Acute coronary syndrome

Atherothrombotic (type 1 MI)

Plaque rupture or erosion with occlusive or subocclusive thrombus — the large majority

Supply-demand mismatch (type 2 MI)

Anaemia, sepsis, tachyarrhythmia, hypotension, hypoxaemia, severe hypertension

Vasospastic

Coronary spasm, cocaine or amphetamine use, ergot derivatives

Embolic

Atrial fibrillation, infective endocarditis, prosthetic valve thrombus, paradoxical embolus

Dissection

Spontaneous coronary artery dissection — young or peripartum women

Inflammatory / other

Vasculitis (Kawasaki, Takayasu), radiation arteriopathy, congenital anomalies, MINOCA

• Ischaemic heart disease is the single leading cause of death globally.
• Incidence rising in South Asia and other low- and middle-income regions with a decade earlier onset than in Western cohorts.
• Women and people with diabetes present later and more often atypically, contributing to excess mortality.

Non-modifiable

• Age, male sex, family history of premature CAD, genetic dyslipidaemia.

Modifiable

• Smoking, hypertension, diabetes, dyslipidaemia, obesity, physical inactivity, unhealthy diet, harmful alcohol, psychosocial stress, CKD, sleep apnoea, inflammatory disease.

1. 1Endothelial injury from shear stress, smoking, hyperglycaemia and dyslipidaemia allows LDL retention in the intima.
2. 2Modified LDL is taken up by macrophages forming foam cells and a lipid-rich necrotic core.
3. 3Smooth-muscle-derived fibrous cap forms; inflammation and matrix metalloproteinases thin it.
4. 4Cap rupture or endothelial erosion exposes thrombogenic core to circulating platelets.
5. 5Platelet adhesion, activation and aggregation with fibrin generate an occlusive thrombus.

Normal physiology → mechanism → tissue change → clinical picture

1. 1Normal physiology: coronary flow reserve allows perfusion to rise 4-5 fold with demand.
2. 2Mechanism: acute thrombotic obstruction abolishes flow to the subtended myocardium.
3. 3Tissue change: subendocardial ischaemia within minutes; a transmural wavefront of necrosis progresses over 6-12 hours.
4. 4Functional effect: regional hypokinesis, raised LV filling pressure, arrhythmogenic electrical instability.
5. 5Clinical manifestation: ischaemic chest pain, ECG ST changes, troponin release, dyspnoea, arrhythmia, hypotension.

Gross

Pale then mottled infarct zone; yellow-tan with hyperaemic border by days 3-7; thin grey-white scar by weeks 6-8

Microscopic timeline

Wavy fibres and coagulative necrosis (hours) → neutrophils (1-3 d) → macrophages (3-7 d) → granulation tissue (1-2 wk) → collagen scar (>4 wk)

Complication correlate

Days 3-7 macrophage phase is the weakest wall — free wall rupture, septal rupture, papillary muscle rupture

Reperfusion pathology

Contraction band necrosis and haemorrhage into the infarct zone

• Central or left-sided pressure, heaviness or crushing pain lasting > 20 minutes
• Radiation to jaw, neck, either arm or interscapular region
• Diaphoresis, nausea and vomiting, marked anxiety or sense of doom
• Dyspnoea, presyncope or syncope
• Silent or atypical in diabetes, older adults, women and after transplant

• Often normal examination — do not use a normal examination to exclude ACS
• Tachycardia or bradycardia (inferior MI with vagal or AV nodal involvement)
• Hypotension, cool peripheries, raised JVP (right ventricular infarction)
• S4, new S3, new murmur of mitral regurgitation, pericardial rub
• Pulmonary crackles and Killip class assessment

Typical

• Exertional or rest chest pressure with autonomic features and dynamic ECG changes.

