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.
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
Historical lecture figure: atherothrombosis accounted for 22.3% of deaths in the source dataset shown in the deck [1]. Do not quote this as a current global estimate without checking a contemporary dataset.
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.
Hospital Mortality Trends (NRMI Registry)
The lecture presents 1994–2006 NRMI registry data showing declining in-hospital mortality over that period [1]:
| Year | STEMI Mortality | NSTEMI Mortality | All ACS Patients |
|---|---|---|---|
| 1994 | ~11.5% | ~7.1% | ~10.4% |
| 2006 | ~8.0% | ~5.2% | ~6.3% |
Mortality by clinical/ECG category [1]:
| Category | In-Hospital Mortality | 30-Day Mortality |
|---|---|---|
| Unstable angina | 0.8% | 1.1% |
| Non-Q-wave MI | 2.9% | 3.8% |
| Q-wave MI | 5.8% | 7.2% |
| ST-elevation | 5.3% | 6.4% |
| No ST-elevation | 2.5% | 3.4% |
These historical figures illustrate improving acute care and greater early risk in STEMI in that registry; they should not be used as present-day counselling figures.
- 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
Contraindications to anticoagulant therapy [1]:
Absolute: Active bleeding, severe bleeding diathesis, severe thrombocytopenia, recent neurosurgery/ocular surgery (excluding cataract)/intracranial bleed.
Relative: Moderate thrombocytopenia, brain metastases, recent major trauma, recent major abdominal surgery (< 1–2 days), GI/GU bleeding within 14 days, endocarditis, severe hypertension (SBP > 200 and/or DBP > 120 mmHg).
Lecture model: NSTE-ACS commonly follows plaque disruption with a non-occlusive or intermittent thrombus. Treat this as a useful model, not an absolute angiographic rule [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, or thyrotoxicosis may produce a supply-demand mismatch. With acute injury and objective ischaemia this is usually classified as type 2 MI, not plaque-rupture (type 1) NSTE-ACS [20] |
| Infection / Inflammation | Systemic inflammation destabilises plaques and promotes thrombosis |
Key Distinction: NSTEMI vs STEMI
NSTEMI/UA often involves non-occlusive or intermittently occlusive atherothrombosis, but the anatomy cannot be inferred reliably from the ECG label alone. NSTEMI may occasionally have a completely occluded culprit artery, and not every STEMI has persistent complete occlusion.
The actionable distinction at presentation is persistent ST elevation (or another ECG pattern suggesting acute coronary occlusion) versus no persistent ST elevation. Both groups require integration of symptoms, serial ECGs, hs-cTn and, when indicated, urgent angiography [18].
Fibrinolysis has proven benefit for eligible STEMI patients when timely primary PCI is unavailable, but it has no established benefit and excess bleeding risk in NSTE-ACS; therefore it is not used for NSTEMI/UA [18].
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 | Family history is relevant, but this does not meet the usual definition of premature CAD in a male first-degree relative (< 55 years) |
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 |
Causes of acute chest pain by frequency (Fruergaard et al.) [1]:
- Gastrointestinal — 42%
- Ischaemic heart disease — 31%
- Chest wall syndrome — 28%
- Pericarditis — 4%
- Pulmonary embolism — 2%
- Pleuritis — 2%
The expanded ESC 2011/2020 differential also includes vascular causes (aortic dissection, symptomatic aortic aneurysm, stroke), haematological causes (sickle cell crisis, anaemia), and orthopaedic/infectious causes (cervical discopathy, rib fracture, herpes zoster) [1].
The slide's body map deliberately shows substantial overlap: cardiac ischaemia may be retrosternal, left- or right-sided, epigastric, interscapular, or radiate to either shoulder, arm, jaw, or neck [1]. Location alone cannot rule ACS in or out. Use the quality, time course, provoking/relieving factors, associated autonomic symptoms, risk profile, examination, ECG and hs-cTn together.
