Acute coronary syndromes (STEMI, NSTEMI and unstable angina)

The acute coronary syndrome (ACS) is the ischaemic spectrum from unstable angina through non-ST-elevation myocardial infarction (NSTEMI) to ST-elevation myocardial infarction (STEMI), and it is the commonest life-threatening presentation the emergency physician manages. It begins with an atherosclerotic plaque that ruptures or erodes, exposing thrombogenic contents to the circulation: platelets adhere, activate and aggregate, coagulation is triggered, and a thrombus forms. A partial occlusion produces the subendocardial ischaemia of NSTEMI or unstable angina; a complete occlusion produces the transmural ischaemia of STEMI.[1] The distinction that drives management is made on the ECG, and because myocardium dies minute by minute while the artery stays occluded, the Fellowship candidate must move from the door to the catheter-lab decision with speed and precision.

Definition and classification

ACS is classified by the ECG and by troponin. Unstable angina is ischaemia at rest or on minimal exertion without biomarker evidence of necrosis. NSTEMI is ischaemia with a rise or fall in cardiac troponin. STEMI is ischaemia with ST elevation or an ST-elevation equivalent on the ECG. The unstable-angina-versus-NSTEMI line is troponin; the NSTEMI-versus-STEMI line is the ECG. A separate entity, type 2 MI, is myocardial necrosis from a supply-demand mismatch (tachyarrhythmia, hypotension, sepsis, severe anaemia) without plaque rupture, and it must not be confused with the type 1 plaque-rupture ACS that drives the reperfusion pathway. [1]

Epidemiology and risk factors

ACS is predominantly a disease of middle and later life, more common in men than in pre-menopausal women, and driven by the conventional vascular risk factors: age, smoking, diabetes, hypertension, dyslipidaemia, family history, prior vascular disease and chronic kidney disease. Cocaine precipitates ACS through both coronary vasospasm and thrombus formation. Mortality from STEMI has fallen steadily with timely reperfusion but remains around 5 to 10 per cent in-hospital, considerably higher when cardiogenic shock complicates the infarct.[1][5]

Pathophysiology

The healthy coronary supplies myocardium with a flow that rises to meet demand. When a plaque ruptures, the exposed lipid core and collagen bind platelets, which aggregate and trigger the coagulation cascade; the resulting thrombus narrows or occludes the lumen. A total occlusion stops flow, producing transmural ischaemia within minutes — the ST elevation of STEMI — and, if unrelieved, full-thickness necrosis over the next six hours, with troponin released into the circulation from three to six hours and peaking around eighteen to twenty-four hours. A partial occlusion produces the subendocardial ischaemia of NSTEMI. This time-course is the entire justification for reperfusion: the myocardium that is ischaemic but not yet dead can be salvaged, and the salvage falls minute by minute. "Time is muscle" is not a slogan; it is the pathophysiology. [1]

Clinical presentation

The classic presentation is unmistakable: crushing or pressure-like central chest pain, radiating to the left arm, jaw or back, with diaphragresis, nausea, dyspnoea and a sense of doom. Examiners, however, deliberately test the atypical presentations, which are common and dangerous: in the elderly, the diabetic and the female patient the pain may be epigastric or mistaken for indigestion, or the presentation may be isolated dyspnoea, syncope, confusion or fatigue. A silent infarct is a well-described diabetic presentation. The clinical assessment alone is never sufficient — the ECG and troponin are mandatory for every patient in whom ACS is plausible. [1]

Differential diagnosis

The differential is the dangerous cause of chest pain, and the task is to distinguish them at the bedside by the tempo and character of the pain and the accompanying signs. [1]

The decisive distinction is tempo: ACS pain builds, whereas dissection pain is sudden and maximal at onset. The lethal trap is that dissection into the right coronary ostium produces an inferior STEMI, and thrombolysing it kills. [1]

Bedside assessment

Take a brief, focused history — the character, onset and tempo of the pain, the risk factors, and any contraindication to fibrinolysis or anticoagulation (prior intracranial haemorrhage, ischaemic stroke, active bleeding, recent surgery, aortic dissection, known bleeding tendency). Examine for the signs of complication: hypotension and shock, pulmonary oedema, a new murmur of mitral regurgitation or a ventricular septal defect, and bradycardia or heart block (particularly in inferior infarction). Site two large-bore intravenous cannulae and draw bloods while the ECG is being obtained. [1]

Investigations and the risk scores

The ECG is the first and the most time-critical investigation, and it must be obtained within ten minutes of arrival[1]; repeat it if pain is ongoing or evolves, and add posterior leads (V7 to V9) when posterior involvement is suspected and right-sided V4R in inferior infarction to seek right-ventricular involvement.

