GC028 Accelerating Chest Pain: Acute Coronary
Acute coronary syndrome encompasses a spectrum of conditions—unstable angina, NSTEMI, and STEMI—caused by sudden reduction in coronary blood flow, typically due to atherosclerotic plaque rupture and thrombosis, presenting with accelerating or new-onset chest pain requiring urgent evaluation and management.
Accelerating Chest Pain: Acute Coronary Syndromes (NSTE-ACS Focus)
This lecture by Prof. Hung-Fat Tse focuses primarily on Non-ST-Segment Elevation Acute Coronary Syndromes (NSTE-ACS), which encompasses Unstable Angina (UA) and Non-ST-Elevation Myocardial Infarction (NSTEMI). STEMI is covered in the companion lecture (GC 088 – Sudden Severe Chest Pain) [1][2]. The lecture uses a single clinical case (CTM, M/51) that threads through the entire session — from presentation to diagnosis, acute management, revascularisation, and secondary prevention.
How this fits into clinical practice and exams:
- ACS is the number-one killer worldwide (atherothrombosis = 22.3% of global mortality) [1]. Every doctor must be able to recognise, risk-stratify, and initiate management.
- In-house exams test the clinical spectrum (UA vs NSTEMI vs STEMI), ECG interpretation (Wellens syndrome, ST changes), troponin interpretation, acute pharmacotherapy (the "MONA-B-H" mnemonic is a simplification — the lecture's framework is more nuanced), and secondary prevention.
- The lecture maps precisely onto the ESC 2023 guidelines framework [1].
Learning objectives (from the lecture structure):
- Epidemiology of ACS
- Pathophysiology of atherothrombosis
- Diagnosis and assessment (clinical features, ECG, troponin, risk stratification)
- Initial therapies and management (anti-ischaemic + antithrombotic + revascularisation strategy)
- Long-term / secondary prevention
Atherothrombosis is the leading cause of death worldwide (22.3% of global mortality), surpassing infectious disease (19.3%), cancer (12.6%), and injuries (9.7%). [1]
High Yield – Exam Framing
The lecture specifically defines atherothrombosis as the combination of ischaemic heart disease AND cerebrovascular disease. This combined statistic (22.3%) is a favourite exam factoid. [1]
Why this matters: It justifies why every medical student must be fluent in ACS management — it is the single largest disease burden globally.
- Atherothrombosis is a generalised and progressive process [1] — it doesn't just affect coronary arteries. The same pathology causes:
- Stable angina / intermittent claudication (atherosclerosis stage)
- Unstable angina, MI, ischaemic stroke/TIA, critical leg ischaemia (atherothrombosis stage — when plaque ruptures and thrombus forms)
This means a patient with ACS likely has diffuse atherosclerotic disease elsewhere (carotid, peripheral arteries) — which is why the physical exam includes checking peripheral pulses, carotid bruits, and arm BP disparity [1].
2. Pathophysiology
Pathophysiology of Atherothrombosis involves TWO parallel processes: Platelet Aggregation (Primary Haemostasis) and Coagulation (Secondary Haemostasis). [1]
From first principles:
- Atherosclerotic plaque develops over decades: fatty streaks → fibroatheroma → vulnerable plaque (thin fibrous cap, large lipid-rich necrotic core, inflammatory infiltrate) [5].
- Plaque rupture or erosion exposes the subendothelial matrix (collagen, tissue factor) to flowing blood.
- Primary haemostasis (0–5 min): Platelets adhere (via vWF–GPIb), activate (releasing ADP, TxA2), and aggregate (via GPIIb/IIIa cross-linking with fibrinogen).
- Secondary haemostasis (5–10 min): Tissue factor activates the coagulation cascade → thrombin generation → converts fibrinogen to fibrin → stabilises the platelet plug into a haemostatic clot.
Why does this matter clinically? Because treatment targets BOTH pathways simultaneously:
- Antiplatelets (aspirin, P2Y12 inhibitors, GPIIb/IIIa inhibitors) → block platelet aggregation
- Anticoagulants (heparin, LMWH, fondaparinux) → block the coagulation cascade / thrombin
NSTE-ACS results from non-occlusive thrombus on a pre-existing plaque (vs. complete occlusion in STEMI). [1]
The lecture lists five mechanisms for NSTE-ACS symptom progression [1]:
| Mechanism | Explanation |
|---|---|
| Non-occlusive thrombus on pre-existing plaque | Plaque rupture with partial luminal obstruction — some flow preserved, hence no ST elevation |
| Dynamic obstruction (coronary spasm/vasoconstriction) | Vasospasm at or near the plaque site transiently worsens ischaemia |
| Progressive mechanical obstruction | Plaque growth gradually narrows the lumen further |
| Increased myocardial oxygen demand | Tachycardia, fever, anaemia, thyrotoxicosis — "demand ischaemia" on top of a fixed stenosis |
| Infection / Inflammation | Systemic inflammation destabilises plaques and promotes thrombosis |
Key Distinction: NSTEMI vs STEMI
NSTEMI/UA = partial coronary occlusion → residual blood flow → subendocardial (not transmural) ischaemia → ST depression or T-wave changes (not ST elevation) → troponin may or may not rise.
