What I've always wanted to know about coronary atherosclerosis (= CAD)

CAD stands for coronary artery disease. The coronary arteries supply the heart muscle with oxygen around the clock; in classic CAD these vessels become diseased through atherosclerosis. Why is this so relevant? According to the German Heart Report, around 126,000 people die each year in Germany from CAD including heart attack⁷ – about 345 a day, 14 an hour.

And CAD can cause far more than chest pain: heart attack, cardiac arrhythmias, heart failure, sudden cardiac death. The real problem often begins long before – the atherosclerosis develops over years in the vessel walls without you noticing anything. That is why we are interested not just in the heart attack, but in the disease from which it arises.

The scale is enormous. For the reporting year 2023, the German Heart Report records around 538,675 hospital admissions for CAD including heart attack⁷ – roughly 1,476 a day, 61 an hour, more than one a minute. Among them, around 185,804 admissions for an acute heart attack alone (about 509 a day).

In 2022, around 126,000 people died from CAD, including 46,608 from an acute heart attack – that works out to around 345 CAD deaths a day, more than 14 an hour, roughly one person every four minutes.

And even that does not fully capture its significance: CAD can contribute to heart failure and be the starting point for serious arrhythmias and sudden cardiac death. These causes of death cannot simply be added up statistically – the groups overlap, and heart failure and arrhythmias have many other causes too. But it is precisely these connections that explain why CAD is so central in medicine.

In short, and honestly: in Germany, cardiovascular diseases claim more lives than all cancers combined – in 2022 the figures were 358,219 versus 231,533. And coronary artery disease (CAD) is the single most common cause of death of all.¹⁴

CAD and its secondary conditions thus claim around 4 times as many lives as lung cancer, around 8 times as many as colorectal cancer, around 10 times as many as breast or pancreatic cancer and almost 13 times as many as prostate cancer.¹⁵ Even the 126,000 deaths coded directly as CAD exceed every single type of cancer many times over.

In the individual case, however, the direct comparison “a tumour versus CAD” is misleading – it depends on the type of tumour, its stage and your personal risk. What matters is the characteristic they share: both often develop silently over years. The difference is that CAD can be made visible early with modern imaging – and that its most important drivers can be influenced. Our aim is therefore not to cause fear, but to provide orientation.

Yes. You can work, do sport, climb stairs, feel completely healthy – and yet there may already be significant deposits in your coronary arteries. Being free of symptoms does not automatically mean your vessels are healthy. How common this silent form is was shown in 2026 by the large REACT study, presented on 29 August 2026 in Munich: around 57 % of symptom-free adults already had deposits.¹

Many years can pass between the onset of atherosclerosis and its first noticeable effects. That is why the key question is not only "Do I have symptoms?", but "Is there already a disease of my coronary arteries?" The cardiac stress MRI examination can make an important contribution to early clarification here – not whether deposits are present, but whether there are early signs of them. And our cardiologist will discuss your personal situation with you.

Because classic CAD is, at its core, a disease of the walls of our coronary arteries – and these walls achieve something remarkable. The heart beats around 100,000 times a day, and by the age of 50 already about 1.6 billion times. Each beat sends a pressure wave through the arteries.

Hold your hand out flat for a moment: a systolic blood pressure of about 120 mmHg corresponds – roughly translated onto the palm of a hand – to a load of 15–20 kilograms. Beat after beat, for decades. That our vessels normally withstand this is the truly astonishing part.

For an artery is not a garden hose. Its innermost lining, the endothelium, is living tissue and at the same time a selectively semi-permeable boundary layer. Certain lipoproteins (LDL- or ApoB-containing) enter the wall both via active transport routes (transcytosis) and through gaps in an already disturbed barrier – and become trapped there, bound to connective-tissue sugars. So they are not merely flushed past, but retained in the wall, damaging the tissue from within.¹⁰

This is where mechanics come into play: high pressure and unfavourable flow, for example at vessel branch points, increase the permeability of the endothelium and damage it further. At lower pressure, fewer particles penetrate and the barrier stays intact for longer. This is precisely why high blood pressure is harmful. So it is both: a biological process amplified by mechanical load and by time. That is why young vessels hardly have the problem – and why atherosclerosis is a core theme of ageing: the endothelium renews itself only slowly, and its repair capacity declines over the years.