[1]

The territories: inferior (II, III, aVF — right coronary or circumflex; check V4R for the right ventricle), anterior (V1 to V4 — left anterior descending), lateral (I, aVL, V5, V6 — circumflex), and posterior (ST depression in V1 to V3 with a tall R wave, confirmed by ST elevation in V7 to V9). The STEMI equivalents must be recognised: a new or presumed-new left bundle branch block (diagnosed with the Sgarbossa criteria), the posterior infarct, the hyperacute T wave, the de Winter pattern and Wellens' syndrome. The high-sensitivity troponin strategy uses serial sampling with the validated 0/1-hour or 0/2-hour algorithms: the delta change (a rise or fall) distinguishes an acute infarction from the chronic troponin elevation of renal failure, sepsis, heart failure or pulmonary embolism.[1] A single negative troponin at presentation does not exclude ACS if the pain is ongoing or recent.

The Sgarbossa criteria identify infarction in a left bundle branch block: (1) concordant ST elevation of at least 1 mm in any lead; (2) concordant ST depression of at least 1 mm in V1 to V3; or (3) discordant ST elevation greater than 25 per cent of the preceding S-wave depth (the Smith-modified criterion, the most useful in practice). Any one criterion is highly specific for an occlusive infarct and activates the catheter laboratory. [1]

Three scores risk-stratify the patient and are reproduced in the topic: [1]

[1]

A HEART score of 0 to 3 carries a very low risk of major adverse cardiac events and supports safe early discharge after a negative troponin strategy; higher scores mandate further workup.[6] The GRACE score (age, heart rate, systolic blood pressure, creatinine, Killip class, cardiac arrest at admission, ST deviation, troponin) estimates in-hospital and six-month mortality and sets the invasive-timing threshold. The TIMI score (one point each: age 65 or older, at least three vascular risk factors, known CAD, aspirin in the last seven days, severe angina, ST deviation, raised biomarkers) is an alternative seven-variable score. The Killip class grades heart failure at the bedside — class I no heart failure, class II rales or a third heart sound, class III pulmonary oedema, class IV cardiogenic shock — and carries strong prognostic weight.

Immediate management — the drug bundle at first medical contact

Resuscitation and the specific therapy begin together. The immediate bundle — the part every Fellowship candidate must be able to recite with doses — is: [1]

[1] [1]

The P2Y12 choice is grounded in the trials: PLATO showed ticagrelor reduced cardiovascular death and all-cause mortality against clopidogrel without a significant increase in major bleeding,[2] and TRITON-TIMI 38 showed prasugrel reduced ischaemic events after primary PCI but increased bleeding.[3] Morphine is reasonable for refractory pain, with the awareness that it may slow the absorption of oral antiplatelets. Nitrates are given for ongoing ischaemic pain or pulmonary oedema — and are contraindicated in the right-ventricular infarct, in hypotension, and within 24 to 48 hours of a phosphodiesterase type-5 inhibitor.

Reperfusion — the core decision

Definitive treatment is reperfusion, and the decision turns on the ECG. [1]

STEMI

For the ST-elevation infarct, primary percutaneous coronary intervention is the preferred reperfusion when it can be delivered within 120 minutes of first medical contact, with a door-to-balloon time under 90 minutes from the PCI-capable hospital.[1] When primary PCI cannot be delivered within that window, fibrinolysis is the alternative, given within 30 minutes of arrival (door-to-needle): tenecteplase as a single weight-based bolus (or alteplase), followed by transfer to a PCI centre (the pharmaco-invasive strategy). The absolute contraindications to fibrinolysis must be known cold — any prior intracranial haemorrhage, a known cerebral vascular lesion or malignant intracranial neoplasm, an ischaemic stroke within six months, active bleeding, a suspected aortic dissection, and significant closed-head or facial trauma — because in their presence the bleeding risk justifies waiting for PCI even at the cost of time.

NSTEMI — risk-stratified invasive timing

The NSTEMI is managed with an early invasive strategy, but the timing is risk-stratified:[1]

Subtypes and special scenarios

The right-ventricular infarct is the scenario most often tested: an inferior STEMI complicated by hypotension, clear lung fields and a raised jugular venous pressure. The right ventricle is preload-dependent, so the treatment is fluid loading and the avoidance of nitrates and diuretics, which drop the preload and collapse the cardiac output. The posterior infarct shows ST depression and a tall R wave in V1 to V3 (the mirror of posterior ST elevation) and is confirmed with posterior leads. Cocaine-induced ACS is managed with benzodiazepines, nitrates and aspirin; beta-blockers are relatively contraindicated in the acute phase because of the risk of unopposed alpha-mediated vasospasm. [1]

