Five conditions arrive looking exactly like a heart attack, are taken to the same catheter laboratory, and then part company with it: the artery is clean, or torn, or the muscle is stunned or inflamed rather than dead. The standard heart-attack drugs are partly wrong for each of them, the follow-up is different, and the commonest error is to send the person home labelled as a heart attack with a heart-attack prescription. This chapter is each one in full.
1. Takotsubo: the stunned heart
What it is. A sudden weakening of part of the left ventricle, usually the apex, which balloons out while the base contracts, giving the shape of the Japanese octopus pot it is named after. The trigger is often a sudden shock — a bereavement, an accident, a violent argument, a fright — or a physical stress: a severe illness, surgery, an asthma attack, a seizure, chemotherapy. In about a third no trigger is found. Nine in ten cases are in women, most between 55 and 75. The mechanism is thought to be a surge of stress hormones stunning the muscle.
How it is found. It cannot be told from a heart attack at the door: chest pain or breathlessness, ST elevation or deep T-wave inversion on the ECG, a raised troponin. It is diagnosed when the angiogram shows no culprit artery and the ventriculogram or echocardiogram shows the characteristic ballooning extending beyond any one artery's territory. The international (InterTAK) criteria add a modest troponin rise relative to the size of the wall abnormality, a markedly raised BNP, and recovery on follow-up imaging. Cardiac MRI shows a stunned wall without the scar of an infarction and excludes myocarditis. A rare tumour of the adrenal gland (phaeochromocytoma) can produce the same picture and is excluded with a urine or blood test for its hormones.
Treatment. Supportive: the first days can bring heart failure, dangerous rhythms, low blood pressure and, rarely, rupture, so the person is monitored as a heart attack would be. An ACE inhibitor and a beta-blocker are usually given while the pump is weak. There is no trial evidence for any drug; in the registries, ACE inhibitors were associated with fewer recurrences and beta-blockers were not. Adrenaline-like drugs are avoided, because they are the mechanism. The antiplatelets and the high-intensity statin given for a plaque-rupture heart attack are not needed for takotsubo unless there is coronary disease as well.
Afterwards. The pump usually recovers fully within days to weeks, and an echocardiogram at four to six weeks should confirm it; the ACE inhibitor and beta-blocker can then be reviewed. It is not benign: around 4% die in hospital, mostly from the complications of the first days, and it recurs in about 1–2% of people a year, sometimes with a different trigger. Long-term, a proportion have persisting fatigue and reduced exercise capacity despite a normal-looking heart. Cardiac rehabilitation applies; psychological support after an emotional trigger is part of the treatment, not an optional extra; and the discharge letter must say takotsubo, not "heart attack", because a future doctor reading "MI" will restart the wrong drugs.
2. SCAD: the torn artery
What it is. Spontaneous coronary artery dissection: a bleed within the wall of a coronary artery, or a tear in its lining, that compresses the channel from outside, in an artery with no plaque. It causes a genuine heart attack — troponin, ECG changes, sometimes ST elevation, sometimes an arrest. It is the cause of up to a quarter of heart attacks in women under 50, and of most heart attacks around childbirth. Around half of people with SCAD have fibromuscular dysplasia, an abnormality of the walls of arteries elsewhere in the body (kidney, neck, pelvis) that is usually silent. Other associations: pregnancy and the weeks after, extreme physical or emotional stress, connective-tissue disorders, hormonal treatment, migraine. Men make up about one in ten cases.
How it is found. On the angiogram, and it is easy to miss: the classic appearance is a long, smooth narrowing rather than a plaque, and the operator has to think of it. Intracoronary imaging (OCT or ultrasound) confirms it when the picture is unclear but carries its own risk of extending the tear, so it is used sparingly. A young woman with a heart attack and no risk factors should have SCAD asked about by name before she leaves the laboratory.