This damaging process is driven above all by: raised lipoproteins (LDL/ApoB), high blood pressure, smoking, diabetes and metabolic disorders, genetic predisposition, lack of exercise – and time. Conversely, what is good for vascular health: not smoking, blood pressure control, regular exercise – and above all the reduction of these lipoproteins through certain medications, diet, endurance and strength training.

And the crucial point: these dangerous deposits are visible neither on ultrasound nor on ECG. These methods only respond indirectly, once the damage caused by the deposits has become so severe that the heart can no longer work properly – valuable treatment time has then already been lost. This is exactly where CAD begins: not first at the heart attack, not first at an 80 % stenosis, not first at chest pain.

No – and that is exactly what is fascinating. During exercise, heart rate, cardiac output and blood pressure rise, and the system works harder. Even so, regular exercise is among the most effective things you can do for your cardiovascular system.⁸ Vessels are not a machine that gets worse with every use: they respond, adapt and become trained.

Physiological load is something different from chronic biological damage. One exception is extreme endurance training that repeatedly goes to and beyond the limit of performance over hours: such repeated pressure peaks can indeed place additional strain on the endothelium and even injure it. This is why sensible training takes place predominantly at around 80 % of capacity – and not constantly at 100 % and above; that is reserved, if at all, for competition. For the vast majority of people the opposite applies anyway – and even excellent fitness does not make you immune to heart disease.

There is an interesting purely physical effect: some people with a narrowing actually feel better under exertion. If the blood pressure at the vessel entrance rises while the pressure drop across the narrowing stays comparable, more pressure remains beyond it to supply the downstream heart muscle – right into the "last meadow". Conversely, some people get their symptoms precisely at night, at rest (with a stenosis then confirmed): that is when blood pressure is lowest and the autonomic control shifts. Feeling well under exertion is therefore no proof of healthy vessels.

Yes. Sport considerably lowers cardiovascular risk – but fitness is not a diagnostic finding. Even a superbly trained person can have a previously undetected heart disease.¹

There is an example from recent German cardiology that is as tragic as it is striking: an internationally renowned clinic director and heart specialist – of all people a scientist whose research concerned the function of the inner vessel wall in coronary artery disease – died suddenly and unexpectedly in his late fifties while road cycling, his great passion.

The specific cause of death cannot be inferred from publicly available sources, and it would be wrong to use his death retrospectively as proof of an undetected CAD. But his fate is a reminder in a way that could hardly be more powerful: even exceptional fitness is no substitute for medical diagnostics.

No – these examinations answer different questions. The ECG shows above all the electrical activity of the heart; the ultrasound above all the movement of the heart muscle, pumping function and valves. Ultrasound can say nothing about the extent of possible deposits in the vessels.

Like the ECG, ultrasound too only becomes abnormal once cardiac function is already affected – often, therefore, late. Both can be unremarkable even though coronary plaques have long been present. This is not a failure of these methods; you just need to know which question to put to which examination: if you want to know how the heart pumps, echocardiography is excellent – if you want to know the state of the vessels and the extent of the deposits, you have to look at the vessels directly – talk to us (cardiac CT).²

Your heart has its own electrical system: normally an impulse arises, spreads in an orderly way and triggers a heartbeat – about 100,000 times a day.

In an arrhythmia this control gets out of step: the heart may beat too fast, too slowly or irregularly – or develop electrical activity from which no adequate pumping performance results any more. The spectrum ranges from the harmless extra beat to life-threatening ventricular fibrillation. More on this on the Arrhythmias page.

Because an effective heartbeat needs two things: orderly electricity and the effective mechanics (pumping movement) arising from it.

In ventricular fibrillation, for example, the heart muscle loses its coordinated pumping movement, the effectiveness of the pumping performance falls – the circulation can collapse within seconds. Other arrhythmias, by contrast, are not immediately threatening. The decisive question is therefore: which arrhythmia is present?

The spectrum ranges from nothing at all, through palpitations, racing heart, dizziness and reduced performance, to loss of consciousness, stroke, heart failure or circulatory arrest.