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 = low-normal blood pressure with tachycardia — concerning in ACS and deserving repeat assessment for hypoperfusion, but not by itself diagnostic of shock
- S3 gallop = indicates ventricular dysfunction / heart failure — volume overload of a failing ventricle
- These findings together raise concern for LV impairment or evolving haemodynamic compromise; shock requires clinical evidence of tissue hypoperfusion, not a single borderline blood-pressure reading
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)
Several ECG slides carry more teaching than their captions [1]:
- De Winter pattern: upsloping ST depression at the J point across the anterior precordial leads with tall, symmetric T waves (often with slight aVR elevation). In the right clinical context this suggests acute proximal LAD occlusion and warrants immediate expert review and an occlusion-MI pathway, not reassurance because there is no classic ST elevation.
- Hyperacute T waves: broad, bulky, symmetric T waves that are disproportionately large for the QRS can precede conventional ST elevation. Compare with prior/serial tracings and the clinical picture; isolated tall T waves also have non-ischaemic mimics.
- Dynamic change matters: the paired ECGs show an initially near-normal tracing evolving into clear precordial ST-T abnormalities. Repeat the ECG when pain recurs, wanes, or the first tracing is non-diagnostic; a single normal ECG does not exclude ACS [18].
- Posterior/RV extensions: with ongoing symptoms and an inconclusive 12-lead ECG, record V7–V9 for suspected posterior occlusion and V3R–V4R for suspected RV infarction [18].
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 high-risk reperfusion pattern classically associated with severe proximal LAD disease. Two morphologies are commonly described:
- Biphasic T waves (initial positive, terminal negative) in V2-V3, about 25% of classic cases
- Deeply inverted, symmetric T waves in V2-V4 (sometimes V1-V6), about 75%
The deck reverses these percentages on its labelled Type 1/Type 2 slide, and Type A/Type B nomenclature is used inconsistently across publications. For exams and practice, identify the morphology and clinical context, not the letter label [21].
Critical exam points:
- These ECG changes appear during pain-FREE intervals (not during chest pain)
- Troponin may be non-elevated or elevated; a significant elevation does not make the pattern safe
- 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 — complicates repolarisation assessment (use concordance-based criteria such as modified Sgarbossa alongside the clinical picture). New LBBB alone is not automatically STEMI, but BBB with ongoing symptoms highly suspicious for ischaemia requires immediate occlusion-MI management [18]
- 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][18]:
- Measure hs-Tn at presentation (0h)
- Repeat at 1h (or 2h depending on assay)
- Rule-out: Very low 0h value and/or a low value with a small absolute delta → MI unlikely, provided the clinical/ECG context is low risk
- Rule-in: High 0h value or a sufficiently large absolute delta → high probability of MI, but still integrate evidence of ischaemia and the cause of injury
- Observe: Intermediate values → repeat at 3h, continue monitoring
Thresholds and deltas are assay-specific; do not transplant a numeric cut-off from one hs-cTnT/hs-cTnI assay to another. An elevated troponin means myocardial injury. Acute MI requires a rise/fall with at least one value above the 99th-percentile upper reference limit plus clinical evidence of acute ischaemia (symptoms, new ischaemic ECG change, new ischaemic wall-motion abnormality/loss of viable myocardium, or coronary thrombus) [18][20].
