After a heart attack, "the tests" means three things: the bloods and scans on the first days that decide the acute treatment; the tests over the following months that set the drugs and decide whether a defibrillator is needed; and the extended blood, genetic and imaging tests for heart attacks that are early, unexplained, or not a plaque at all. This chapter lists all three in the same form as the other clot topics, with what each result changes and a list of what is sold but not worth doing.
1. Tier one: the first days, everyone
| Test | Why | What an abnormal result changes |
|---|---|---|
| 12-lead ECG, repeated | The road: STEMI or not; then rhythm and evolution | ST elevation → the catheter laboratory within 120 minutes; new block or VT → monitoring and the rhythm chapter |
| High-sensitivity troponin, at 0 and 1–3 hours, then the peak | Infarction or not; the size of it | A rise and fall confirms it; a flat raised level points to another cause (kidney, sepsis, PE, myocarditis, a fast rhythm); the peak roughly tracks the size |
| Full blood count | Anaemia (a cause of a type 2 heart attack, and a bleeding risk on two antiplatelets); platelets before the anticoagulant | Anaemia is investigated, not just transfused; a low platelet count changes the antithrombotic plan |
| Kidney function and electrolytes, including potassium and magnesium | Contrast, drug dosing, rhythm risk | Low potassium or magnesium provokes rhythms and is corrected; kidney function sets the ACE inhibitor and DOAC doses |
| Glucose and HbA1c | Undiagnosed diabetes is found in around one in five heart attacks | 48 or over is diabetes and changes the drugs (SGLT2 inhibitor, GLP-1); 42–47 is prediabetes and changes the plan |
| Lipid profile within 24 hours | The baseline; after 24 hours the illness lowers cholesterol for weeks and the number is meaningless | Sets the baseline for the target; an LDL over 4.9, or over 4.0 with a family history, raises familial hypercholesterolaemia (tier three) |
| Liver function | Statin and drug baseline | Rarely changes the plan |
| Clotting screen, and an INR or DOAC level if anticoagulated | Before the catheter and the anticoagulant | Changes the anticoagulant given in the laboratory |
| Thyroid function | Thyrotoxicosis causes AF and provokes angina; hypothyroidism raises cholesterol and causes block | Treat the thyroid; the rhythm often follows |
| BNP or NT-proBNP | Heart failure; markedly raised in takotsubo | Guides the heart failure drugs and, with the echo, the prognosis |
| CRP | Pericarditis and myocarditis; infection | Very high with a normal angiogram points away from a plaque |
| Pregnancy test | Anyone who could be pregnant | Changes imaging, drugs and the diagnosis (SCAD is the commonest heart attack of pregnancy) |
| Toxicology | Younger people; an unexplained event | Cocaine and amphetamines cause spasm and heart attacks; beta-blockers are then avoided |
| Echocardiogram, before discharge | The ejection fraction; wall motion; valves; fluid around the heart; a clot in the ventricle | Decides half the drugs; sets up the 90-day defibrillator question; finds mechanical complications |
| Coronary angiogram, or CT coronary angiography for the low-risk and for stable chest pain | The arteries, and the treatment of them | A stent or surgery; or, if clean, MINOCA and the search that follows |
| Cardiac MRI | For MINOCA, suspected myocarditis or takotsubo, an unexplained weak pump, or an arrest without a cause | The deciding test between infarct, inflammation and stunning; scar burden for the defibrillator decision; sarcoid and amyloid |
| Chest X-ray | Heart size, lung fluid, the aorta | A widened mediastinum is an aortic dissection until proved otherwise |
2. Tier two: the months after
- Lipids on treatment at 2–3 months (UK) or 4–8 weeks (US), against the target, with the next drug if not met; then annually. The test most often not done.
- Lipoprotein(a), once in a lifetime: inherited, not lowered by statins, a cause of early heart attacks and aortic stenosis; a high level (over 120 nmol/L, or over 50 mg/dL) intensifies the other lipid treatment, prompts testing of relatives, and identifies people for the trials and, when they arrive, the drugs that lower it. Recommended once by HEART UK and by the American lipid guideline for anyone with premature or unexplained disease.
