Medicine chapters
Acute coronary syndrome: STEMI and NSTEMI
The spectrum of unstable angina, NSTEMI and STEMI: risk factors, ECG leads for each heart wall, troponin, first treatment, primary PCI or thrombolysis, complications and discharge drugs.
- ACS = unstable angina (no troponin rise), NSTEMI (troponin rise, no persistent ST elevation) and STEMI (persistent ST elevation or new LBBB: a fully blocked artery).
- Give aspirin 300 mg, a P2Y12 inhibitor, an anticoagulant, pain relief and oxygen only if SpO2 below 90%; STEMI needs immediate reperfusion: primary PCI, or thrombolysis if PCI cannot happen within 120 minutes.
- ECG leads map to walls: II, III, aVF inferior (RCA); V1–V4 anterior/septal (LAD); I, aVL, V5–V6 lateral (circumflex); tall R and ST depression V1–V2 posterior.
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Overview
Acute coronary syndrome (ACS) is the sudden reduction of blood flow in a coronary artery, usually from a thrombus on a ruptured or eroded atheromatous plaque. It includes:
- Unstable angina: ischaemic pain, no troponin rise.
- NSTEMI (non-ST-elevation MI): troponin rises, but no persistent ST elevation; the artery is usually partly blocked.
- STEMI (ST-elevation MI): persistent ST elevation or new LBBB; the artery is usually completely blocked.
ACS is a leading cause of death worldwide. "Time is muscle": fast diagnosis and reperfusion save heart muscle and lives.
Pathophysiology
- An atherosclerotic plaque with a large lipid core and thin fibrous cap is prone to rupture.
- Rupture or erosion exposes collagen and tissue factor, so platelets stick and aggregate, a thrombus forms, and released thromboxane A2 and serotonin cause spasm.
- Partial or intermittent blockage → unstable angina or NSTEMI (subendocardial injury).
- Complete, lasting blockage → STEMI. Cell death begins after about 15–30 minutes and spreads from the subendocardium outwards to become transmural (Q-wave infarct).
Universal types of MI (short form)
| Type | Mechanism |
|---|---|
| 1 | Spontaneous plaque rupture/erosion with thrombus (classic ACS) |
| 2 | Supply–demand mismatch (anaemia, arrhythmia, hypotension, spasm) |
| 3 | Sudden cardiac death with features of MI |
| 4 | Related to PCI (4a) or stent thrombosis (4b) |
| 5 | Related to CABG |
Risk factors
| Non-modifiable | Modifiable |
|---|---|
| Age | Smoking |
| Male sex (women catch up after menopause) | Diabetes mellitus |
| Family history of early coronary disease | Hypertension |
| South Asian ethnicity | Dyslipidaemia (high LDL, low HDL) |
| Obesity, inactivity, heavy alcohol | |
| Cocaine and amphetamine use | |
| Chronic kidney disease, chronic inflammatory disease |
Clinical features
- Central crushing or heavy chest pain, often more than 20 minutes, not relieved by GTN.
- Spreads to the left arm, neck or jaw.
- Autonomic features: sweating, nausea, vomiting, pallor, clamminess.
- Breathlessness, palpitations, collapse.
- Atypical or silent presentations are common in the elderly, diabetics and women: breathlessness, fatigue, confusion, syncope, epigastric pain.
Examination: may be normal. Look for hypotension, tachycardia or bradycardia, raised JVP, basal crackles, S3 or S4, new murmurs (mitral regurgitation, VSD), and signs of other diagnoses (dissection, PE).
Investigations
ECG
- Record within 10 minutes; repeat every 15–30 minutes while pain continues if non-diagnostic.
- STEMI criteria: new ST elevation at the J point in two contiguous leads: ≥0.2 mV (2 mm) in V1–V3 or ≥0.1 mV (1 mm) in other leads; or new (or presumed new) LBBB with a typical history.
- NSTEMI/unstable angina: ST depression, T-wave inversion, or a normal ECG.
Evolution of STEMI ECG:
- Minutes: tall, peaked (hyperacute) T waves.
- Hours: ST elevation (convex), then Q waves appear and R waves shrink.
- Days: ST returns to baseline; T waves invert.
- Weeks to months: T waves may recover; Q waves stay.