Atypical

• Isolated dyspnoea or fatigue (especially women, elderly, diabetes)
• Epigastric pain with vomiting mimicking gastritis — inferior MI
• New arrhythmia, syncope, or unexplained heart failure
• Delirium or a fall in a frail older adult

1. 1ECG within 10 minutes of first contact; repeat every 15-30 minutes if non-diagnostic and symptoms persist.
2. 2Classify: ST elevation → STEMI pathway; no ST elevation → risk-stratify with troponin and clinical score.
3. 3High-sensitivity troponin at presentation and at 1-3 hours using a validated rule-in/rule-out algorithm.
4. 4Bedside assessment for shock, murmur, and alternative catastrophic diagnoses (dissection, PE, tamponade).
5. 5Score risk: GRACE for NSTE-ACS; HEART for undifferentiated chest pain in the emergency department.
6. 6Decide reperfusion or invasive timing; start antithrombotic and anti-ischaemic therapy in parallel.
7. 7Echocardiography for wall motion, ejection fraction and complications.

• Myocardial infarction (Fourth Universal Definition): rise and/or fall of cardiac troponin with at least one value above the 99th percentile PLUS evidence of ischaemia — symptoms, new ischaemic ECG change, pathological Q waves, imaging evidence of new loss of viable myocardium, or intracoronary thrombus.
• STEMI ECG criteria: new ST elevation at the J point in ≥ 2 contiguous leads — ≥ 1 mm in most leads; ≥ 2 mm in men ≥ 40 y (≥ 2.5 mm if < 40 y) and ≥ 1.5 mm in women in V2-V3.
• Unstable angina: ischaemic symptoms without troponin elevation.

Initial

• 12-lead ECG, high-sensitivity troponin, capillary glucose, FBC, renal function, electrolytes, chest radiograph.

Confirmatory

• Serial troponin per 0/1 h or 0/3 h algorithm, echocardiography, invasive coronary angiography.

Severity

• Lactate, blood gas, BNP, Killip class, LV function; right heart assessment in shock.

Risk / prognostic

• Lipid profile, HbA1c, thyroid function; CT coronary angiography or functional imaging in low-risk undifferentiated pain.

Monitoring

• Telemetry for arrhythmia, renal function post-contrast, potassium and magnesium, repeat echo before discharge.

Aortic dissection

Rule in: abrupt tearing pain to back, pulse/BP asymmetry, widened mediastinum. Rule out: CT angiography — critical before antithrombotics.

Pulmonary embolism

Rule in: pleuritic pain, hypoxaemia, RV strain on ECG/echo, raised D-dimer. Rule out: CTPA.

Pericarditis / myocarditis

Rule in: positional pleuritic pain, rub, diffuse concave ST elevation with PR depression. Rule out: regional wall motion abnormality and coronary occlusion.

Oesophageal spasm / GORD

Rule in: relation to food, acid regurgitation, response to PPI. Rule out: dynamic ECG change and troponin rise.

Takotsubo syndrome

Rule in: emotional/physical trigger, apical ballooning, unobstructed coronaries. Rule out: culprit occlusion on angiography.

Musculoskeletal chest pain

Rule in: reproducible focal tenderness. Rule out: never on tenderness alone in a high-risk patient.

Killip classification

Killip I

No heart failure — mortality lowest

Killip II

Crackles < 50% lung fields, raised JVP or S3

Killip III

Frank pulmonary oedema

Killip IV

Cardiogenic shock — highest mortality

• GRACE score stratifies in-hospital and 6-month death in NSTE-ACS and guides invasive timing (< 24 h if high risk).
• TIMI risk score is an alternative for NSTE-ACS and a separate score exists for STEMI.

Immediate

• Attach monitor and defibrillator, IV access, oxygen only if SpO2 < 90%
• Aspirin loading dose chewed, plus a P2Y12 inhibitor per local pathway
• Anticoagulation (unfractionated heparin, enoxaparin or bivalirudin) per strategy
• Sublingual or IV nitrate for pain if not hypotensive and no RV infarction or recent PDE5 inhibitor
• IV opioid for refractory pain; treat nausea

Reperfusion / revascularisation

• STEMI: primary PCI within 120 min of diagnosis; otherwise fibrinolysis within 10 min of decision and transfer for angiography.
• NSTE-ACS: invasive strategy timing by risk — immediate (very high risk), within 24 h (high risk), selective/early for others.