Complications and pitfalls

The complications follow a timeline. Arrhythmia dominates the first hours — ventricular fibrillation and tachycardia (defibrillate), complete heart block (often transient in inferior infarction because the right coronary artery supplies the AV node, but a sign of extensive necrosis in anterior infarction), and sinus bradycardia from vagal tone. Cardiogenic shock complicates extensive infarction; the intra-aortic balloon pump has no routine mortality benefit (IABP-SHOCK II) and is reserved as a bridge to definitive support or revascularisation.[5] The mechanical complications appear three to five days after the infarct as the necrotic wall weakens: a ventricular septal rupture (a new pansystolic murmur at the lower left sternal edge with shock), papillary-muscle rupture (acute mitral regurgitation), and free-wall rupture (tamponade and arrest). Pericarditis appears early (epistenocardiac) or weeks later (Dressler syndrome). The recurring pitfalls are well-described: delaying the ECG; accepting a single negative troponin as a rule-out; missing a posterior, right-ventricular or LBBB-equivalent infarct; giving oxygen routinely; giving a beta-blocker in acute heart failure or a right-ventricular infarct; giving a nitrate in a right-ventricular infarct or after a phosphodiesterase inhibitor; and thrombolysing an unrecognised dissection.

Prognosis and disposition

STEMI in-hospital mortality is around 5 to 10 per cent, lower with timely reperfusion; cardiogenic shock raises it substantially, to around 40 per cent.[5] Every patient is admitted to a monitored bed or coronary care unit via the reperfusion pathway. Long-term survival depends on optimal secondary prevention: dual antiplatelet therapy for twelve months, a beta-blocker, an ACE inhibitor (especially with left-ventricular dysfunction, diabetes or hypertension), a high-intensity statin, an aldosterone antagonist with left-ventricular dysfunction and heart failure or diabetes, and cardiac rehabilitation.

Special populations

The elderly more often present atypically and carry a higher bleeding risk with aggressive antithrombotic regimens. Diabetic patients may have a silent infarct and uniformly worse outcomes. Women present atypically more often and are under-recognised. Chronic kidney disease produces a chronically raised troponin (so the delta matters more than the absolute value) and demands contrast-dose care and anticoagulant dose adjustment. Pregnancy is rare but modifies the workup (radiation avoidance) and the drug choice. [1]

Evidence and regional guidelines

The contemporary framework is the 2023 ESC ACS guideline[1] and the ACC/AHA chest-pain and ACS guidance. The antiplatelet evidence is PLATO (ticagrelor)[2] and TRITON-TIMI 38 (prasugrel),[3] the oxygen evidence is AVOID,[4] the mechanical-support evidence is IABP-SHOCK II,[5] and the chest-pain risk-stratification evidence is the HEART score.[6] The drug bundle and the risk scores are broadly global, but the reperfusion thresholds and the troponin algorithm are regional — the local cardiology pathway governs door-to-balloon and door-to-needle targets, and the candidate must know their own hospital's STEMI and NSTEMI pathways.

STEMI ECG criteria — the explicit thresholds

The STEMI diagnosis is an ECG diagnosis, and the Fellowship candidate must be able to state the threshold and the leads cold. The criteria require ST elevation measured at the J-point, in two anatomically contiguous leads, sustained through the window: at least 1 mm (0.1 mV) in any limb lead (I, II, III, aVF, aVL) or at least 2 mm in V2 to V3 in men (at least 1.5 mm in women), recognising that the precordial thresholds are sex- and age-dependent (a threshold of 2.5 mm in men under 40 is applied in some schemas). The "two contiguous leads" rule is what catches the single-lead elevation of early repolarisation and benign variants.[1]

[1] [1]

The STEMI equivalents — the occlusions the standard criteria miss

A coronary artery can be occluded without meeting the conventional ST-elevation thresholds, and the Fellowship examiner tests these "STEMI equivalents" relentlessly because missing them delays the catheter-lab activation. Each of them activates the same primary-PCI pathway as a frank STEMI. [1]

[1] [1]

The ACS mimics — the troponin rise that is not a plaque rupture

Not every troponin rise is a type 1 MI, and the over-treatment of the type 2 MI or the non-coronary troponin rise is a recurring pitfall. The universal definition of the MI distinguishes five types: the type 1 (the plaque rupture with the thrombus), the type 2 (the supply-demand mismatch), the type 3 (the sudden cardiac death with the ECG or imaging evidence before the troponin), the type 4 (the PCI-related: 4a, 4b the stent thrombosis, 4c the restenosis) and the type 5 (the CABG-related). The type 2 MI (the tachyarrhythmia, the hypotension, the sepsis, the severe anaemia, the hypertensive emergency, the hypoxia) is treated for the underlying cause — the rate control of the atrial fibrillation, the transfusion of the anaemia, the antibiotic and the fluid of the sepsis — and the antithrombotic regimen is reserved for the documented coronary disease. [1]

[1] [1]