STEMI = complete coronary occlusion → no blood flow → transmural ischaemia → ST elevation → troponin always rises.
This is why thrombolysis is used in STEMI (to dissolve the complete occlusion) but NOT in NSTEMI/UA (partial occlusion — lysing the thrombus could paradoxically worsen things or is simply unnecessary). [5]
3. Clinical Presentation
A 51-year-old male with history of stable CAD and hyperlipidaemia, on aspirin/statin/metoprolol (betaloc), defaulted medications for 6 months. Presents with sudden onset of chest pain at rest for 1 day. Pain is constricting in character and NOT relieved by TNG. Father died of CAD at age 65. Chronic smoker (1 pack/day). [1]
Why each detail matters:
| Feature | Significance |
|---|---|
| Known CAD | Pre-existing disease — this is "accelerating" from stable → unstable |
| Defaulted meds × 6 months | Lost cardioprotection (aspirin = antiplatelet, statin = plaque stabilisation, BB = reduces O₂ demand) |
| Chest pain at rest | Implies ACS (not stable angina which only occurs with exertion) |
| Constricting character | Typical ischaemic quality |
| Not relieved by TNG | Distinguishes from simple stable angina (which typically responds to GTN) |
| Smoking 1 pack/day | Major modifiable risk factor |
| Family Hx: father died CAD age 65 | Premature CAD in first-degree male relative ( < 55) — actually 65 is borderline, but still significant |
Four principal presentations of NSTE-ACS [1]:
| Presentation | Definition | Key Point |
|---|---|---|
| Rest Angina | Angina at rest, usually > 20 minutes | Most patients with NSTEMI present this way |
| New-onset Angina | New angina of at least CCS Class III severity | First-ever angina that is already moderately severe |
| Increasing (Crescendo) Angina | Previously diagnosed angina becoming more frequent, longer, or lower threshold (↑ by ≥ 1 CCS class to at least CCS III) | The "accelerating" in the lecture title |
| Post-MI Angina | Recurrence of angina after a recent MI | Suggests incomplete revascularisation or new event |
CCS Classification Reminder
CCS I: Angina only with strenuous exertion. CCS II: Slight limitation — angina walking > 2 blocks or climbing > 1 flight. CCS III: Marked limitation — angina walking 1-2 blocks or 1 flight of stairs. CCS IV: Angina at rest or with any activity.
The lecture's differential diagnosis slides [1] and the CFB History Taking slides [3] emphasise that ACS can present atypically:
- Diabetics may have painless ("silent") MI — due to autonomic neuropathy [5]
- Elderly, women, diabetics may present with dyspnoea, nausea, syncope, or fatigue rather than typical chest pain
- Epigastric pain can mimic GI pathology
The lecture's differential diagnosis table (ESC 2020/2011) includes [1]:
| Category | Conditions |
|---|---|
| Cardiac | ACS (UA/NSTEMI/STEMI), myocarditis/pericarditis, aortic dissection (Type A), takotsubo, aortic stenosis, HCM |
| Pulmonary | Pulmonary embolism, pneumothorax, pneumonia, pleuritis |
| Gastrointestinal | GERD, oesophageal spasm, peptic ulcer, pancreatitis, cholecystitis |
| Musculoskeletal | Costochondritis, rib fracture, muscle strain |
| Other | Herpes zoster, anxiety/panic |
The CFB slides provide a detailed SOCRATES comparison table for chest pain aetiologies — angina vs MI vs aortic dissection vs pericardial vs oesophageal pain [3]. Key discriminators:
| Feature | Angina | MI | Aortic Dissection | Pericarditis | Oesophageal |
|---|---|---|---|---|---|
| Onset | Progressive ↑ over 1-2 min | Rapid over few min | Very sudden, max at onset | Gradual | Over 1-2 min |
| Character | Constricting, heavy | Constricting, heavy | Tearing, ripping | Sharp, stabbing, pleuritic | Gripping, burning |
| Duration | 2-10 min | Prolonged (> 30 min) | Prolonged | Variable | Variable |
| Radiation | Arm, neck | Arm, neck, jaw | Back, between shoulders | Left shoulder | Back, arms |
| Relieving | Rest, TNG | NOT rest/TNG | Nothing | Sitting up, NSAIDs | Antacids; nitrates sometimes |
| Severity | Mild-moderate | Usually severe | Very severe | Can be severe | Usually mild |
4. Physical Examination
The lecture provides a comprehensive P/E framework organised by GOAL [1]:
| Finding | Significance |
|---|---|
| BP > 15 mmHg arm disparity | Increased risk for PAD and cardiovascular death (also think aortic dissection!) |
| BMI > 30 kg/m² | Obesity — metabolic syndrome |
| Cutaneous xanthomas, xanthelasma, corneal arcus | Hyperlipidaemia |