Atrial fibrillation, for instance, can promote the formation of blood clots and thus strokes.¹¹ Persistently fast rhythms can impair heart function. Certain ventricular arrhythmias can become immediately life-threatening.

A great deal. The heart muscle needs oxygen, and the coronary arteries deliver it. If the supply to a section of muscle is impaired, this can also change its electrical stability.

In a heart attack, muscle tissue can die off; the scar tissue left behind alters the spread of electrical excitation. In this way CAD can promote arrhythmias via several routes: acute reduced blood flow, heart attack, scar formation and remodelling of the heart muscle.

Put simply: the heart can no longer adequately fulfil its task – it no longer supplies the body with enough blood under all conditions, or manages this only at raised filling pressures.¹²

Possible consequences are breathlessness, loss of performance, exhaustion, fluid retention (such as ankle oedema), night-time shortness of breath – up to sleeping with the upper body raised – and more frequent night-time trips to the toilet. Heart failure is therefore not simply "a bit of a weak heart" – it can dominate everyday life. More on this on the Heart failure page.

Many conditions can lead to heart failure: CAD and heart attack, high blood pressure, heart valve disease, cardiomyopathies, myocarditis, certain arrhythmias.¹²

Heart failure is therefore often not the original disease, but the result of years of damage to the heart.

A great deal. If the heart muscle is permanently supplied with too little blood, or if muscle tissue is lost in a heart attack, the pumping function suffers.¹²

After a larger heart attack, strong heart muscle can turn into scar tissue that no longer pumps as before; the rest of the heart compensates, remodelling processes follow – and heart failure can develop from this. That is why we would prefer not to first encounter CAD once it has already turned into a heart attack, arrhythmia or heart failure.

It is not only the large vessels that count: disease of the smallest heart vessels (microangiopathy) can also contribute to heart failure. A disturbed function of the inner vessel wall (endothelial dysfunction) plays a role here – it is also discussed in connection with conditions following viral infections, such as Long Covid. Such disorders of the smallest vessels often remain hidden in standard examinations and only become visible with functional imaging such as stress MRI.

Atherosclerosis does not develop overnight. What is decisive is the long-term burden of risk factors.

These include in particular: certain lipoproteins, high blood pressure, smoking, diabetes and metabolic disorders, genetic factors, lack of exercise – and one factor no one can switch off: time.¹⁰

A plaque is not simply "calcium in the vessel", but a change in the vessel wall. And here lies a widespread misconception: "Calcium is hard – so stable – so harmless."

A pure calcium plaque is indeed comparatively stable. But plaques usually consist of a mixture: calcified, partly calcified or predominantly non-calcified. That is why the equation "no calcium = no atherosclerosis" is too simple.

The dangerous parts of a plaque are above all the soft, fat- and inflammation-rich components: they can rupture, a blood clot forms – and a heart attack results. So it is not the narrowing alone but the composition that determines the danger.¹⁰

Not necessarily. A score of 0 initially means: no detectable coronary calcium. That is important and, in principle, favourable information.

What is coronary calcium anyway? You can picture it as hard, calcified deposits in the vessel wall – genuinely solid, chalk-like material that the body incorporates into older deposits, similar to small calcifications. A pure calcium component is more a sign of a mature, quieter deposit.

However, the more a plaque consists of different materials – soft, firm and partly fatty components – the more unstable it can become. There is then a risk that parts break loose and a heart attack results. It is precisely the non-calcified ("soft") plaques that remain invisible on the calcium score² – the contrast-enhanced coronary CT therefore answers the further question: what do my coronary arteries actually look like?

Put simply, a plaque that is not yet calcified and is rich in fat and cells – you can picture it as a soft, swollen spot in the vessel wall, not as a hard stone. It is precisely this that can remain invisible on the pure calcium score.

Important: even such rather unstable plaques can be made visible on cardiac CT – exactly those the calcium score misses. Modern coronary CT shows, in addition to calcifications, non-calcified plaques and certain plaque features too. This turns "How narrow is the vessel?" into the additional question "What is inside the vessel wall?"

These are two different pieces of information: the degree of stenosis describes how narrow the vessel is; the plaque morphology, what the underlying atherosclerosis looks like.