Treatment: mostly, do not stent. This is the reversal that matters. In a plaque-rupture heart attack, opening the artery is the treatment; in SCAD, the artery usually heals itself over weeks and stenting a fragile, dissected wall often makes the tear longer, so the guidance from both the American and European statements is conservative management unless the person is unstable, the artery is completely blocked with ongoing damage, or the left main stem is involved. Over 90% of conservatively managed dissections heal on follow-up imaging. Clot-busting drugs are avoided (they can extend the bleed into the wall); anticoagulants are stopped once the diagnosis is made. Aspirin is usually given; whether to add a second antiplatelet is contested, and a large registry (DISCO) found dual therapy associated with worse outcomes, so many centres now use aspirin alone. A beta-blocker is associated with fewer recurrences in the largest cohort and is usually continued. A statin is not needed unless there is coronary disease or high cholesterol as well. The person is kept in hospital for several days because early extension of the tear is the main risk.
Afterwards. A CT or MR angiogram from head to pelvis to look for fibromuscular dysplasia and aneurysms in other arteries, once, after recovery. Recurrent SCAD happens in around one in ten over three years and is not predictable by the first event; blood pressure control, the beta-blocker, and avoiding the identified triggers (heavy lifting and straining, adrenaline-driven activities, hormonal contraception, stimulants) are the measures. Pregnancy after SCAD is possible but carries a real recurrence risk and needs a joint cardiology and obstetric plan before conception. Cardiac rehabilitation adapted for SCAD (no heavy resistance work) is recommended. Anxiety and post-traumatic symptoms are common and under-treated. Family screening is not routine, but a first-degree relative with SCAD or fibromuscular dysplasia is a reason for a specialist opinion.
3. MINOCA: the heart attack with clean arteries
What it is. A heart attack by every criterion — troponin rise and fall, symptoms, ECG or imaging evidence — but an angiogram with no artery more than half narrowed. About one heart attack in twenty, and more often in women and younger people. It is a working diagnosis, not a final one: the job is to find the cause, and the causes are different diseases.
What is behind it. A plaque that ruptured or eroded without leaving a significant narrowing (found on intracoronary imaging); coronary spasm; a small embolus from the heart (atrial fibrillation, a valve, a hole in the heart); SCAD missed on the first look; microvascular disease; a type 2 heart attack from a fast rhythm, anaemia or sepsis; and, once cardiac MRI has been done, a proportion turn out not to be heart attacks at all: myocarditis or takotsubo. Cardiac MRI within the first weeks is the deciding test, and the American and European guidance both say it should be done in everyone with MINOCA; in practice it often is not.
Treatment. By cause. For plaque disruption and microvascular disease: the standard secondary prevention, and the Swedish registry found statins and ACE inhibitors associated with better outcomes; the value of the second antiplatelet is less clear. For spasm: calcium-channel blockers and nitrates, and stop smoking and stimulants. For an embolus: treat the source, often with an anticoagulant. For myocarditis or takotsubo: their own sections. The outcome is better than for an obstructive heart attack but not benign: about one in ten has a further event within a few years. "Your arteries are clear, nothing to worry about" is the sentence that should prompt the question "then what caused it, and has the MRI been done?"
4. Myocarditis: the inflamed muscle
What it is. Inflammation of the heart muscle, most often after a viral illness (enteroviruses, adenovirus, parvovirus, herpesviruses, SARS-CoV-2, influenza), sometimes from an immune disease, a drug reaction, or — rarely, and mostly in young men after the second dose — an mRNA vaccine. It ranges from a chest pain with a small troponin rise in a fit twenty-year-old who recovers in a week, to a fulminant illness with heart failure and dangerous rhythms needing intensive care. The first dedicated European guideline for it was published in 2025.
How it is found. Chest pain, breathlessness, palpitations or collapse in someone often young with a recent infection; a raised troponin; ECG changes that are widespread rather than in one artery's territory; an echocardiogram that may be normal or show a weakened pump. The angiogram (or a CT coronary angiogram in the young) is normal. Cardiac MRI makes the diagnosis in most: oedema and a characteristic pattern of enhancement in the muscle. A heart muscle biopsy is reserved for the severe or unexplained. Blood tests for the virus rarely help.