The case patient's hs-TnT = 100 is elevated and, together with acute ischaemic symptoms and the dynamic anterior T-wave pattern, supports 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 (acute or chronic myocardial injury; not a laboratory false positive) |
| Post-procedural | Cardioversion, catheter ablation/biopsy, PCI |
ESC 2011 comprehensive list of conditions associated with elevated troponin [1]:
- Chronic or acute renal dysfunction
- Severe congestive heart failure (acute and chronic)
- Hypertensive crisis
- Tachy- or bradyarrhythmias
- Pulmonary embolism, severe pulmonary hypertension
- Inflammatory diseases (e.g. myocarditis)
- Acute neurological disease (stroke, subarachnoid haemorrhage)
- Aortic dissection, aortic valve disease, hypertrophic cardiomyopathy
- Cardiac contusion, ablation, pacing, cardioversion, endomyocardial biopsy
- Hypothyroidism
- Apical ballooning syndrome (Takotsubo cardiomyopathy)
- Infiltrative diseases (amyloidosis, haemochromatosis, sarcoidosis, scleroderma)
- Drug toxicity (adriamycin, 5-fluorouracil, Herceptin, snake venoms)
- Burns (> 30% BSA)
- Rhabdomyolysis
- Critically ill patients (respiratory failure, sepsis)
Renal insufficiency and troponin prevalence (creatinine > 1.5 mg/dL) [1]:
- Before dialysis: Troponin T elevated in 15–20%, Troponin I in 10%
- On dialysis: Troponin T elevated in 17–30%, Troponin I in 4–15%
Troponin in Renal Dysfunction
Chronically elevated troponin in CKD is common and usually represents real chronic myocardial injury, not a false-positive assay. Diagnose acute MI using the trajectory plus evidence of acute ischaemia; a changing value alone may still reflect acute non-ischaemic injury. Age, renal function, time from symptom onset and sex all influence measured hs-cTn concentrations [18][20].
The lecture's biomarker timeline slide shows [1]:
- CK-MB: The historical curve rises and falls faster than conventional troponin, but hs-cTn is the preferred contemporary biomarker; routine parallel CK-MB testing adds little in most ACS pathways
- 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
The lecture's hs-cTn diagnostic pathway also provides illustrative risk estimates for each category [1]:
| hs-cTn Category | MI at Index Visit | 30-Day MACE |
|---|---|---|
| Rule-out (low risk) | < 0.3% | < 0.5% |
| Observe (intermediate risk) | ~10% | 15–20% |
| Rule-in (high risk) | > 65% | > 70% |
These percentages are deck-specific and must not be applied to a different assay, population or pathway. A biochemical zone is not a disposition order.
Disposition after hs-cTn categorisation [1][18]:
- Rule-out → consider discharge only after clinical risk assessment, ECG review and exclusion of other dangerous diagnoses; outpatient testing is selective rather than automatic
- Observe → Ward admission, repeat hs-cTn at 3h + echocardiography
- Rule-in → CCU admission + early coronary angiography
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
It is not the test for haemodynamically unstable patients, confirmed MI requiring an invasive strategy, or an ECG suggesting acute coronary occlusion. Heavy calcium and stents can produce blooming artefact and overestimate stenosis; therefore a normal high-quality study is generally more decisive than an apparently moderate lesion in a heavily calcified vessel.
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
The slide juxtaposes perfusion imaging (a map of inducible downstream ischaemia) with CTCA/invasive angiography (a map of coronary anatomy). These answer different questions. They are used primarily after MI has been ruled out in stable, non-high-risk patients or for later risk stratification—not as a delay to angiography in high-risk ACS.
The ESC 2023 guidelines recommend intravascular imaging to guide PCI in ACS [1]:
- Clear culprit lesion suitable for PCI → IVUS or OCT can define lesion morphology, vessel size, stent expansion and edge complications; the deck displays this as a Class IIa strategy, not “Class Ia” [1]
- No clear culprit lesion (e.g. multivessel disease, hazy lesion, calcification) → Intravascular imaging, preferably OCT, to identify the culprit (Class IIb)
Intravascular imaging findings that may be identified include: plaque rupture, plaque erosion, calcified nodule, spontaneous coronary artery dissection (SCAD), or no significant lesion.
If angiography shows no clear culprit, do not stop at “normal coronaries.” The slide's right-hand pathway uses OCT/IVUS to look for subtle plaque disruption or SCAD, then echocardiography and cardiac MRI when needed to distinguish MINOCA mechanisms from mimics such as myocarditis or takotsubo [1].
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 |
This table is useful for recognising ominous clinical features, but its fixed troponin cut-offs and age bands pre-date hs-cTn assays and current pathways. Do not use it to overrule an assay-specific hs-cTn algorithm or contemporary GRACE-based assessment [18].
The case patient (CTM) has multiple high-risk features: accelerating rest symptoms, an S3, tachycardia/low blood pressure, anterior ischaemic T-wave changes and 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.