Persistent ST elevation weeks after an anterior MI suggests a left ventricular aneurysm.
ECG leads and heart walls
| Wall | Leads with ST elevation | Usual artery |
|---|---|---|
| Inferior | II, III, aVF | Right coronary artery (sometimes circumflex) |
| Anteroseptal | V1–V3 | Left anterior descending (LAD) |
| Anterior | V3–V4 | LAD |
| Extensive anterior | V1–V6, I, aVL | Proximal LAD or left main |
| Anterolateral | V4–V6, I, aVL | LAD or circumflex |
| Lateral | I, aVL, V5–V6 | Left circumflex (or diagonal branch) |
| Posterior | ST depression with tall R waves in V1–V2; ST elevation in posterior leads V7–V9 | Circumflex or RCA |
| Right ventricle | ST elevation in V4R (right-sided chest leads) | Proximal RCA |
"II, III, aVF look at the floor." The inferior leads look up at the diaphragmatic (floor) surface of the heart, fed by the RCA.
In right ventricular infarction (with inferior MI), the patient is preload-dependent: avoid nitrates and diuretics; give IV fluids for hypotension.
Cardiac biomarkers
- Troponin I or T is the marker of choice. High-sensitivity assays detect small rises; repeat after about 3 hours if the first is normal. Troponin also predicts risk: higher levels, higher mortality.
- CK-MB: rises and falls faster; useful for detecting re-infarction.
- Myoglobin: rises earliest but is not specific to heart muscle.
- LDH: rises late; a flipped pattern (LDH1 above LDH2) was used historically.
Troponin can also rise without ACS: PE, myocarditis, heart failure, sepsis, renal failure, tachyarrhythmia.
Other tests
- FBC, renal function and electrolytes, glucose, lipids.
- Chest X-ray: pulmonary oedema, widened mediastinum (dissection).
- Echocardiography: regional wall motion loss, LV function, mechanical complications, alternative diagnoses.
Initial management (all ACS)
| Step | Detail |
|---|---|
| Aspirin | 300 mg chewed or dispersible, then 75 mg daily |
| P2Y12 inhibitor | Ticagrelor 180 mg then 90 mg twice daily, prasugrel 60 mg then 10 mg daily (if going to PCI), or clopidogrel 300–600 mg then 75 mg daily |
| Oxygen | Only if SpO2 is below 90% (routine oxygen is not given) |
| Pain relief | IV morphine or diamorphine with an antiemetic (e.g. metoclopramide) |
| Nitrates | Sublingual or IV GTN for ongoing pain if systolic BP is above 90 mmHg |
| Anticoagulant | Fondaparinux 2.5 mg s.c. daily, enoxaparin 1 mg/kg s.c. twice daily, or unfractionated heparin (bivalirudin is an option during PCI) |
| Beta-blocker | Oral, if no asthma, AV block, heart failure or hypotension; aim for resting rate 50–60/min |
| Statin and ACE inhibitor | Start in hospital (e.g. atorvastatin 80 mg) |
The first drug in suspected ACS is aspirin 300 mg. Oxygen is not routine; give it only when saturation is low.
STEMI: reperfusion
Primary PCI
- The preferred reperfusion for STEMI when it can be done promptly; the target is to cross the blocked artery with a wire within about 60 minutes in a PCI centre.
- Radial artery access, drug-eluting stents, and treatment of other significant narrowings during the same admission.
- Given within 12 hours of symptom onset (and later if pain, shock or instability continues).
- Glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban) are no longer routine; kept for heavy thrombus or complications.
Thrombolysis (fibrinolysis)
- Used if primary PCI cannot be delivered within 120 minutes of diagnosis.
- Greatest benefit within 6 hours; little benefit after 12 hours.
- Aim to give the bolus within 10 minutes of the decision to treat.
- Drugs convert plasminogen to plasmin: streptokinase, alteplase, tenecteplase (tenecteplase is a single bolus).
- Give with aspirin and clopidogrel and an anticoagulant.
- Failed reperfusion: less than 50% resolution of ST elevation at 60–90 minutes → rescue PCI.
- After successful lysis, patients are moved to a PCI centre for angiography.
Streptokinase produces antibodies, so it should not be given again to the same patient; use a different agent.
