comprehensive cardiovascular check-up should include several parameters. The standard lipid profile, including total cholesterol, LDL, HDL, and triglycerides, forms the basis and is covered by health insurance as a preventative measure. ApoB should also be measured, as it may be more informative than LDL alone—especially in cases of metabolic disorders, obesity, or diabetes. Lp(a) should be measured at least once in a person's lifetime, as it is genetically determined. A family history of atherosclerosis or elevated levels can influence treatment decisions. HsCRP, an inflammatory marker, can provide additional risk information but is influenced by many factors. Blood glucose and HbA1c are also important for risk assessment, as diabetes is a strong driver of atherosclerosis.

When should you get tested?

A basic blood lipid check is recommended as part of a health check-up starting at age 35. An earlier and more comprehensive check may be advisable if there is a family history of heart disease or other risk factors. Specifically, you should know your status if parents or siblings suffered a heart attack or stroke at a young age (before 55 or 65), if you smoke or have smoked in the past, if you are overweight, have high blood pressure or diabetes, or if you simply want to know the health of your blood vessels. A home test like the DoctorBox Cardiovascular Check allows for convenient determination of important parameters from home. Blood is drawn via finger prick, and the results are presented in an easy-to-understand way.

Understand results and act

The test results should not be viewed in isolation, but interpreted within the context of your overall risk. A single elevated value in an otherwise optimal profile has a different meaning than several borderline findings. If the results are abnormal, a consultation with a doctor is advisable to plan further steps. Whether lifestyle changes are sufficient or medication should be considered depends on the overall picture.

Atherosclerosis is a serious disease, but not inevitable. Although genetic factors play a role, the majority of the risk lies in modifiable factors. With knowledge of modern risk markers and the right strategies, you can actively protect your vascular health and significantly reduce your risk of heart attack and stroke.

Key findings

Atherosclerosis is a gradual process that develops over years, usually without causing any symptoms. By the time it manifests itself through an event like a heart attack, significant damage has already occurred. This is why prevention is so important. The classic risk factors remain relevant: high blood pressure, elevated LDL cholesterol, smoking, diabetes, and obesity are the main drivers. The good news is that all of these factors are modifiable. ApoB may be a better cholesterol marker than LDL because it measures the number of atherogenic particles. ApoB can reveal an underestimated risk, especially in people with metabolic disorders. Lp(a) is a genetically determined risk factor that should be measured once in a lifetime. If elevated levels are found, other risk factors must be optimized even more rigorously, as Lp(a) itself is not modifiable.

What you can do

A Mediterranean diet rich in vegetables, olive oil, nuts, and fish is the best-documented heart-protective diet. Regular exercise improves virtually every risk factor and is a strong, independent protective factor. Quitting smoking is the single greatest benefit—the risk begins to decline immediately and approaches that of a non-smoker within a few years. Stress management and adequate sleep are often underestimated but have demonstrable effects on cardiovascular risk. If lifestyle changes are insufficient, medications such as statins can further reduce risk. In high-risk individuals or after a cardiovascular event, they are often lifesaving.

The first step

Know your risk. A comprehensive blood test, which includes ApoB and ideally Lp(a) in addition to the classic parameters, gives you a picture of your current vascular health. Based on this, you can take targeted action – with lifestyle changes and, if necessary, with medical support. Your blood vessels will thank you.