The deck includes the GRACE nomogram to make an important visual point: risk rises continuously, not in neat steps. A score > 140 is one ESC high-risk criterion for considering angiography within 24 hours, but current ESC 2023 strategy is not a universal “< 109 / 109–140 / > 140” timing table. Confirmed NSTEMI warrants an inpatient invasive strategy; immediate angiography is driven by very-high-risk clinical instability, and early angiography (< 24 h) should be considered for high-risk features [18].
7. Management
Primary anti-ischaemic therapeutic measures [1]:
| Measure | Details | Rationale |
|---|---|---|
| Monitoring and activity | Continuous ECG/defibrillation readiness for suspected ACS; titrate activity to stability rather than prescribing prolonged bed rest automatically | Detects life-threatening arrhythmia and deterioration |
| Oxygen | Give for SpO₂ < 90%; do not give routinely to a normoxic patient | Corrects hypoxaemia; routine oxygen above 90% has no clinical benefit [18] |
| Nitrates | Sublingual for symptom relief; IV only for selected persistent symptoms with adequate BP | Venodilation reduces preload; symptom response is not diagnostic of ACS |
| Morphine / opioid | Consider carefully for severe ongoing pain, IV and titrated—not a routine component of “MONA” | Can cause hypotension, nausea and delayed absorption/onset of oral P2Y12 inhibitors [18] |
| 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 | |
| Symptomatic bradycardia | Treat according to the current local resuscitation algorithm | Atropine is a bradycardia intervention, not routine ACS therapy |
Anti-ischaemic therapies — how to read the historical slide [1]:
| Agent | Mechanism | Mortality Effect |
|---|---|---|
| Beta-blockers | ↓ HR, BP, contractility via β1 antagonism | Useful when tachycardic/hypertensive and stable; avoid in shock risk, acute HF, significant bradycardia or AV block. Do not infer a universal mortality benefit for every modern NSTE-ACS patient |
| Nitrates | Venodilation ↓ preload; coronary vasodilation | No mortality benefit |
| Calcium channel blockers | Vasodilation ± ↓ HR ± ↓ contractility | No clear mortality benefit; short-acting nifedipine alone increases reinfarction |
| Ranolazine / trimetazidine / nicorandil | Alternative anti-anginal mechanisms | These are not routine acute ACS mortality-reducing therapies; use is jurisdiction- and indication-specific |
Short-Acting Nifedipine Warning
Short-acting nifedipine used alone (without a beta-blocker) is associated with increased reinfarction rate in NSTE-ACS. If a dihydropyridine CCB is needed, always combine with a beta-blocker. [1]
Nitrates Caution
Do NOT give nitrates if:
- Hypotension or a clinically important fall from baseline (case BP 98/65 is borderline—reassess before dosing)
- Known RV infarction (nitrates ↓ preload → catastrophic drop in RV output)
- Phosphodiesterase-5 inhibitor use within the relevant interval (commonly 24 h for sildenafil/vardenafil and 48 h for 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 promptly to ACS patients unless there is a true contraindication; assess active bleeding and allergy. A PPI is used for patients at increased GI-bleeding risk, not automatically as a substitute for evaluating intolerance [19].
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 | Used when proceeding to PCI after anatomy is known; contraindicated after prior stroke/TIA. Age ≥75 and weight < 60 kg require caution/dose adjustment rather than being identical absolute contraindications [18] |
| Cangrelor | Reversible P2Y12 antagonist (direct-acting, ATP analogue) | IV bolus + infusion | Onset 2 min, offset 30–60 min; used in P2Y12-naïve patients undergoing PCI; no CYP interaction [1] |
High Yield – DAPT Duration
Default DAPT after ACS is at least 12 months when bleeding risk is not high, but duration and possible transition to P2Y12 monotherapy are individualised to bleeding risk, ischaemic risk, PCI details and any need for long-term anticoagulation. The old BMS-versus-DES minimum-duration rule is not the contemporary organising principle [19].
