GC032 Chest Pain On Exertion: Ischaemic Heart Disease; Angina Pectoris
Angina pectoris is episodic chest pain or discomfort caused by transient myocardial ischemia due to an imbalance between myocardial oxygen supply and demand, typically provoked by exertion or stress and relieved by rest or nitrates.
Chest Pain on Exertion: Ischaemic Heart Disease & Angina Pectoris
The Big Idea: This lecture, delivered by Prof. Hung-Fat Tse (Chair Professor of Cardiovascular Medicine, HKU), walks through a clinical case of a 49-year-old male smoker presenting with exertional chest pain. It covers the full spectrum of stable ischaemic heart disease (IHD) — from the pathophysiology of atherosclerosis driving myocardial oxygen supply-demand mismatch, through systematic clinical assessment (history, examination, non-invasive and invasive investigations), to comprehensive management including lifestyle, pharmacotherapy, and revascularisation. It also touches on special entities: Prinzmetal variant angina, cardiac syndrome X, and congenital coronary anomalies. [1]
How it fits in the curriculum:
- This is the foundation lecture for coronary artery disease. The ACS lecture (GC 028 / WCS28) builds directly on it — same patient, a few years older, disease progressed because he didn't quit smoking [2].
- Links to: hypertension (GC 058), lipid disorders, heart failure (GC 084), sudden severe chest pain/STEMI (GC 088), cardiology interactive tutorial, clinical pharmacology of antiplatelets/anticoagulants, and CVS investigations (ECG).
Learning Objectives (inferred from slide structure and supporting tutorial):
- Understand the pathophysiology and etiologies of IHD
- Describe clinical characteristics of angina pectoris using SOCRATES
- Identify cardiovascular risk factors and their physical signs
- Outline non-invasive and invasive investigation strategies
- Describe pharmacological and non-pharmacological management of stable CAD
- Recognise special variants: Prinzmetal angina, cardiac syndrome X, congenital coronary anomalies
Core Concepts and Mechanisms
Angina pectoris is generally defined as a discomfort in the chest or adjacent areas that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. [1]
From first principles: The heart is a muscle that needs oxygen. It gets oxygen from coronary arteries. When a coronary artery is narrowed (usually by atherosclerosis), there is adequate flow at rest but inadequate flow during increased demand (exertion). The myocardium becomes ischaemic → metabolites (adenosine, lactate, bradykinin) accumulate → stimulate chemosensitive and mechanosensitive cardiac receptors → afferent signals travel via cardiac sympathetic nerves → upper 5 thoracic sympathetic ganglia → upper 5 thoracic spinal cord dorsal roots → convergence with somatic afferents from the chest wall, arm, jaw → this is why angina is "referred" to these areas. [1]
Why Diabetics Get Silent Ischaemia
Silent ischaemia in diabetic patients has been proposed to be related to failed development of the cardiac sensory system because of reduced nerve growth factor. [1] This is why up to 25% of patients with myocardial ischaemia (especially elderly and diabetics) may not experience angina but present with "angina equivalents" — dyspnoea, fatigue, syncope. [3]
The ischaemic cascade is driven by an imbalance between myocardial oxygen supply and demand:
| Factor | Increases O₂ Demand | Decreases O₂ Supply |
|---|---|---|
| Physiological | Exercise, emotion, eating, cold environment (the "4 Es") | — |
| Pathological | Hypertension, aortic stenosis, HOCM, tachycardia, thyrotoxicosis | Coronary atherosclerosis, coronary spasm, anaemia, hypoxia, hyperviscosity |
Why does this matter clinically? A patient with stable angina from a fixed 70% coronary stenosis may be fine at rest. But add anaemia (reduced O₂ carrying capacity), or thyrotoxicosis (increased heart rate and demand), and you can tip them into ischaemia even with the same degree of stenosis. This is why the lecture emphasises checking TFT and haemoglobin. [1]
The dominant cause is ATHEROSCLEROSIS OF CORONARY ARTERIES. [1]
| Category | Specific Causes |
|---|---|
| Atherosclerotic | The overwhelming majority |
| Primary cardiac (non-atherosclerotic) | Coronary spasm, coronary arteritis, coronary dissection, coronary artery anomalies, radiation-induced disease, myocardial bridging, aortic stenosis, HOCM, dilated cardiomyopathy, tachycardia |
| Primary non-cardiac | Anaemia, sickle cell disease, hypoxaemia, CO poisoning, hyperviscosity (polycythaemia), hyperthyroidism, phaeochromocytoma |
The lecture devotes multiple slides (slides 12–16) to this. The process in sequence:
- Endothelial injury — from risk factors (smoking, hypertension, dyslipidaemia, diabetes)
- LDL accumulation in intima → oxidised LDL provokes inflammatory response
- Monocyte recruitment → differentiate into macrophages → engulf oxidised LDL → become foam cells → form fatty streaks
- Smooth muscle cell migration from media to intima → produce collagen → fibrous cap forms over lipid/necrotic core → atheromatous plaque
- Plaque progression → stable plaque (thick cap, small core) vs. vulnerable/unstable plaque (thin cap, large lipid core) → rupture → thrombus → ACS
Accumulated LDL-C years concept — the longer and higher your LDL exposure, the greater your CAD risk. This is why early intervention matters. [1]
CVD is the #1 Killer
IHD remains the number one cause of death in men and women (27% of deaths). [1] The initial manifestation of IHD is angina pectoris in 50% of cases, and about 50% of patients presenting with ACS have preceding angina.