| Acanthosis nigricans, skin tags | Insulin resistance / diabetes mellitus |
| Tobacco staining, odour, premature wrinkling | Smoking |
| Ear lobe creases (Frank sign) | Controversial but classically associated with CAD |
| Finding | Suggests |
|---|---|
| JVD, S3, S4, displaced PMI, hepatomegaly, pulmonary/peripheral oedema | Congestive heart failure |
| New murmur (pansystolic at apex) | Ischaemic mitral regurgitation (papillary muscle dysfunction) |
| Hypotension, tachycardia | Low-output cardiac failure or cardiogenic shock |
| Ectopy, irregularly irregular pulse | Arrhythmias (AF, VT) |
| Carotid bruits, absent peripheral pulses, skin discolouration | Peripheral arterial disease |
| Finding | Suggests |
|---|---|
| Late-peaking systolic murmur, pulsus parvus et tardus | Aortic stenosis |
| Harsh crescendo-decrescendo systolic murmur varying with provocation | HCM |
| Loud P2, right S4, TR murmur, RV heave | Pulmonary hypertension |
P/E: Weight 80 kg, height 165 cm (BMI 29), waist 93 cm, BP 98/65, HR 102, S3 present, nil murmur, chest clear. [1]
Interpretation:
- BMI 29 = overweight (approaching obesity) with central obesity (waist 93 cm > 90 cm for Asian males)
- BP 98/65, HR 102 = hypotension with compensatory tachycardia — suggests significant myocardial injury with reduced cardiac output → this is a HIGH-RISK feature
- S3 gallop = indicates ventricular dysfunction / heart failure — volume overload of a failing ventricle
- These findings together suggest this patient is in the early stages of cardiogenic shock or at least significant LV impairment
Clinical Pearl – S3 in ACS
An S3 gallop in the context of ACS is an ominous sign — it indicates significant LV systolic dysfunction and predicts higher mortality. It should prompt urgent echocardiography and consideration of early invasive strategy. Do NOT dismiss an S3 as benign in this context.
5. Investigations
5.1 ECG
The ECG is the FIRST and most important test in ACS — must be done within 10 minutes of presentation. [1]
The lecture shows that NSTE-ACS can produce [1]:
- ST depression (> 0.5 mm in ≥ 2 contiguous leads)
- T-wave inversion (> 1 mm in leads with dominant R wave)
- Biphasic T waves (especially V1-V4 → Wellens syndrome)
- Transient ST elevation (if coronary spasm)
- Normal ECG (does NOT rule out ACS — up to 6% of patients with normal ECGs have NSTEMI)
Wellens Syndrome: History of angina + T-wave inversion or biphasic T waves in V2-V4 + normal or minimally elevated cardiac enzymes + no pathologic Q waves. 75% of patients with this pattern develop acute MI within a mean of 6-8.5 days. ALL patients have > 50% LAD stenosis. Incidence 10-15%. [1]
Wellens Syndrome – Must Know for Exams
This is a pre-infarction ECG pattern indicating critical proximal LAD stenosis. Two types:
- Type A (more common, 75%): Deeply inverted, symmetric T waves in V2-V4 (sometimes V1-V6)
- Type B (25%): Biphasic T waves (initial positive deflection then negative) in V2-V3
Critical exam points:
- These ECG changes appear during pain-FREE intervals (not during chest pain)
- Troponin is normal or minimally elevated
- Exercise stress testing is CONTRAINDICATED — it may precipitate acute MI
- Urgent coronary angiography is required
- The case patient (CTM) had "biphasic T-wave inversion over V1-V6" → this IS Wellens syndrome [1]
The lecture slides show that ECG interpretation in ACS can be confounded by [1]:
- LBBB / IVCD — makes ST changes uninterpretable (use Sgarbossa criteria)
- LVH — baseline ST-T changes from strain pattern
- Paced rhythm — similar issue to LBBB
5.2 Cardiac Biomarkers
High-sensitivity troponin (hs-Tn) is the gold standard biomarker for diagnosing myocardial injury in ACS. [1]
From first principles: Troponin is a structural protein of the cardiac myocyte contractile apparatus (troponin I and T are cardiac-specific isoforms). When myocardial cells die (necrosis), troponin leaks into the bloodstream. High-sensitivity assays can detect very small amounts, enabling earlier diagnosis.
The ESC 2023 0h/1h algorithm [1]:
- Measure hs-Tn at presentation (0h)
- Repeat at 1h (or 2h depending on assay)
- Rule-out: Very low 0h value AND minimal change at 1h → ACS very unlikely
- Rule-in: High 0h value OR significant rise at 1h → NSTEMI confirmed
- Observe: Intermediate values → repeat at 3h, continue monitoring
The case patient's hs-TnT = 100 — this is elevated (normal is typically < 14 ng/L for hs-TnT), confirming NSTEMI [1].