Do Not Routinely Pretreat NSTE-ACS
If an early invasive strategy is planned within 24 hours and coronary anatomy is unknown, routine upstream P2Y12 loading is not recommended. Load at PCI once the strategy/anatomy is defined. If angiography will be delayed beyond 24 hours, upstream clopidogrel or ticagrelor may be considered after bleeding-risk assessment [18][19].
Incremental benefit of antiplatelet regimens (lecture slide data) [1]:
| Regimen | CV Death/MI/Stroke | Major Bleeding |
|---|---|---|
| No antiplatelet | 20% | 0.8% |
| Aspirin alone | 15% (↓25%) | 1.3% |
| Aspirin + clopidogrel | 12% (↓20%) | 1.8% |
| Aspirin + prasugrel | 10% (↓18%) | 2.4% |
| Aspirin + ticagrelor | 10% (↓33% vs clopidogrel) | 1.8% |
This historical graphic combines results from different trials and eras; it illustrates the efficacy–bleeding trade-off but is not a valid head-to-head numerical comparison between all regimens.
C. GP IIb/IIIa Inhibitors
GP IIb/IIIa inhibitors (principally tirofiban or eptifibatide in current practice) — cath-lab bailout rather than routine upstream therapy [1][18]
- Mechanism: Block the final common pathway of platelet aggregation (GPIIb/IIIa receptor cross-linking)
- Consider bailout for no-reflow or a thrombotic complication during PCI
- Do not routinely add them before angiography; the deck's abciximab dosing table is historical and should not be memorised as a standing protocol [18]
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 (usual ACS dose 1 mg/kg Q12h) | More predictable pharmacokinetics; renal dose adjustment is required, and extremes of weight/renal function need protocol-based review [18] |
| 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 |
Detailed anticoagulant comparison [1]:
| Feature | UFH | Enoxaparin | Fondaparinux | Bivalirudin |
|---|---|---|---|---|
| Half-life | 1–2 h | 5–7 h | 17–21 h | 25 min |
| Molecular weight | 3–30 kDa | 2–10 kDa | 1.7 kDa | 2.2 kDa |
| Metabolism | Hepatic | Hepatic | Excreted largely unchanged | Plasma proteases |
| Elimination | Extra-renal | Renal | Renal | Renal |
| HIT incidence | 1–3% | ≤0.2% | Negligible | None |
| Antidote | Protamine | Protamine (partial) | None | None |
| Clot-bound thrombin | Inactive | Inactive | Inactive | Active (inhibits clot-associated thrombin) |
Advantages of LMWH over UFH [1]:
- Better bioavailability → SC administration sufficient
- Reduced protein binding → more predictable response, no routine monitoring
- Longer half-life → once- or twice-daily dosing
- Lower incidence of HIT (reduced platelet factor 4 binding)
- Lower risk of heparin-associated osteoporosis
The slide visually stacks aspirin, a P2Y12 inhibitor, parenteral anticoagulation and optional GP IIb/IIIa therapy. It is a menu of drug classes, not a prescription to give every drug immediately [1]:
- Give aspirin unless contraindicated.
- Choose one parenteral anticoagulant according to the invasive plan, renal function, bleeding risk and local protocol.
- Choose/timestamp the P2Y12 inhibitor according to anatomy and strategy; avoid routine pretreatment before early angiography.
- Reserve GP IIb/IIIa inhibition for cath-lab bailout, not routine “plus/minus” use [18].
What the lecture case received (historical case record, not a universal order set): [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
The ticagrelor load before anatomy reflects the case/deck. Under current guidance, routine P2Y12 pretreatment would be avoided when early (< 24 h) angiography is planned; the decision also depends on bleeding risk and expected delay [18][19].