By anatomy we mean the location in the vessel tree: a plaque in the main stem or at the beginning of a large vessel weighs more heavily than one further out in a small branch. The functional significance asks whether a narrowing really impairs blood flow – with main-stem involvement, for example, a lot of heart muscle lies behind it.

Reducing coronary disease to a single percentage figure therefore falls short. Anatomy (location), plaque burden (amount), plaque morphology (composition) and functional significance (blood flow) each answer different questions.

Yes. Because "not high-grade" does not mean "no atherosclerosis".

A moderate narrowing can be part of a much more extensive coronary atherosclerosis. That is why we are not interested exclusively in the narrowest spot.

And there is a surprising point: it is precisely such moderate, not-yet-high-grade plaques that are often more likely to rupture and trigger a heart attack than very tight, already mature and calcified stenoses. It is not the narrowest spot alone that determines the risk – but the total burden and the composition of the deposits.⁵

For treatment this means: the aim is to "freeze" the extent of the atherosclerosis at this level, as it were – above all through a consistent reduction of the harmful lipoproteins (medication, diet, exercise). In this way it is precisely the vulnerable plaques that can be "stabilised" with medication and their progression slowed.¹⁰

If, on the other hand, the disease continues unnoticed, this is exactly where decisive treatment time is lost – time in which the course could still have been influenced favourably. That is why it is worth taking even the seemingly "small" findings seriously.

Not only "Where is the narrowest spot?", but "How much atherosclerosis is there in my coronary arteries overall?"

A single localised plaque is something different from a coronary tree with numerous altered segments. That is why we look, as far as possible, at the entire coronary disease.

Because a laboratory value and the state of your coronary arteries are not the same thing. Laboratory values describe a statistical risk.

Imaging can answer a different question: has this risk already manifested itself anatomically? Only then does a probability become a finding.

No. A risk factor is not a CT scan.

People with similar laboratory values can show a different atherosclerotic burden. That is why we distinguish risk from demonstrable disease.

A family history – especially an early heart attack in parents or siblings – leads to a markedly raised individual risk and is one of the established risk factors.⁸ It does not, however, yet tell you what your own coronary arteries actually look like.

Family history, age, blood pressure, lipid metabolism, diabetes and smoking belong together. Particularly important here is the lipoprotein content in the blood (such as LDL and Lp(a)): it is strongly hereditary, drives atherosclerosis and can be treated in a targeted way. Especially with a family history, it should definitely be measured and, if raised, consistently lowered.¹⁰

At some point this gives rise to a concrete question: do I just want to calculate my risk – or to know whether atherosclerosis is already present? In such a case it is best to talk to us. Depending on the situation, it may make sense to begin with a cardiac stress MRI examination – it is sensitive and involves no radiation and no catheter.⁹

The coronary arteries themselves. Coronary CT angiography can depict and assess the vessel lumen, calcifications, non-calcified and even unstable plaques, stenoses and the distribution of atherosclerosis.

These are exactly the details that remain hidden from a heart ultrasound (echocardiography); the ECG too – with or without exertion – cannot detect them. This allows precisely those structures to be examined that the previous questions were about. Technical details on the cardiac CT page.

Yes. Coronary CT depicts the entire coronary tree.

Assessed in particular are the three large vessels (RCA, LAD/RIVA, RCX) including diagnostically depictable branches. This gives an anatomical overview of the coronary atherosclerosis.

No. The further course of action depends on the specific finding. A normal CT in particular can often avoid an invasive procedure.⁶

Sometimes consistent prevention or medication therapy is the priority, sometimes additional functional diagnostics are needed, and sometimes an invasive assessment or treatment makes sense.

Because diagnostic information does not necessarily require and justify an invasive procedure.² A cardiac catheter is usually only necessary when the atherosclerosis is far advanced or is to be treated straight away. In most cases, by contrast, one first wants to know whether the medication therapy needs to be optimised in order to stop the disease from progressing.

For stable chest pain, CT-based assessment led in large studies to results comparable to direct catheterisation – with fewer procedure-related complications.⁶ The European guideline therefore recommends CT as the first-line examination when chronic CAD is suspected,² and in Germany it has been recognised as covered by statutory health insurance since 2024.³

Anatomy alone does not always answer this question.