Causes of elevated troponin that are NOT ACS [1]:
| Category | Examples |
|---|---|
| Non-coronary cardiac | Myocarditis, acute/chronic LV failure, arrhythmias |
| Non-cardiac | Pulmonary embolism, septic shock, renal dysfunction ("false positive") |
| Post-procedural | Cardioversion, catheter ablation/biopsy, PCI |
Troponin in Renal Dysfunction
Chronically elevated troponin in CKD patients is common (reduced clearance + chronic myocardial stress). The key to diagnosing ACS in these patients is looking for a rise-and-fall pattern (delta change), not just a single elevated value. The lecture specifically flags renal dysfunction as a cause of "false positive" troponin. [1]
The lecture's biomarker timeline slide shows [1]:
- CK-MB: Rises 4-6h, peaks 12-24h, normalises 48-72h — useful for detecting re-infarction (because it falls quickly)
- Troponin (conventional): Rises 4-6h, peaks 12-24h, remains elevated 7-14 days
- hs-Troponin: Detectable as early as 1-3h post-injury — enables the rapid rule-in/rule-out algorithms
- Myoglobin: Rises earliest (1-2h) but not cardiac-specific — largely supplanted by hs-Tn
5.3 Imaging
CTCA limitations: radiation exposure (especially young patients — mitigated by ECG-triggering, low HR, faster scanners), calcified vessels or prior stenting (artefact), and rapid or irregular heart rate (motion artefact). [1]
CTCA is most useful in:
- Low-to-intermediate risk patients to rule out significant CAD (high negative predictive value)
- Patients with non-diagnostic ECG and normal troponin
The lecture references the role of non-invasive assessment [1] — this includes:
- Exercise ECG (treadmill test) — for patients who can exercise and have interpretable baseline ECG
- Stress echocardiography (exercise or dobutamine)
- Myocardial perfusion imaging (MPI/SPECT) — using pharmacological stress (adenosine/dipyridamole)
- Cardiac MRI — stress perfusion or late gadolinium enhancement
These are used primarily for stable patients or post-ACS risk stratification, NOT during the acute presentation.
ECG: Biphasic T-wave inversion V1-V6. FBS 6.2, TG 2.0, HDL 1.0, LDL 4.6, hs-TnT 100. [1]
| Test | Result | Interpretation |
|---|---|---|
| ECG: biphasic T inversions V1-V6 | Wellens pattern | Critical proximal LAD disease |
| FBS 6.2 mmol/L | Impaired fasting glucose (IFG: 5.6-6.9) | Pre-diabetes — cardiovascular risk factor |
| TG 2.0 mmol/L | Mildly elevated (> 1.7) | Component of metabolic syndrome |
| HDL 1.0 mmol/L | Low (< 1.0 for males = metabolic syndrome criterion) | Borderline |
| LDL 4.6 mmol/L | Markedly elevated | Very high-risk patient → target LDL < 1.4 mmol/L |
| hs-TnT 100 | Elevated | Confirms NSTEMI |
6. Risk Stratification
The Braunwald Classification stratifies patients into High, Intermediate, and Low Risk based on History, Character of Pain, Clinical Findings, ECG, and Cardiac Markers. [1]
| Feature | High Risk | Intermediate Risk | Low Risk |
|---|---|---|---|
| History | Accelerating ischaemic symptoms in preceding 48h | Prior MI, PVD, CVD, CABG, prior aspirin use | — |
| Pain | Prolonged ongoing (> 20 min) rest pain | Prolonged rest angina (> 20 min), now resolved | New-onset or progressive CCS III-IV in past 2 weeks |
| Clinical | Pulmonary oedema, new/worsening MR, S3, new rales, hypotension, brady/tachycardia, age > 75 | Age > 70 | — |
| ECG | Rest angina with transient ST changes > 0.5 mm, new/presumed new BBB, sustained VT | T inversions > 2 mm, pathological Q waves | Normal or unchanged ECG during symptoms |
| Markers | TnT/TnI > 0.1 ng/mL | Slightly elevated (0.01-0.1 ng/mL) | Normal |
The case patient (CTM) falls into HIGH RISK: accelerating symptoms, rest pain > 20 min, S3 present, hypotension + tachycardia, biphasic T waves, elevated troponin.