ESC 2023: Timing of invasive strategy based on risk [1]:
| Risk Category | Criteria | Timing |
|---|---|---|
| Very high risk | Haemodynamic instability/cardiogenic shock, refractory/recurrent ongoing chest pain, life-threatening arrhythmia/cardiac arrest after presentation, mechanical complication, acute HF from ongoing ischaemia, recurrent dynamic ECG changes (especially intermittent ST elevation) | Immediate—as soon as possible |
| High risk | Confirmed NSTEMI by a recommended hs-cTn algorithm, dynamic ST/T changes, transient ST elevation, or GRACE > 140 | Inpatient invasive strategy; early < 24 h should be considered |
| Non-high risk | No very-high/high-risk feature | Inpatient angiography for high suspicion of UA; selective invasive strategy after appropriate testing when suspicion is low [18] |
Early vs delayed invasive strategy — meta-analysis of 17 RCTs (n = 10,209) [1]:
| Outcome | RR (95% CI) | Significance |
|---|---|---|
| All-cause mortality | 0.90 (0.78–1.04) | NS |
| Myocardial infarction | 0.86 (0.63–1.16) | NS |
| Recurrent ischaemia | 0.57 (0.40–0.81) | Favours early |
| Admission for heart failure | 0.66 (0.43–1.03) | NS (trend) |
| Major bleeding | 0.86 (0.68–1.09) | NS |
Key finding: Early invasive strategy significantly reduces recurrent ischaemia without increasing major bleeding, supporting the ESC recommendation for early angiography in high-risk patients.
The case patient had elevated troponin and extensive ischaemic T-wave changes, so he is at least high risk and needs an inpatient invasive strategy. He becomes very high risk only if the low BP/S3 corresponds to genuine haemodynamic instability or acute HF, or if he has refractory pain or other very-high-risk criteria.
ESC 2023 risk stratification and therapeutic strategy [1]:
Note the ESC 2023 simplification: patients are categorised as very high risk, high risk, or non-high risk (rather than the previous four-tier system). Non-high-risk patients may undergo either selective or inpatient invasive strategy depending on clinical suspicion [1].
CTM underwent successful PCI with stenting to LAD. [1]
The image-only angiogram sequence is the visual confirmation of the case narrative: the initial left-coronary runs show the critical LAD culprit with poor downstream opacification; after PCI the LAD lumen and distal flow are restored. The final case slide explicitly confirms successful LAD stenting [1]. This closes the diagnostic loop from anterior reperfusion T waves → LAD culprit → revascularisation.
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].
Default after ACS: low-dose aspirin plus an oral P2Y12 inhibitor for at least 12 months if bleeding risk is not high; individualise shortening, de-escalation, monotherapy and treatment with concomitant oral anticoagulation. [19]
Secondary prevention anti-ischaemic therapy: [1]
- Beta-blockers — indicated particularly with LVEF ≤40%, HF, arrhythmia, hypertension or ongoing angina; avoid assuming every patient with preserved EF requires indefinite therapy solely because of a remote 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
For this case, LVEF 40% gives a clear reason for evidence-based post-MI LV-dysfunction therapy. Reassess EF and symptoms after recovery rather than treating the slide's discharge list as immutable.
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)
- Individualised glycaemic control (the slide shows HbA1c < 7% / < 53 mmol/mol as a common goal, not a universal target)
- Individualised blood-pressure control (the slide's < 130/80 mmHg goal is “if tolerated” and must account for frailty, symptoms and comorbidity)
- Aggressive lipid lowering with statin: LDL target < 1.4 mmol/L (< 55 mg/dL) (ESC 2023 for very high-risk patients)
- Diet and weight control
- Annual influenza vaccination
- Promote drug adherence and persistence
- Psychosocial management
The ESC 2023 lipid-lowering algorithm [1]:
During admission:
| Prior Treatment | Action |
|---|---|
| LLT-naïve (irrespective of LDL-C) | Initiate high-potency, high-dose statin (Class I); consider combination with ezetimibe (Class IIb) |
| On low-potency/low-dose statin | Change to high-potency, high-dose statin (Class I); consider adding ezetimibe (Class IIb) |
| On highest tolerated statin, LDL-C ≥1.4 mmol/L | Add ezetimibe (Class I) |
| On highest tolerated statin + ezetimibe, LDL-C ≥1.4 mmol/L | Add PCSK9 inhibitor (evolocumab or alirocumab) (Class I) |
Outpatient follow-up (4–6 week intervals):
- Reassess LDL-C at each visit
- If LDL-C ≥1.4 mmol/L on max statin → add ezetimibe (Class I)
- If LDL-C ≥1.4 mmol/L on max statin + ezetimibe → add PCSK9 inhibitor (Class I)
Target: LDL < 1.4 mmol/L (< 55 mg/dL) AND ≥50% reduction from baseline for very high-risk patients.