Contraindications to thrombolysis
| Absolute | Relative |
|---|---|
| Haemorrhagic stroke or stroke of unknown cause at any time | Recent transient ischaemic attack |
| Recent ischaemic stroke (Kumar and Clark gives the previous 3 months) | Oral anticoagulant therapy |
| CNS tumour, damage or vascular malformation | Pregnancy or within 1 week after delivery |
| Major trauma, surgery or head injury in the last 3 weeks | Refractory hypertension (systolic above 180 mmHg) |
| Gastrointestinal bleeding in the last month | Advanced liver disease |
| Known bleeding disorder | Active peptic ulcer |
| Suspected aortic dissection | Non-compressible punctures; traumatic resuscitation |
NSTEMI and unstable angina
- Treat with aspirin, a P2Y12 inhibitor, an anticoagulant (fondaparinux or LMWH), nitrates, beta-blocker, statin and ACE inhibitor.
- Thrombolysis is NOT used in NSTEMI or unstable angina.
Inferior MI = ST elevation in II, III, aVF from right coronary occlusion; watch for bradycardia, AV block and right ventricular infarction.
- Risk stratify with the TIMI or GRACE score to decide how quickly to do angiography.
TIMI risk score for UA/NSTEMI (one point each)
- Age over 65 years
- Three or more coronary risk factors
- Known coronary stenosis of 50% or more
- Aspirin use in the past 7 days
- Severe angina (two or more episodes of rest pain in 24 hours)
- ST deviation of 1 mm or more
- Raised cardiac markers
A 70-year-old smoker with diabetes and hypertension, taking aspirin, has rest pain, ST depression and a raised troponin. No known coronary disease; one episode of pain.
Age >65 (1) + ≥3 risk factors (1) + aspirin in last 7 days (1) + ST deviation (1) + raised troponin (1) = 5
Kumar and Clark's table gives about a 12% rate of death or MI at 14 days for a score of 5 → high risk, early invasive approach.
Timing of coronary angiography
| Risk | Features | Angiography |
|---|---|---|
| Very high | Ongoing pain despite treatment, heart failure, shock, life-threatening arrhythmia | Within 2 hours |
| High | Rising/falling troponin, dynamic ST–T changes, GRACE above 140 | Within 24 hours |
| Intermediate | Diabetes, eGFR below 60, LVEF below 40%, early post-infarct angina, previous PCI or CABG, GRACE 109–140 | Within 72 hours |
| Low | None of the above | Non-invasive testing; invasive approach still often preferred |
Complications of myocardial infarction
| Complication | Typical timing and clues |
|---|---|
| Ventricular fibrillation | First hours; commonest cause of death before reaching hospital |
| Other arrhythmias | VT, AF, bradycardia; treat VT with amiodarone or cardioversion; keep K+ above 4.5 mmol/L |
| Heart block | Especially inferior MI (RCA supplies the AV node), often temporary; atropine or temporary pacing; permanent pacing if it lasts beyond about 2 weeks |
| Heart failure and cardiogenic shock | Graded by Killip class; large anterior infarcts |
| Papillary muscle rupture | Usually within the first week; sudden pulmonary oedema with new pansystolic murmur at the apex; posteromedial muscle after inferior MI |
| Ventricular septal rupture | Usually within the first week; new harsh pansystolic murmur at the left sternal edge; step-up in oxygen saturation in the right ventricle |
| Ventricular wall rupture | Usually within the first week; sudden tamponade and electromechanical dissociation (PEA) |
| Left ventricular aneurysm | Weeks later; persistent ST elevation, heart failure, emboli, VT |
| Mural thrombus | Large anterior MI; systemic emboli (stroke) |
| Early pericarditis | First few days; pleuritic pain, rub |
| Dressler syndrome | Weeks later; autoimmune pericarditis with fever, raised ESR |
Killip classification
| Class | Findings |
|---|---|
| I | No crackles, no S3 |
| II | Crackles in less than half the lung fields, or S3 |
| III | Crackles in more than half the lung fields (pulmonary oedema) |
| IV | Cardiogenic shock |
"Day one rhythm, first week rupture, weeks later aneurysm and Dressler."