- Kidney function and potassium after each ACE inhibitor or antagonist step, then annually.
- HbA1c at three months if borderline, then annually.
- A repeat echocardiogram at 6–12 weeks if the pump was weakened, to see whether it has recovered; if the ejection fraction is still 35% or lower at 40 days after a heart attack (90 days after a stent or surgery) on full treatment, the defibrillator question is asked. After takotsubo, an echo at 4–6 weeks to confirm recovery; after myocarditis, at 3–6 months.
- A rhythm monitor if there are palpitations, faints, or a weak pump: 24 hours to 7 days, a patch, or a loop recorder for infrequent symptoms.
- An exercise test only for a reason: symptoms, a Group 2 driving licence, a return to a demanding job, or as the prescription for rehabilitation. Not as a routine "check the stent is working" after a successful PCI in someone without symptoms: neither guideline recommends it, and it generates false alarms.
- Blood pressure at home, with the target in the after-hospital chapter.
3. Tier three: early, unexplained or unusual heart attacks
Justified by a heart attack under 55 (men) or 60 (women), a strong family history, an event with clean arteries, an arrest or a dangerous rhythm without an acute cause, a sudden death in a relative, or a specific clinical clue. Ordered through cardiology, the lipid clinic, or the inherited cardiac conditions clinic.
| Test | Looks for | Clue that justifies it | What a positive changes |
|---|---|---|---|
| Familial hypercholesterolaemia assessment: the Simon Broome or Dutch criteria, then genetic testing (LDLR, APOB, PCSK9) | An inherited cholesterol disorder, present in about 1 in 250, that causes heart attacks decades early | Untreated LDL over 4.9 mmol/L; tendon xanthomas; a heart attack or a relative's heart attack under 60 (men) or 55 (women); a known family diagnosis | Lifelong intensive treatment with lower thresholds for the injectables; cascade testing of first-degree relatives, half of whom will carry it; children tested from about 10 |
| Lipoprotein(a) | As tier two | Any premature or unexplained event | As above; relatives tested |
| Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-β2-glycoprotein I; repeated at 12 weeks) | Antiphospholipid syndrome, which causes arterial as well as venous clots | A young heart attack with clean or minimally diseased arteries; previous clots or miscarriages; lupus | Warfarin rather than antiplatelets, long term; the venous rules are in the PE topic |
| Inherited thrombophilia | Venous clotting variants | Rarely: only where a paradoxical embolus through a hole in the heart is the plausible mechanism | Usually nothing; the venous variants do not cause arterial events |
| Autoimmune screen (ANA, ENA, ANCA, complement, ESR) | Lupus, vasculitis, Kawasaki aneurysms in the young | Systemic symptoms; coronary aneurysms; a young event with clean arteries | Rheumatology; immunosuppression treats the cause |
| Homocysteine | Homocystinuria, rare and inherited | A very young event with the marfanoid build, dislocated lenses or learning difficulty. Not as a routine risk marker | Metabolic referral; specific treatment |
| Metanephrines (plasma or 24-hour urine) | A phaeochromocytoma, an adrenal tumour that secretes adrenaline | Takotsubo, especially recurrent or with hypertension crises, headaches and sweats | Surgery cures it and stops the recurrences |
| CT or MR angiography head to pelvis | Fibromuscular dysplasia and aneurysms in the arteries of the neck, kidneys and pelvis | Every SCAD, once, after recovery | Surveillance of any aneurysm found; blood-pressure control; occasionally treatment of a renal artery lesion |
| Cardiac MRI | Scar, inflammation, infiltration (sarcoid, amyloid), the cardiomyopathies | Any arrest or sustained VT without an acute cause; an unexplained weak pump; heart block in the middle-aged | The defibrillator decision; a diagnosis with its own treatment |