The MONA bundle and its traps

The mnemonic MONA (morphine, oxygen, nitrates, aspirin) is taught because it is memorable — but every component carries a trap the examiner probes. The correct recital is the bundle with the doses and the caveats, not the bare letters. [1]

[1] [1]

The ED STEMI — the first 30 minutes

The STEMI pathway is choreographed. The Fellowship candidate must move from the door to the catheter-lab activation (or the fibrinolytic decision) inside 30 minutes without missing a step. [1]

[1]

The fibrinolysis pathway and its contraindications

When the primary PCI cannot be delivered within 120 minutes of the first medical contact, fibrinolysis is the reperfusion, given within 30 minutes of arrival (the door-to-needle). The agent is tenecteplase as a single weight-based bolus (the maximum 30 mg, with the dose 0.5 mg/kg for the weight under 60 kg, stepped up to the 30 mg ceiling at the weight over 90 kg), or the alteplase as the 90-minute weight-based infusion. The fibrinolysis is followed by the transfer to a PCI centre and the routine early angiography at 3 to 24 hours (the pharmaco-invasive strategy), because the fibrinolysis fails in 20 to 30 per cent and the failed fibrinolysis (the ongoing pain, the under-50 per cent ST resolution at 60 to 90 min) is the indication for the rescue PCI. [1]

[1] [1] [1]

NSTEMI risk stratification — the scores compared

The NSTEMI timing is set by the risk stratification. The GRACE score is the validated mortality estimate and sets the invasive threshold; the TIMI score is the simpler bedside tool; the HEART score is the emergency-department rule-out for the low-risk chest pain. [1]

[1]

Cardiogenic shock complicating the infarct

The cardiogenic shock complicates 5 to 8 per cent of the acute MIs and carries a mortality around 40 to 50 per cent. The definition is the persistent hypotension (the systolic under 90 mmHg or the mean under 65) with the end-organ hypoperfusion (the cool peripheries, the oliguria, the altered mental state, the raised lactate) and the haemodynamic or the imaging evidence of the cardiac dysfunction. The early revascularisation is the survival therapy (the SHOCK trial established the survival benefit of the early revascularisation in the cardiogenic shock complicating MI), and the culprit-lesion-only PCI is preferred over the multivessel PCI in the shock (the CULPRIT-SHOCK trial).[5]

[1]

The mechanical complications — the timeline

The mechanical complications appear three to five days after the infarct as the necrotic wall weakens — the timeline is the diagnostic clue. The new murmur with the shock in this window is the mechanical complication until proven otherwise, and the bedside echo is the immediate investigation. [1]

[1]

Post-MI secondary prevention — the four pillars

The post-MI mortality depends on the secondary prevention, and the Fellowship candidate must be able to recite the four pillars and their evidence. The post-MI bundle reduces the mortality by a large margin and is non-negotiable in the discharged patient. [1]

[1] [1]

The special scenarios revisited — the pearls

[1] [1]

The landmark trials — the evidence base

The Fellowship candidate must know the trials that underpin the recommendations, because the viva probes the evidence as much as the practice. [1]

[1] [1] [1]

Additional red flags

[1]

Exam pearls

• ECG within 10 minutes; oxygen only if the saturation is under 90 per cent; aspirin 300 mg + a P2Y12 inhibitor + an anticoagulant.
• Primary PCI under 90 minutes door-to-balloon; else fibrinolysis within 30 minutes door-to-needle (120 minutes from first medical contact the decision point).
• Inferior STEMI plus hypotension plus clear lungs plus a raised JVP is a right-ventricular infarct — fluids, no nitrates, no diuretics.
• Inferior STEMI plus a widened mediastinum may be dissection into the right coronary ostium — exclude dissection before any thrombolysis.
• A single troponin does not rule out ACS; use the delta with the 0/1h or 0/2h algorithm.
• GRACE above 140 sends the high-risk NSTEMI to invasive management within 24 hours.
• A new pansystolic murmur with shock three to five days after the infarct is a mechanical complication until proven otherwise — echo, urgent surgery, mechanical support (not lytics). [1]

SAQs

[1] [1]

Red flags

[1]

References

1. [1]Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the management of acute coronary syndromes Eur Heart J, 2023.PMID 37622654
2. [2]Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes N Engl J Med, 2009.PMID 19717846
3. [3]Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes N Engl J Med, 2007.PMID 17982182
4. [4]Stub D, Smith K, Bernard S, et al. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction Circulation, 2015.PMID 26002889
5. [5]Thiele H, Akin I, Sandri M, et al. Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial Circulation, 2019.PMID 30586721
6. [6]Poldervaart JM, Langedijk M, Backus BE, et al. Effect of Using the HEART Score in Patients With Chest Pain in the Emergency Department: A Stepped-Wedge, Cluster Randomized Trial Ann Intern Med, 2017.PMID 28437795