Complaints & connections · borters.ch
A vessel closes and heart muscle dies — every minute counts: call 144 at once.
Also known as: myocardial infarction · MI · STEMI/NSTEMI · heart attack
Open in the tool — with search and all the links →This compilation is for information and replaces neither medical diagnosis nor treatment. If you have symptoms, see a doctor.
A clot blocks a coronary artery — usually where an atherosclerotic plaque ruptures. The muscle beyond it dies unless the vessel is reopened quickly. Typical: lasting chest pressure/tightness, radiating to arm or jaw, breathlessness, cold sweat, nausea. Emergency — call at once. Often atypical in women and people with diabetes. The guideline also lists signs that on their own indicate an immediately threatening situation — regardless of how the pain is described: a **faint or collapse** just before, **confusion or clouding**, **newly arisen breathlessness at rest**, cold sweat, distended neck veins — and, expressly included, **marked fear in the person affected**. That last point is not there as decoration: someone who feels their life is at stake is often right, and that feeling belongs taken seriously rather than soothed.
The strongest dietary lever for LDL: replace saturated fats (fatty meat, butter, palm oil) and trans fats with unsaturated ones (olive oil, nuts, fish).
Soluble fibre binds bile acids in the gut; the body pulls LDL from the blood to replace them. Well established and dose-dependent.
They block cholesterol absorption in the gut and lower LDL by about 10 %. In fortified products or as a supplement.
After a heart attack each medicine has its own job: antiplatelets keep the stent open, statins stabilise the deposits, beta blockers unload the heart, ACE inhibitors prevent remodelling. None of them can be felt — which is exactly why they are most often dropped in the second year, when things have long been going well.
From the moment of blockage the muscle begins to die within twenty to thirty minutes; after six to twelve hours the damage is largely fixed. Hence “time is muscle”. The target for catheter treatment is ninety to a hundred and twenty minutes from first medical contact. Troponin rises three to four hours after the start and stays raised for seven to fourteen days. Rehabilitation lowers mortality by about twenty per cent in reviews.
Emergency — call at once, don’t wait to see if it eases.
The large studies at 1 g a day found no difference after a heart attack. One study with 4 g of a pure EPA preparation showed fewer events — the same amount of mixed fish oil capsules did not. Amount and form decide here.
In heart failure a study at 300 mg a day over 2 years showed fewer events; it has not been convincingly repeated. For muscle complaints on statins the results are contradictory.
One of the clearest examples of a refuted expectation: in large prevention trials for heart events no benefit showed, and at high sustained doses rather more bleeding strokes.
Heart attacks cluster in the first hours after waking — adrenaline, cortisol and blood pressure rise together then, and the blood clots more readily. That is one of the clearest daily rhythms in medicine.
After a heart attack this hormone shows how badly the pump has suffered. A high value after weeks argues for lasting weakness — and it helps decide which medicines then belong permanently.
Sustained heavy strain raises the risk measurably — through blood pressure, sugar and clotting at once. Broken heart syndrome is the extreme case: heart weakness from an adrenaline storm alone, with no blocked vessel.
Reduces cardiovascular events.
Cardiac rehabilitation is not an extra but part of the treatment. Supervised training after a heart attack lowers mortality and repeat events in studies.
Depression after a heart attack is common and linked with a poorer course. Stress methods act on mood; on the vessels only indirectly.
AWMF 053-023 · S3 · 2025-07 — in force
Brustschmerz — DEGAM-Leitlinie für die primärärztliche Versorgung
checked 2026-09