Treatment. Rest, painkillers other than anti-inflammatories in the acute phase if the pump is weak, and the heart failure drugs if it is; immunosuppression for the specific immune-driven forms (giant cell, sarcoid, immune-checkpoint-inhibitor myocarditis, eosinophilic); mechanical support and consideration of transplant in the fulminant few. The rule that matters most to most people: no competitive or strenuous sport for three to six months, because exercise during the inflamed phase provokes dangerous rhythms and is the mechanism of the rare deaths. Return is guided by a normal echocardiogram, a normal troponin, no arrhythmia on a monitor, and often a repeat MRI.
Afterwards. Most recover completely. Around one in five is left with a weakened pump (a dilated cardiomyopathy), which is treated as heart failure and, if it persists with a low ejection fraction, may need a defibrillator. Follow-up includes an echocardiogram at three to six months and a rhythm monitor before returning to sport. Vaccine myocarditis has been mild in the great majority and the guidance is that the relevant vaccine is not repeated.
5. Pericarditis: the inflamed sac
What it is. Inflammation of the pericardium, the two-layered sac around the heart, usually viral or unexplained, sometimes after a heart attack or heart surgery, sometimes from an autoimmune disease, tuberculosis (rare in the UK, common globally), kidney failure or cancer.
How it is found. A sharp, stabbing chest pain that is worse lying flat and on breathing in, and better sitting forward; a scratching rub heard over the heart; an ECG with widespread saddle-shaped ST elevation and PR depression that does not fit one artery; a raised inflammatory marker; a normal or only mildly raised troponin (if it is raised, the muscle is involved too — "myopericarditis" — and the myocarditis rules apply). An echocardiogram looks for fluid around the heart; a large or rapidly growing collection can compress it (tamponade), which is an emergency drained with a needle.
Treatment. High-dose anti-inflammatories (ibuprofen or aspirin) for one to two weeks then tapered, plus colchicine for three months, which halves the chance of recurrence (the COPE and CORP trials); steroids only where the anti-inflammatories cannot be used, because they increase recurrence; and rest from strenuous exercise until symptoms, the inflammatory marker and the ECG have settled — several weeks for the ordinary case, three months for athletes. Around one in five to one in three has a recurrence; recurrent pericarditis gets a longer course of colchicine and, for the refractory few, an interleukin-1 blocker (rilonacept in the US, anakinra in the UK), which has transformed the worst cases.
6. Coronary spasm and microvascular angina
Two causes of chest pain with normal arteries that were long dismissed. Spasm is an artery clamping down, classically at rest in the early morning, with ST elevation during the pain that resolves; it is provoked by smoking, cocaine, amphetamines, some migraine drugs and cold, and can cause a heart attack or an arrest. The treatment is a calcium-channel blocker with long-acting nitrates, and stopping the provocations; beta-blockers can make it worse. Microvascular angina is the small vessels of the heart muscle failing to dilate; it is commoner in women, causes typical angina with a normal angiogram, is diagnosed with specialised coronary flow testing, and is treated with the anti-anginal drugs, risk-factor control and cardiac rehabilitation. Both carry a real, if lower, risk of future events and both are diagnoses, not reassurance.
7. Where UK and US guidance differ
- Takotsubo: no national guideline in either country; both follow the international expert consensus. The same supportive approach.
- SCAD: the American scientific statement (2018) and the European position paper (2018) agree on conservative management, the beta-blocker, and screening for fibromuscular dysplasia; the dual-antiplatelet question is open in both, and practice has moved towards aspirin alone since the DISCO registry.
- MINOCA: both say cardiac MRI for everyone; the UK's delivery of it is patchier.
- Myocarditis and pericarditis: Europe published the first dedicated guideline in 2025; the US works from the 2015 European pericarditis guideline and its own statements; the exercise-restriction and colchicine positions are the same. Rilonacept is licensed in the US and not the UK; anakinra is used off-label in the UK.