That is why we distinguish two questions: "What does the vessel look like?" and "What does this finding mean for the blood supply to the heart muscle?" This brings us to functional diagnostics – the stress MRI. It helps to clarify whether an existing narrowing really warrants intervention (catheter/stent) or whether medication optimisation is sufficient.⁹

The stress MRI asks a different question: is my heart muscle adequately supplied with blood under load?

Put simply: the cardiac CT shows what the coronary arteries look like; the stress MRI shows whether enough blood reaches the heart muscle under load. Compared with an exercise ECG, the stress MRI is considerably more sensitive and detects an impairment of blood flow more reliably.⁹ Anatomy (cardiac CT) and function (stress MRI) are not competitors – they complement each other.

The honest answer: the number alone is not enough.

What can be relevant: location, vessel size, plaque morphology, plaque burden, further stenoses – and above all: does the stenosis cause a relevant impairment of blood flow?

Of course the link to the clinical picture must not be missing either – though it often does not yet make itself felt: such stenoses often cause no (or not yet any) symptoms. The most important thing is that the danger is recognised and thus, one hopes, averted. With unclear symptoms in particular, an additional stress MRI can be useful. If in doubt, do feel free to call us.

Then it becomes particularly interesting – because the blood is not concerned with the isolated percentage of each individual spot.

Several serial stenoses can influence one another haemodynamically. That is why the entire course of the vessel must be considered: a single 50 % stenosis is not the same as several 50 % stenoses one behind another. Unfortunately, the actual effective narrowing does not result from simply adding up the individual stenoses.

Because we need the heart to be as calm and regular as possible for the scan. A lower heart rate can improve image quality and reduce motion artefacts. How much of a beta-blocker is needed depends above all on the absolute heart rate.

Modern devices such as our dual-source CT are particularly tolerant here: it is, so to speak, two CTs in one device – two X-ray sources circle the heart offset from each other, and what one does not capture, the other sees. This high temporal resolution makes it possible to examine even higher heart rates well – a small beta-blocker dose is then often enough, and sometimes none at all.¹³

Modern cardiac CT technology has advanced considerably. The actual radiation exposure depends on the scanner, body build, heart rate and protocol, and with current technology it can already be reduced markedly compared with devices from around ten years ago.

The decisive question is therefore not "Does a CT involve radiation?" – of course it does – but: "Is the diagnostic information worth this radiation exposure in my specific situation?"

To put it in context: the danger comes from the undetected disease, not from the examination. The more than 500,000 hospital admissions for CAD and around 186,000 for a heart attack per year in Germany arise from coronary artery disease – not from a CT.⁷ Details on the technology on the cardiac CT page.

Why contrast agent at all? Because only then do the coronary arteries stand out clearly from their surroundings, and their interior (the lumen) as well as non-calcified plaques become assessable. Without any contrast agent, only the calcium can be measured (calcium score) – but not the actual course of the vessel with soft plaques and narrowings. That is why we are often asked whether it can be done "without": for the actual depiction of the vessels, unfortunately not.

Iodine-containing contrast agent is used routinely and is as a rule well tolerated. Of course there are situations that call for particular caution – which is why relevant previous contrast-agent reactions and kidney function are part of the preparation. If no current kidney value is available, we determine one directly before the examination here as needed. A good examination begins not with the scanner, after all, but with the right indication and preparation.

The decisive scan: a few seconds.

The whole examination takes longer – explanation, preparation, heart-rate optimisation if needed, and the administration of nitro and contrast agent take more time than the actual scan. And it is precisely this preparation that largely determines the diagnostic quality.

Yes – though with differences.

Bypasses can often be depicted very well thanks to their larger diameter and course. With stents, the assessability depends more strongly on diameter, material, position, calcifications and CT technology – but with modern technology, non-invasive stent monitoring is an established application of cardiac CT, especially for larger stents.

Perhaps not only "Do I have chest pain today?" and also not solely "How severe is my narrowest stenosis?", but: "Do I already have coronary atherosclerosis – how pronounced is it, and is it already impairing the supply to my heart muscle?"¹

Different examinations answer different questions – it is not about having as many as possible, but about the right question and the examination that fits it.

If in doubt, call us if you have questions – our Cardiology and Radiology teams are happy to talk everything through with you. And as a general rule: do not put off diagnoses.