"Heart attack" is used for a dozen different things, and the differences matter: a heart attack from a burst plaque, a heart attack from a torn artery, a heart attack with clean arteries, a heart that stops from a rhythm rather than a blockage, and a heart that is stunned by stress and recovers completely are treated differently and carry different futures. This chapter is the map. Each entry says what the thing is, how it is told apart, and what that changes. The chapters that follow go into each group.
1. The words
Ischaemia is heart muscle short of blood. Infarction is heart muscle that has died from it; a myocardial infarction (MI) is what the public calls a heart attack. Angina is the pain of ischaemia without infarction. Acute coronary syndrome (ACS) is the hospital's umbrella for the three things that arrive the same way: unstable angina, NSTEMI and STEMI. Troponin is the protein that leaks from injured heart muscle into the blood, and a rise and fall of it is what turns "chest pain" into "infarction". Arrest is the heart stopping as a pump, whatever the cause. Heart failure is the pump weakened, chronically, which any of the above can leave behind.
2. Blocked or narrowed arteries: the coronary syndromes
| What | What is happening | How it is told apart | What that changes |
|---|---|---|---|
| Stable angina | A narrowed artery that supplies enough blood at rest and not enough on exertion. Predictable: pain with effort, relieved by rest or a GTN spray within minutes | History; an ECG usually normal at rest; troponin normal; a CT coronary angiogram (the UK first-line test) shows the narrowing | Not an emergency, but a diagnosis: antiplatelet, statin, symptom control, and stenting or surgery when the narrowing is severe or symptoms persist. A change in the pattern — pain at rest, more easily, or lasting longer — is unstable angina and is an emergency |
| Unstable angina | A plaque has cracked and a clot is forming on it, but not enough muscle has died to raise troponin | Rest pain or a changed pattern; ECG may show changes; troponin normal on the timed pathway | Treated as ACS: aspirin, a second antiplatelet, an anticoagulant, and an angiogram within days. Increasingly rare as a label, because sensitive troponin tests reclassify most cases as NSTEMI |
| NSTEMI (non-ST-elevation myocardial infarction) | The same cracked plaque; the artery is partly blocked, or fully blocked with some flow around it; muscle is dying | Troponin rises and falls; the ECG shows no ST elevation (it may show depression or T-wave changes, or be normal) | The commonest heart attack. Antiplatelets and an anticoagulant now; an angiogram within 72 hours, sooner if unstable; usually a stent |
| STEMI (ST-elevation myocardial infarction) | The artery is completely blocked and the full thickness of the wall is dying, minute by minute | ST elevation on the ECG in a pattern that matches an artery; troponin will rise but nobody waits for it | The emergency within the emergency: the artery is opened by primary PCI within 120 minutes, or a clot-busting drug is given if PCI cannot be reached in time |
| Type 2 infarction | Muscle dies because supply and demand have parted company — a very fast rhythm, severe anaemia, a crashing blood pressure, sepsis — often with a narrowed artery that would otherwise have coped | A troponin rise and fall in the setting of the other illness, without a cracked plaque | Treat the cause; antiplatelets and stents help less. Common in hospital and often mislabelled. Carries a worse prognosis than a type 1, because of the company it keeps |
| MINOCA (infarction with non-obstructive coronary arteries) | A true infarction, but the angiogram shows no artery more than half narrowed. About 1 in 20 heart attacks, more often women | Angiogram; then cardiac MRI, which distinguishes a small infarct from myocarditis or takotsubo; sometimes intracoronary imaging | Depends entirely on the cause found: plaque rupture without narrowing, spasm, a tiny embolus, SCAD, or a cause outside the arteries. "Your arteries are fine" is where the investigation should start, not stop |
| Coronary spasm (Prinzmetal or vasospastic angina) | An artery clamps down, usually at rest, at night or early morning, and often in smokers or with cocaine | ECG during pain shows transient ST elevation that resolves; angiogram normal; sometimes a provocation test | Calcium-channel blockers and nitrates; stop smoking and the drugs that provoke it; beta-blockers can make it worse |
| Microvascular angina | The small vessels in the muscle do not dilate properly; the big arteries are clean | Typical angina with a normal angiogram; specialised testing of coronary flow | A real diagnosis, commoner in women, treated with the anti-anginal drugs and risk-factor control; long dismissed as "nothing wrong" |
3. The torn artery: SCAD
Spontaneous coronary artery dissection is a tear within the wall of a coronary artery that lets blood in and squeezes the channel shut from outside, in someone with no plaque at all. It causes a real heart attack, with troponin and sometimes ST elevation, and it causes up to a quarter of heart attacks in women under 50 and a large share of those around childbirth. It is associated with fibromuscular dysplasia (an abnormality of artery walls elsewhere), pregnancy, extreme physical or emotional stress, and connective-tissue conditions. The treatment is different from a plaque: stents often make the tear worse, so most SCAD is managed with medicines and time while the artery heals itself; anticoagulants are avoided; and the follow-up includes imaging of the other arteries in the body. A woman under 50 with a heart attack and "no risk factors" should have SCAD asked about by name.
4. The stunned heart: takotsubo
Takotsubo, or stress cardiomyopathy, is a heart attack in every respect but one: severe chest pain, a raised troponin, an abnormal ECG, part of the heart wall not moving on the scan — and clean arteries, with the muscle stunned rather than dead, usually after a sudden emotional or physical shock. Nine in ten cases are in women, most after the menopause. It looks exactly like a STEMI at the door and is taken to the catheter lab, where the angiogram is normal and the ventricle balloons in a characteristic shape. Most recover fully within weeks, but it is not benign: in-hospital death is around 4–5%, similar to a heart attack, and it recurs in a few per cent a year. Treatment is supportive; the drugs that help after a plaque-rupture heart attack are not all needed after this one, and that decision needs a cardiologist who has named the condition.