The ESC 2023 guidelines recommend the GRACE score for risk assessment in NSTE-ACS. [1]
The GRACE score incorporates: age, heart rate, systolic BP, creatinine, Killip class, cardiac arrest at admission, ST deviation, and troponin elevation. It predicts in-hospital and 6-month mortality.
| GRACE Score | Risk Category | 6-month Mortality | Management Strategy |
|---|---|---|---|
| < 109 | Low | < 3% | Non-invasive assessment or selective invasive |
| 109-140 | Intermediate | 3-8% | Invasive within 72h |
| > 140 | High | > 8% | Early invasive within 24h |
7. Management
Primary anti-ischaemic therapeutic measures [1]:
| Measure | Details | Rationale |
|---|---|---|
| Bed rest + ECG/BP monitoring | General measure | Reduces myocardial O₂ demand; enables early detection of arrhythmia |
| Oxygen | 4-8 L/min if SpO₂ < 90% | Corrects hypoxaemia (but supplemental O₂ in normoxic patients may paradoxically cause harm via coronary vasoconstriction) |
| Nitrates | Sublingual or IV; caution if SBP < 90 mmHg | Venodilation → ↓ preload → ↓ myocardial O₂ demand; also coronary vasodilation |
| Morphine | 3-5 mg IV or SC | Analgesia + anxiolysis + ↓ sympathetic drive → ↓ HR, ↓ BP, ↓ O₂ demand |
| Oral beta-blocker or CCB | Particularly if tachycardia or HTN without signs of HF | ↓ HR → ↓ O₂ demand, ↑ diastolic filling time → ↑ coronary perfusion |
| Diltiazem or verapamil if BB failed or CI | Rate-limiting CCBs as alternative | |
| Atropine | 0.5-1 mg IV if bradycardia or vagal reaction | Reverses parasympathetic-mediated bradycardia |
Nitrates Caution
Do NOT give nitrates if:
- SBP < 90 mmHg (case patient had BP 98/65 — borderline! Proceed with extreme caution or avoid)
- Known RV infarction (nitrates ↓ preload → catastrophic drop in RV output)
- Phosphodiesterase-5 inhibitor use within 24-48h (sildenafil, tadalafil)
- Severe aortic stenosis
7.3 Antithrombotic Therapy
This is the core of NSTE-ACS pharmacotherapy. The lecture organises it into antiplatelets and anticoagulants [1].
A. Aspirin (COX-1 inhibitor)
Aspirin: Loading dose 150-300 mg, then 75-100 mg daily maintenance. [1]
- Mechanism: Irreversibly acetylates COX-1 → blocks TxA₂ synthesis → inhibits platelet aggregation
- Given to ALL ACS patients unless true allergy (not GI intolerance — use PPI cover)
B. P2Y12 Receptor Inhibitors (Dual Antiplatelet Therapy = DAPT)
A P2Y12 inhibitor is recommended in addition to aspirin, maintained over 12 months unless contraindications or excessive bleeding risk. [1]
| Drug | Mechanism | Dosing | Key Features |
|---|---|---|---|
| Clopidogrel | Irreversible P2Y12 antagonist (prodrug) | 300-600 mg loading → 75 mg daily | Slower onset; variable response (CYP2C19 polymorphism); cheapest |
| Ticagrelor | Reversible P2Y12 antagonist (direct-acting) | 180 mg loading → 90 mg BD | Faster onset, more potent, more predictable; SE: dyspnoea, bradycardia |
| Prasugrel | Irreversible P2Y12 antagonist (prodrug) | 60 mg loading → 10 mg daily | Most potent; PCI-planned only; CI in prior stroke/TIA, age > 75, weight < 60 kg |
High Yield – DAPT Duration
Standard DAPT duration = 12 months post-ACS. Can be shortened to 6 months (high bleeding risk) or extended beyond 12 months (high ischaemic risk, low bleeding risk). After bare-metal stent (BMS): minimum 1 month DAPT. After drug-eluting stent (DES): minimum 6 months, ideally 12 months. [1]
C. GP IIb/IIIa Inhibitors
GP IIb/IIIa inhibitors (abciximab, tirofiban, eptifibatide) — used as adjunct during PCI [1]
- Mechanism: Block the final common pathway of platelet aggregation (GPIIb/IIIa receptor cross-linking)
- Used mainly in cathlab during PCI for heavy thrombus burden
- Not routinely used upstream anymore (increased bleeding risk without clear benefit in the era of potent oral antiplatelets)
Anticoagulants for ACS target the coagulation cascade (thrombin generation and fibrin formation). [1]