The lower-right mechanism diagram shows where the add-on drugs act: ezetimibe blocks intestinal NPC1L1-mediated cholesterol absorption; statins inhibit hepatic HMG-CoA reductase; bempedoic acid inhibits upstream ATP citrate lyase; monoclonal PCSK9 inhibitors and inclisiran increase LDL-receptor availability by inhibiting PCSK9 protein or synthesis, respectively [1].
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
The discharge plan should also include [1]:
- Explain long-term treatment rationale to the patient
- Educate about lifestyle modification (diet, exercise, smoking cessation)
- Consider mental and emotional health — screen for depression and anxiety
- Arrange outpatient review to manage comorbidities and discuss patient goals and preferences
| 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 |
|---|---|
| Calling every non-elevated troponin “UA” | UA requires a compatible ischaemic syndrome after MI is excluded; many such patients have a non-ACS diagnosis. NSTEMI requires acute injury plus evidence of ischaemia, not merely any 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 commonly causes real chronic myocardial injury; use serial change and evidence of ischaemia, not “false positive” language |
| Treating PPI as automatic with DAPT | Co-prescribe a PPI when GI-bleeding risk is increased; assess history, age, concomitant anticoagulants/NSAIDs and local guidance [19] |
| Loading a P2Y12 inhibitor before early angiography in every NSTEMI | Routine pretreatment before anatomy is known is not recommended when angiography is expected within 24 h [18] |
| 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" | Presentation phenotype: persistent ST elevation/occlusion-equivalent pattern versus no persistent ST elevation, then integrate hs-cTn and clinical evidence. Do not infer culprit patency from the label alone |
High Yield Summary
-
Acute Coronary Syndromes (NSTE-ACS)
- encompass UA and NSTEMI. NSTEMI requires a rise/fall in hs-cTn above the 99th percentile plus evidence of acute ischaemia; UA is less common in the hs-cTn era. Avoid equating ECG labels rigidly with “partial” versus “complete” occlusion.
-
Diagnosis
- 12-lead ECG within 10 min plus serial ECGs and an assay-specific hs-cTn 0/1h or 0/2h pathway. Recognise de Winter/hyperacute T waves and other occlusion equivalents that need immediate reperfusion assessment.
-
Wellens syndrome
- = biphasic/inverted T waves V2-V4 in pain-free interval → critical proximal LAD → urgent angiography (NO stress testing).
-
Acute Mx
- Monitor; oxygen only if SpO₂ < 90%; nitrates only if haemodynamically suitable; opioid only for severe pain. Give aspirin and one protocol-selected anticoagulant. Do not routinely pretreat with a P2Y12 inhibitor before early angiography; match invasive timing to clinical risk.
-
Secondary prevention (ABCDE)
- Individualised antiplatelet strategy (default DAPT for at least 12 months if bleeding risk is not high), high-intensity statin with stepwise add-on therapy, ACEI/ARB and beta-blocker when indicated by LV dysfunction/HF or another indication, smoking cessation, cardiac rehab, and individualised BP/glycaemic control.
-
Fibrinolysis is not used for NSTEMI/UA
- it is reserved for eligible STEMI presentations when timely primary PCI (within 120 min from diagnosis) cannot be delivered [18].
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) [18] Byrne RA, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J. 2023;44:3720–3826. [19] Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes — Top Things to Know. American Heart Association, 2025. [20] Thygesen K, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018;72:2231–2264. [21] Patel S, et al. Wellens' Syndrome: a sign of impending myocardial infarction. Cureus. 2022;14:e25584.
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.