First-line ongoing therapy

• High-intensity statin regardless of baseline LDL-C
• Beta-blocker once stable and not in shock
• ACE inhibitor or ARB, especially with LV dysfunction, diabetes or hypertension
• MRA if LVEF ≤ 40% with heart failure or diabetes
• SGLT2 inhibitor where indicated for heart failure or diabetes
• Dual antiplatelet therapy typically 12 months, individualised by bleeding risk

Severe / refractory

• Mechanical circulatory support and inotropes in cardiogenic shock; surgical repair for mechanical complications; CABG for unsuitable anatomy.

Supportive

• Cardiac rehabilitation, smoking cessation, diet and exercise prescription, psychological support, immunisation.

Monitoring

• Continuous ECG for 24-48 h, troponin trend, renal function, bleeding assessment, repeat echo, adherence review at follow-up.

Linked drug entities

• aspirin — irreversible COX-1 inhibition, loading then lifelong maintenance
• atorvastatin — high-intensity statin for plaque stabilisation and LDL reduction
• metoprolol — reduces ischaemic burden, arrhythmia and remodelling
• enoxaparin — parenteral anticoagulation during the acute phase

Early (0-48 h)

• Ventricular arrhythmia, AV block, cardiogenic shock, acute pulmonary oedema, RV failure, reinfarction, stroke.

Intermediate (3-14 d)

• Papillary muscle rupture with acute mitral regurgitation, ventricular septal rupture, free wall rupture and tamponade, pericarditis, LV thrombus.

Late

• LV remodelling and chronic heart failure, ventricular aneurysm, Dressler syndrome, depression, recurrent ACS.

• In-hospital mortality for reperfused STEMI is roughly 4-6%; cardiogenic shock raises it above 40%.
• Prognosis is driven by time to reperfusion, infarct size, LVEF, Killip class, age, renal function and diabetes.
• One-year outcomes improve substantially with completed cardiac rehabilitation and adherence to four-drug secondary prevention.
• Recurrence risk is highest in the first 90 days; residual disease and untreated risk factors dominate long-term risk.

• Primary: lipid and blood-pressure control, smoking cessation, weight and glycaemic management, physical activity; risk scoring (e.g. ASCVD) to guide statin initiation.
• Secondary: antiplatelet therapy, high-intensity statin, ACEi/ARB, beta-blocker, structured rehabilitation, influenza vaccination.
• No population screening for CAD in asymptomatic low-risk adults; use risk calculators instead.

• Review at 2-6 weeks: symptoms, adherence, blood pressure, heart rate, lipids, renal function.
• Lipid panel 4-8 weeks after starting or intensifying statin, targeting guideline LDL-C goals.
• Repeat echo at 6-12 weeks if LVEF was reduced, to reassess device or therapy needs.
• Cardiac rehabilitation enrolment and return-to-work/driving advice per local rules.

Pregnancy

Rare but serious; consider SCAD; multidisciplinary care; avoid ACEi/ARB and statins during pregnancy

Elderly

Higher bleeding risk — adjust antithrombotic dose and duration; still benefit from reperfusion

CKD

Adjust anticoagulant dosing, minimise contrast, hydrate; higher event and bleeding risk

Diabetes

More silent ischaemia and diffuse disease; prioritise SGLT2 inhibitor/GLP-1 RA with proven benefit

Recent bleeding / anticoagulated

Shorten DAPT duration, use gastroprotection, individualise triple therapy

• ESC Guidelines for the management of acute coronary syndromes (2023)
• ESC heart failure guideline (2021, 2023 focused update) for post-MI LV dysfunction

• Radial-first access and drug-eluting stents are established standards in contemporary PCI practice.
• Complete revascularisation of significant non-culprit lesions improves outcomes after STEMI in selected patients.
• De-escalation and shortened DAPT strategies are an active area of evidence for high bleeding risk patients.

• ESC 2023 ACS guideline (guideline, Europe).
• Fourth Universal Definition of Myocardial Infarction (consensus document).
• DrZep editorial summary, demo dataset v0.1.