| Drug | Mechanism | Route | Key Points |
|---|---|---|---|
| Unfractionated Heparin (UFH) | Potentiates antithrombin III → inhibits thrombin (IIa) and Xa | IV infusion (weight-based, monitor aPTT) | Short half-life, reversible with protamine; preferred if PCI planned soon |
| Low Molecular Weight Heparin (LMWH) — Enoxaparin | Predominantly anti-Xa (via antithrombin III) | SC (1 mg/kg Q12h) | More predictable pharmacokinetics; no routine monitoring needed |
| Fondaparinux | Pure anti-Xa (synthetic pentasaccharide) | SC 2.5 mg daily | Lowest bleeding risk; recommended by ESC for NSTE-ACS if no early invasive strategy; needs UFH supplement if going to PCI |
| Bivalirudin | Direct thrombin inhibitor | IV | Used during PCI; alternative to UFH + GPIIb/IIIa |
ACS Antithrombotic Therapies Summary [1]:
- Aspirin (loading 150-300 mg → 75-100 mg) +
- SC LMWH or IV Heparin (or Fondaparinux, or Bivalirudin if PCI planned) +
- Clopidogrel or Ticagrelor (or Prasugrel if PCI planned) +/-
- GP IIb/IIIa inhibitor (abciximab/tirofiban/eptifibatide — during PCI)
CTM treated as NSTEMI ACS: [1]
- Aspirin 300 mg stat then 100 mg daily
- Enoxaparin 80 mg Q12h (1 mg/kg for 80 kg patient)
- Ticagrelor 180 mg loading then 90 mg BD
- Pantoloc (pantoprazole) 40 mg daily (PPI for GI protection with DAPT)
- Rosuvastatin 20 mg daily
- Echo showed impaired LVEF 40%
- Arranged for coronary angiogram +/- revascularisation
ESC 2023: Timing of invasive strategy based on risk [1]:
| Risk Category | Criteria | Timing |
|---|---|---|
| Very high risk | Haemodynamic instability/cardiogenic shock, recurrent/refractory chest pain, life-threatening arrhythmias, mechanical complications, acute HF, recurrent dynamic ST/T changes | Immediate ( < 2h) |
| High risk | Rise/fall in troponin consistent with MI, dynamic ST/T changes (symptomatic or silent), GRACE score > 140 | Early ( < 24h) |
| Intermediate risk | DM, renal insufficiency (eGFR < 60), LVEF < 40%, early post-infarction angina, prior PCI/CABG, GRACE 109-140 | Within 72h |
| Low risk | No high-risk features | Non-invasive evaluation first |
The case patient had: hypotension, tachycardia, S3, LVEF 40%, elevated troponin, diffuse T-wave changes → very high to high risk → early invasive strategy.
CTM underwent successful PCI with stenting to LAD. [1]
The angiogram images in the lecture show pre-PCI stenosis and post-PCI result [1]. This is consistent with the Wellens syndrome ECG pattern pointing to proximal LAD disease.
Types of revascularisation:
- PCI (Percutaneous Coronary Intervention): Balloon angioplasty + stent deployment. Drug-eluting stents (DES) preferred over bare-metal stents (BMS) — lower restenosis rate.
- CABG (Coronary Artery Bypass Grafting): Preferred for left main disease, 3-vessel disease (especially with DM or reduced LVEF), or anatomy unsuitable for PCI.
8. Secondary Prevention (Long-Term Management)
This is the final and arguably most exam-tested section. The lecture explicitly covers this under "Secondary Prevention" [1].
Aspirin 75-100 mg daily indefinitely. P2Y12 inhibitor (ticagrelor 90 mg BD or clopidogrel 75 mg daily) for 12 months. Clopidogrel if aspirin not tolerated due to hypersensitivity or GI intolerance. [1]
Secondary prevention anti-ischaemic therapy: [1]
- Beta-blockers unless contraindicated — reduce HR, BP, contractility → ↓ O₂ demand; proven mortality benefit post-MI
- ACEI for patients with CHF, LV dysfunction (EF < 40%), hypertension, or diabetes — prevent adverse remodelling; proven mortality benefit
- Calcium antagonists (diltiazem or verapamil) if CI to beta-blockers AND no heart failure — rate-limiting CCBs reduce O₂ demand but can worsen HF
- Nitrates (long-acting or short-acting PRN) in the presence of angina — symptom relief only; no mortality benefit
Why ACEI in ACS with LVEF < 40%?