5. Inflamed rather than blocked: myocarditis and pericarditis
Myocarditis is inflammation of the heart muscle, usually after a viral illness and occasionally after a vaccine, drug or immune disease. It mimics a heart attack — chest pain, troponin, ECG changes — in someone typically young with a recent infection; the angiogram is normal and cardiac MRI shows the pattern of inflammation. Most recover; a minority develop heart failure or dangerous rhythms, which is why sport is restricted for months afterwards. Pericarditis is inflammation of the sac around the heart: sharp pain worse lying flat and better sitting forward, a rub on listening, a characteristic ECG, and usually a normal or only slightly raised troponin. Treated with anti-inflammatories and colchicine; it recurs in a minority. Both are covered in full in the unusual-ones chapter.
6. The rhythm problems
A heart can be in trouble without any artery being blocked. The rhythm disorders are a separate family and have their own chapter; the map entry for each:
| What | What is happening | Why it matters |
|---|---|---|
| Atrial fibrillation (and its cousin atrial flutter) | The upper chambers quiver chaotically instead of beating; the ventricles follow irregularly, often fast | The commonest sustained arrhythmia. Not immediately dangerous in itself, but it causes a fifth of strokes by letting clot form in the atrium, and a fast rate for weeks weakens the heart. Can present as palpitations, breathlessness, fatigue, or nothing until the stroke |
| Supraventricular tachycardia (SVT) | A short circuit above the ventricles; sudden regular racing at 150–220, sudden stop | Frightening, rarely dangerous; curable by ablation |
| Ventricular tachycardia (VT) | A fast rhythm arising in the ventricles, usually in a heart already damaged by a previous infarction or a cardiomyopathy | Can cause collapse and can degenerate into fibrillation. A reason for an implantable defibrillator |
| Ventricular fibrillation (VF) | The ventricles quiver; no output; this is cardiac arrest | A shockable rhythm: the one a defibrillator treats, and the reason public-access defibrillators exist. Survival falls about 10% for every minute without a shock; good compressions keep the rhythm shockable for longer |
| Heart block | The electrical signal from atria to ventricles is delayed (first degree), intermittently dropped (second degree, two types), or completely cut, leaving the ventricles to beat at their own slow escape rate (third degree, "complete") | First degree is usually nothing. Mobitz type II second degree and complete block cause faints and can cause arrest, and need a pacemaker. Causes include a heart attack (particularly of the inferior wall), age-related fibrosis, drugs, Lyme disease and some inherited conditions |
| Sick sinus syndrome and bradycardia | The heart's own pacemaker fails or slows | Fatigue, faints, breathlessness; a pacemaker if symptomatic |
| Inherited rhythm conditions (long QT, Brugada, ARVC, CPVT) | Electrical or structural faults present from birth, often silent | A cause of sudden death in the young and of unexplained faints; found by ECG, genetics and family screening after an arrest or a sudden death in a relative |
7. The pump failing: cardiogenic shock
When enough muscle has died, or a rhythm is bad enough, the heart cannot keep the blood pressure up and the organs start to fail. This is cardiogenic shock; it complicates around 5–10% of heart attacks and kills around 40% of those it affects even with treatment. The treatment is to open the artery at once, support the circulation with drugs, and in selected cases a mechanical pump threaded into the heart, which in 2024 became the first such device shown to save lives. It is covered in the clock chapter.
8. The heart stopping: cardiac arrest
An arrest is the end point any of the above can reach: no pulse, no breathing, no output. In adults out of hospital it is usually a rhythm — ventricular fibrillation from a heart attack or a scarred heart — and the treatment is CPR and a defibrillator within minutes. It has its own chapter, Cardiac arrest and resuscitation, which covers what to do, what the machine says and why, and what happens after the heart restarts; this topic covers what is looked for afterwards, including the inherited conditions, in the rhythm and every-test chapters.
9. Told apart, in one table
| ECG | Troponin | Angiogram | Cardiac MRI | |
|---|---|---|---|---|
| STEMI | ST elevation | Rises | Blocked artery | Not needed |
| NSTEMI | Depression, T-wave change, or normal | Rises and falls | Narrowed or partly blocked artery | Sometimes |
| Unstable angina | May change | Normal | Narrowing | — |
| Type 2 MI | Variable | Rises and falls | Often narrowed, no rupture | Sometimes |
| MINOCA | Variable | Rises and falls | No artery over 50% narrowed | The deciding test |
| SCAD | Often ST elevation | Rises | A tear, sometimes subtle | Sometimes; plus imaging of other arteries |
| Takotsubo | Looks like STEMI | Rises, modestly | Normal | Stunned, not scarred |
| Myocarditis | Variable, often widespread | Rises | Normal | Inflammation pattern |
| Pericarditis | Widespread saddle-shaped elevation | Normal or slight rise | Not needed | If troponin raised |
| Pulmonary embolism | Fast, right-heart strain | Can rise | — | —; CTPA is the test (the PE topic) |
| Aortic dissection | Often normal | Usually normal | Dangerous to do first | —; CT aortogram is the test |
Two mimics that kill if missed. A pulmonary embolism and an aortic dissection (a tear in the body's main artery) both present as chest pain with a raised troponin, and both are made worse by the drugs a heart attack gets. Tearing pain radiating to the back, a pulse or pressure difference between the arms, and a history of high blood pressure or Marfan syndrome point to dissection; breathlessness out of proportion, a swollen leg, and a normal ECG point to a PE. Both are why the emergency department's first job is to decide which chest pain this is.
10. Where UK and US guidance differ
Not on definitions: both use the Universal Definition of Myocardial Infarction and the same categories. The differences are in what happens next to each category and are in the chapters that follow.