Discharge medications (secondary prevention)
| Drug | Notes |
|---|---|
| Aspirin 75 mg daily | Lifelong |
| P2Y12 inhibitor (ticagrelor, prasugrel or clopidogrel) | With aspirin as dual antiplatelet therapy, usually for 12 months after ACS |
| Beta-blocker | Reduces re-infarction and sudden death; aim heart rate below 60/min |
| ACE inhibitor (or ARB) | Especially if LVEF below 40%, diabetes or hypertension; check renal function and potassium |
| High-intensity statin | Atorvastatin 80 mg; LDL target below 1.8 mmol/L |
| Aldosterone antagonist (eplerenone, spironolactone) | If LVEF below 40% with heart failure or diabetes, and creatinine and potassium allow |
| Proton pump inhibitor | If high bleeding risk on dual antiplatelet therapy |
| GTN spray | For any further angina |
Patients with AF who need anticoagulation are given a short period of combined therapy, then an anticoagulant with a single antiplatelet; the length depends on bleeding risk.
Calcium channel blockers are not routine after MI. Rate-limiting ones (verapamil, diltiazem) may be used only if beta-blockers are contraindicated and LV function is good.
Lifestyle after ACS
- Cardiac rehabilitation with supervised exercise; then about 30 minutes of moderate exercise on most days.
- Stop smoking (nicotine replacement is safe).
- Mediterranean-style diet, less salt and saturated fat; BMI below 25.
- Alcohol within safe limits.
- Control BP (systolic below 140 mmHg) and diabetes (HbA1c below 53 mmol/mol, 7%).
- In Pakistan, check local rules and current guidance for return to driving and work.
Expect: the difference between unstable angina, NSTEMI and STEMI; STEMI ECG criteria and new LBBB; which leads show inferior, anterior, lateral and posterior infarction and the artery involved; posterior MI as ST depression with tall R in V1–V2; aspirin 300 mg as the first drug; oxygen only when SpO2 is below 90%; primary PCI preferred and thrombolysis if PCI is not possible within 120 minutes; absolute contraindications to thrombolysis (previous haemorrhagic stroke, aortic dissection, recent GI bleed); no thrombolysis in NSTEMI; streptokinase antibodies; complications by timing (VF early, papillary muscle and septal rupture in the first week, aneurysm and Dressler later); heart block with inferior MI; the standard discharge drugs and that calcium channel blockers are not routine.
Quick revision
- ACS = unstable angina (troponin normal), NSTEMI (troponin up), STEMI (ST elevation or new LBBB).
- Inferior II, III, aVF (RCA); anterior V1–V4 (LAD); lateral I, aVL, V5–V6 (circumflex); posterior: tall R and ST depression V1–V2.
- Aspirin 300 mg + P2Y12 inhibitor + anticoagulant; morphine; GTN; oxygen only if SpO2 <90%.
- STEMI: primary PCI; thrombolysis if PCI not within 120 minutes; rescue PCI if ST fails to settle by half at 60–90 minutes.
- NSTEMI: no thrombolysis; TIMI/GRACE; angiography within 2, 24 or 72 hours by risk.
- RV infarct: avoid nitrates and diuretics; give fluids.
- Complications: VF early; rupture in the first week; aneurysm and Dressler weeks later.
- Discharge: aspirin, P2Y12 inhibitor, beta-blocker, ACE inhibitor, statin, ± aldosterone antagonist, GTN.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What is the difference between NSTEMI and unstable angina?
Both lack persistent ST elevation, but NSTEMI has a rise in troponin showing heart muscle death, while unstable angina does not.
Which leads show an inferior myocardial infarction?
Leads II, III and aVF; the right coronary artery is usually blocked.
When should thrombolysis be given instead of primary PCI?
In STEMI when primary PCI cannot be performed within 120 minutes of diagnosis, ideally within 12 hours of symptom onset and with no contraindication.
Why does an inferior MI often cause heart block?
The right coronary artery usually supplies the AV node, so its blockage makes the node ischaemic; the block is often temporary.
Which drugs are given at discharge after an MI?
Aspirin, a second antiplatelet drug for about a year, a beta-blocker, an ACE inhibitor, a high-intensity statin, an aldosterone antagonist if LVEF is low, and GTN spray.