After MI, the injured myocardium undergoes adverse remodelling — the infarcted area thins and expands, while the non-infarcted myocardium hypertrophies. This leads to progressive ventricular dilatation and heart failure. ACEI block the RAAS → reduce afterload and preload → reduce wall stress → slow remodelling → improve survival. ARBs are an alternative if ACEI not tolerated (cough). [5]
Risk factor modification: [1]
- Stop smoking (single most important modifiable intervention)
- Optimal glycaemic control: HbA1c target 7%
- Blood pressure control in hypertensive patients
- Aggressive lipid lowering with statin: LDL target 1.4-1.8 mmol/L (ESC 2023 for very high-risk patients)
- Diet and weight control
The ESC 2023 lipid-lowering algorithm [1]:
- Start high-intensity statin (e.g. rosuvastatin 20-40 mg or atorvastatin 40-80 mg)
- If LDL not at target after max-dose statin → add ezetimibe
- If still not at target → add PCSK9 inhibitor (evolocumab or alirocumab)
- Target: LDL < 1.4 mmol/L AND ≥ 50% reduction from baseline for very high-risk patients
CTM's discharge medications: [1]
- Aspirin 100 mg daily
- Ticagrelor 90 mg BD
- Pantoloc 40 mg daily
- Rosuvastatin 20 mg daily
- Betaloc (metoprolol) 12.5 mg daily
- Ramipril 1.25 mg daily (ACEI — because LVEF 40%)
- Cardiac rehabilitation arranged — lifestyle modification including smoking cessation
High Yield – Post-ACS Discharge Medications (Mnemonic: ABCDE)
A = Aspirin + another Antiplatelet (DAPT) + ACEI/ARB B = Beta-blocker C = Cholesterol-lowering (statin ± ezetimibe ± PCSK9i) D = Diet, Diabetes control, Don't smoke E = Exercise (cardiac rehab), Education
The lecture ends with arrangement of cardiac rehabilitation [1], which includes:
- Exercise training — structured, supervised programme
- Dietary counselling — Mediterranean diet, weight management
- Smoking cessation — pharmacological (varenicline, NRT) and behavioural support
- Psychosocial support — depression and anxiety screening
- Patient education — understanding medications, warning signs, when to seek help
| Related Lecture | Key Connection |
|---|---|
| GC 088: Sudden Severe Chest Pain (STEMI + Aortic Dissection) [2] | Covers STEMI reperfusion (primary PCI, thrombolysis) and aortic dissection — the other half of the ACS spectrum |
| GC 032: Chest Pain on Exertion (Stable IHD/Angina) [6] | Stable angina is the precursor; the case patient progressed from stable → unstable |
| GC CP02: Clinical Pharmacology of Antiplatelets and Anticoagulation [7] | Detailed pharmacology of aspirin, P2Y12 inhibitors, DOACs, heparin |
| CFB: CVS History Taking [3] | SOCRATES framework for chest pain differentiation |
| GC 089: Syncope and Irregular Heart Beat [8] | Post-MI arrhythmias (VT/VF) as complications |
| GC 084: SOB on Exertion [9] | Post-MI heart failure |
10. Exam Intelligence
| Format | Example Stem |
|---|---|
| MCQ | "A 55-year-old man presents with rest chest pain for 2 hours. ECG shows biphasic T waves in V2-V3. Troponin is mildly elevated. What is the most likely diagnosis?" → Wellens syndrome / NSTEMI |
| SAQ | "List the 4 principal presentations of NSTE-ACS." / "Describe the acute management of NSTEMI." |
| Mini-case | Full case → identify risk factors, interpret ECG/troponin, propose management plan, list discharge medications |
| Data interpretation | ECG showing ST depression or Wellens pattern → identify and manage |
| Trap | Correct Approach |
|---|---|
| Confusing UA with NSTEMI | Both are NSTE-ACS. The only difference is troponin: UA = normal troponin; NSTEMI = elevated troponin |
| Thinking thrombolysis works in NSTEMI | Thrombolysis is ONLY for STEMI — not NSTEMI or UA [5] |
| Giving nitrates to RV infarction | RV infarct depends on preload; nitrates ↓ preload → shock. Check for inferior STEMI + RV involvement (V4R) |
| Missing Wellens syndrome | Pattern appears during pain-free intervals; stress testing is contraindicated |
| Ignoring renal function when interpreting troponin | CKD → chronically elevated troponin; look for rise/fall pattern |
| Forgetting PPI with DAPT | Increased GI bleeding risk with aspirin + P2Y12 → always co-prescribe PPI |
| Not starting ACEI post-MI | If LVEF < 40% or HF or DM or HTN → ACEI is mandatory for secondary prevention |
| Question | Discriminator |
|---|---|
| "Clopidogrel vs Ticagrelor" | Ticagrelor is reversible, faster onset, more potent, given BD, causes dyspnoea. Clopidogrel is a prodrug with CYP2C19-dependent activation (variable response) |
| "UFH vs LMWH" | UFH = IV, short half-life, aPTT monitoring, reversible with protamine → preferred pre-PCI. LMWH = SC, predictable, no monitoring, partially reversible |
| "Fondaparinux vs LMWH" | Fondaparinux = lowest bleeding risk but needs UFH supplement during PCI; LMWH preferred if early invasive planned |
| "STEMI vs NSTEMI" | ECG (ST elevation vs depression/T changes) + the complete vs partial occlusion pathophysiology |
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Q: A 60-year-old man with diabetes presents with 3 hours of rest chest pain. ECG shows 2 mm ST depression in V4-V6. Troponin is elevated. What is the diagnosis and immediate management?
- A: NSTEMI. Immediate: Aspirin 300 mg loading, Ticagrelor 180 mg loading, Enoxaparin 1 mg/kg SC, IV nitrate (if SBP > 90), morphine for pain, beta-blocker (if no HF/hypotension), PPI. Arrange early coronary angiography within 24h (high risk).
-
Q: What are the four principal presentations of NSTE-ACS?
- A: Rest angina (usually > 20 min), new-onset angina (at least CCS III), increasing/crescendo angina (↑ by ≥ 1 CCS class to ≥ CCS III), post-MI angina.