| The inherited cardiac conditions workup: resting and exercise ECG, signal-averaged ECG, a drug challenge for Brugada (ajmaline or flecainide), an echocardiogram and MRI, and gene panels for long QT, Brugada, CPVT, ARVC and the cardiomyopathies | The inherited rhythm and muscle conditions | An arrest or VT without an acute cause; a faint with exercise or a startle; a QT interval over 480 ms; a sudden death in a relative under 40; the ECG patterns | Beta-blockers, drug-avoidance lists, an ICD, activity advice; screening of first-degree relatives with an ECG and echo, and with the gene once found; a post-mortem genetic test (the "molecular autopsy") after a sudden unexplained death |
| Lyme serology | Lyme carditis | New heart block with a tick exposure, a rash or arthritis in the preceding weeks; any unexplained block under 50 | Antibiotics; the block usually resolves and the pacemaker is avoided |
| Sarcoid and amyloid imaging (cardiac MRI, FDG-PET; a bone-tracer scan and serum free light chains for amyloid) | Infiltrative disease of the heart | Unexplained heart block, VT or a thick heart in someone middle-aged or older; a thick heart with low ECG voltages | Sarcoid: immunosuppression and often a device; amyloid: specific treatment now exists (tafamidis) and changes prognosis |
| Sleep study | Obstructive sleep apnoea | Snoring, witnessed pauses, daytime sleepiness, resistant hypertension, AF | CPAP improves blood pressure and AF control |
| Coronary function testing (acetylcholine provocation, coronary flow reserve) | Spasm and microvascular disease | Angina with clean arteries; MINOCA without a cause on MRI | Calcium-channel blockers and nitrates for spasm; a named diagnosis for microvascular disease |
4. For your relatives
Three situations where a heart attack in you is a reason to test someone else. Familial hypercholesterolaemia: cascade testing of first-degree relatives is NICE policy and finds a carrier in half of them, most of whom had no idea. An inherited rhythm or muscle condition: first-degree relatives are offered an ECG and an echocardiogram, and the gene test once the family variant is known. A sudden unexplained death in a relative under 40, or an arrest survived without a cause: the inherited cardiac conditions clinic assesses the family, and a post-mortem genetic test on the person who died is requested through the coroner. A family history of ordinary heart attacks in the 60s and 70s is a risk factor for you, not a reason to test them.
5. Tests that are sold but not worth doing
- The routine stress test after a successful stent in someone without symptoms: neither guideline recommends it.
- A private "cardiac screen" of ECG, echo, calcium score and a stress test in someone who has just had a heart attack: the diagnosis is already made, and the score adds nothing to a known blocked artery.
- A coronary calcium score after a heart attack: it is a test for people without known disease (the CAC chapter).
- Homocysteine as a risk marker, and vitamin treatment to lower it: no benefit in the trials.
- MTHFR, and broad thrombophilia panels for an ordinary arterial event.
- Direct-to-consumer polygenic risk scores after an event: the event has already told you the risk.
- Repeated lipoprotein(a): once.
- Viral serology after myocarditis: rarely changes anything.
6. The list, in one paragraph, for the clinic
"What was my ejection fraction, and has it been repeated?" "What were my lipids in the first 24 hours, and have they been rechecked on treatment against the target?" "Has lipoprotein(a) been measured once, and my HbA1c?" If you were under 60, or a relative had an early heart attack: "Have I been assessed for familial hypercholesterolaemia, and should my family be tested?" If your arteries were clean: "Has the cardiac MRI been done, and what caused it?" If it was SCAD: "Has the head-to-pelvis angiogram been done?" If you had an arrest or a dangerous rhythm without a cause: "Have I been referred to the inherited cardiac conditions clinic, and should my family be screened?" And for any test offered: "What would the result change?"
7. Where UK and US guidance differ
The US guideline specifies the fasting lipid panel at 4–8 weeks; NICE says 2–3 months. Both recommend lipoprotein(a) once for premature or unexplained disease. NICE's familial hypercholesterolaemia guideline is more prescriptive about cascade testing than any US document. The inherited cardiac conditions pathway, with its clinics and the coroner's molecular autopsy, is a UK structure the US lacks in that form. Both say no routine stress testing after PCI.