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Q: What is Wellens syndrome? What is the management?
- A: Pre-infarction ECG pattern: history of angina + biphasic or deeply inverted T waves in V2-V4 + normal/minimally elevated troponin + no pathological Q waves. Indicates critical proximal LAD stenosis. 75% progress to MI within days. Management: urgent coronary angiography — stress testing is CONTRAINDICATED.
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Q: List 5 causes of elevated troponin that are NOT ACS.
- A: Myocarditis, pulmonary embolism, acute/chronic heart failure, septic shock, arrhythmias (tachycardia-mediated), renal dysfunction, post-cardioversion, post-ablation.
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Q: What discharge medications would you prescribe for a patient post-NSTEMI with LVEF 35% who underwent PCI with DES?
- A: Aspirin 100 mg daily (indefinite), Ticagrelor 90 mg BD (12 months), PPI, high-intensity statin, beta-blocker (bisoprolol/carvedilol — LVEF < 40%), ACEI/ARB (LVEF < 40%), ± MRA if symptomatic HF. Smoking cessation, cardiac rehab.
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Q: Why is thrombolysis NOT indicated in NSTEMI?
- A: NSTEMI has partial coronary occlusion (non-occlusive thrombus) with preserved flow. Thrombolysis carries bleeding risk without benefit (the artery is already partially patent). Thrombolysis is reserved for STEMI (complete occlusion) when PCI is not available within 2 hours.
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Q: A patient with ACS has BP 85/55 and ECG showing inferior ST elevation with ST depression in aVL. What should you NOT give and why?
- A: Do NOT give nitrates (↓ preload in RV-dependent circulation → haemodynamic collapse). Check V4R for RV involvement. Give IV fluids instead to maintain preload.
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Q: What are the ESC 2023 LDL targets for a patient post-ACS?
- A: LDL < 1.4 mmol/L AND ≥ 50% reduction from baseline. Achieve with high-intensity statin ± ezetimibe ± PCSK9 inhibitor.
High Yield Summary
Acute Coronary Syndromes (NSTE-ACS) encompass UA and NSTEMI — distinguished by troponin (negative in UA, elevated in NSTEMI). Both result from non-occlusive coronary thrombus on ruptured plaque (vs. complete occlusion in STEMI).
Diagnosis: 12-lead ECG within 10 min (look for ST depression, T-wave inversion, Wellens pattern) + serial hs-troponin (0h/1h algorithm).
Wellens syndrome = biphasic/inverted T waves V2-V4 in pain-free interval → critical proximal LAD → urgent angiography (NO stress testing).
Acute Mx: Anti-ischaemic (O₂ if SpO₂ < 90%, nitrates if SBP > 90, morphine, BB, bed rest) + Antithrombotic (DAPT: aspirin + ticagrelor/clopidogrel + anticoagulant: LMWH or UFH) + risk-stratify → invasive strategy based on GRACE score.
Secondary prevention (ABCDE): Aspirin + P2Y12 inhibitor (12 months), ACEI (if EF < 40%/HF/DM/HTN), Beta-blocker, statin (LDL < 1.4), smoking cessation, cardiac rehab, glycaemic and BP control.
Thrombolysis is NEVER used in NSTEMI/UA — only in STEMI when PCI unavailable within 2h.
Active Recall - Accelerating Chest Pain: ACS
[1] Lecture slides: GC 028. Accelerating chest pain_Acute coronary.pdf (all pages) [2] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (p1, p63) [3] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (p15, p19) [4] Senior notes: Block A - Accelerating chest pain_ Acute Coronary Syndromes.pdf (p1-2) [5] Senior notes: Maksim Medicine Notes.pdf (p7, p11) [6] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf [7] Lecture slides: GC CP02 Clinical pharmacology of anti-platelets and anticoagulation.pdf [8] Lecture slides: GC 089. Syncope and irregular heart beat.pdf [9] Lecture slides: GC 084. Shortness of breath on exertion.pdf [10] Senior notes: Block A - Cardiology Data Interpretation.pdf (p6) [11] Senior notes: Block A - Cardiology Interactive Tutorial.pdf (p4-5) [12] Senior notes: Ryan Ho Cardiology.pdf (p54, p56, p58) [13] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p384) [14] Senior notes: Block A - WCS32 Chest pain on exertion_ ischaemic heart disease; angina pectoris.pdf (p21) [15] Senior notes: Block A - Chest Pain - Department of Medicine.pdf (p1)
GC027 Abnormal Bleeding After Tooth Extraction
Prolonged or excessive hemorrhage following tooth extraction, often indicating a local complication such as disrupted clot (dry socket) or an underlying coagulopathy.
GC029 Am I Prescribing The Right Drug
A clinical decision-making framework that guides physicians in evaluating whether a selected medication is the most appropriate choice for a patient based on indication, efficacy, safety profile, patient-specific factors, and evidence-based guidelines.