Within 12 months of initial diagnosis, 10% to 20% of patients with diagnosis of stable angina progress to MI or unstable angina. [1]
This was directly examined:
Past paper 2022 Q34: "What is the percentage of patients presenting with stable angina that progress to ACS within 12 months?" → Answer: C. 10–20% [4]
Other key epidemiological points from the lecture:
- Among persons 60–79 years: ~25% of men and ~16% of women have CHD; these figures rise to 37% and 23% in those > 80 years [1]
- Incidence in women after menopause is similar to that of men [1]
- Annual MI rate in patients with symptomatic angina: 3–3.5%/year [1]
Clinical Approach: The Case of CTM, M/49
The lecture is anchored around a clinical case that reappears throughout:
Presentation (Slides 2, 26):
- 49-year-old male, 3-month history of on-and-off retrosternal discomfort while walking back to office after lunch
- Constricting in character, relieved by rest
- Family Hx: Father died of CAD at age 60–65
- Social Hx: Chronic smoker, non-drinker
- No past history of cardiovascular disease [1]
Clarify the details of the pain using SOCRATES [1]
| SOCRATES | Angina Pectoris Features | Why This Matters |
|---|---|---|
| Site | Retrosternal or slightly to left, occasionally at extrathoracic sites | Cardiac pain is visceral → poorly localised; patient often uses palm/fist (Levine's sign), NOT a pointing finger |
| Onset | Gradual increase and fading away, usually 2–10 minutes | Sudden maximal-at-onset pain = think dissection/PE/pneumothorax instead |
| Character | Tightness, pressure, squeezing, heaviness, burning, aching, fullness, "heavy weight" or "band across chest" | Sharp/stabbing/knife-like pain is ATYPICAL for angina → think pleuritic/MSK |
| Radiation | Neck, throat, lower jaw, L shoulder or arm (ulnar distribution), occasionally R arm, interscapular, epigastrium or back | Due to convergence of cardiac afferents with somatic dermatomes T1–T5 |
| Associations | SOB, dizziness, syncope | These can be "angina equivalents" — important in elderly/DM |
| Time course | Worsening/improving/fluctuating | Progressive worsening → think unstable/ACS |
| Exacerbating/Relieving | 4 "E"s – Eating, Exertion, Emotion, Environment (hot/cold) vs. Rest, cessation of activity/stress, NTG | If NOT relieved by rest or NTG → think ACS or non-cardiac |
| Severity | Scale 0–10 | Important for monitoring and comparison |
| Grade | Description |
|---|---|
| 0 | Asymptomatic |
| I | Angina with strenuous exertion only |
| II | Angina with moderate exertion (slight limitation of ordinary activities) |
| III | Angina with mild exertion, e.g. 100–200m, 1 flight of stairs (great limitation) |
| IV | Angina at rest |
This slide is crucial for recognising atypical presentations:
Dyspnoea (exertional, rest, PND), non-chest locations of discomfort (neck, mandible, throat, shoulder, arm — more often left), mid-epigastric burning, nausea/vomiting (especially inferior MI with increased vagal tone), diaphoresis, excessive fatigue, dizziness and syncope. [1]
Why this matters: The 2021 past paper Q11 described a 62-year-old woman with "severe epigastric pain associated with dyspnoea on climbing stairs, subsiding after resting for 5 minutes" — the answer is IHD, not dyspepsia, because of the exertional pattern and relief with rest. [6]
Pre-test probability is determined by:
- Demographic data — age, sex
- Symptoms — typical vs. atypical vs. non-anginal
- Cardiovascular risk factors
This determines which investigation pathway to pursue (see below).
The majority of cases present with NORMAL physical findings. [1]
The physical exam has three goals:
| Goal | What to Look For | Clinical Significance |
|---|---|---|
| Assess risk factors | BP (> 15 mmHg arm disparity = ↑ risk PAD/CVD death), BMI > 30, xanthelasma, corneal arcus, cutaneous xanthomas, acanthosis nigricans, skin tags, tobacco staining, ear lobe crease (Frank sign) | Identifies modifiable and non-modifiable CVD risk factors |
| Assess for complications | JVP distension, S3/S4, displaced apex, hepatomegaly, pulmonary/peripheral oedema (CHF); ischaemic MR; arrhythmias; carotid bruits, absent peripheral pulses (PAD) | CHF and MR are complications of IHD; PAD indicates generalised atherosclerosis |
| Assess for other causes of angina | AS (late-peaking systolic murmur, pulsus parvus et tardus), HOCM (harsh crescendo-decrescendo murmur with dynamic provocation), pulmonary hypertension (loud P2, RV heave) | These conditions cause angina by mechanisms other than coronary atherosclerosis |
In the case (Slide 28):
- BP 130/85
- Xanthelasma on bilateral upper eyelids, no tendon xanthoma
- Normal cardiovascular examination [1]
Physical Exam Pearl
Acanthosis nigricans is associated with insulin resistance and diabetes mellitus. Ear lobe crease (Frank sign) is a potential marker of increased risk for coronary artery disease. [1] These are the kind of visual recognition points that can appear in OSCE stations.
C. Investigations
1. Blood Tests (Slides 32–36)
| Category | Tests | Why |
|---|---|---|
| Lipid levels | LDL-C, HDL-C, triglycerides, Lipoprotein(a) | Assess dyslipidaemia — major modifiable risk factor |
| Metabolic evaluation | Fasting glucose, HbA1c (if DM suspected), creatinine, thyroxine | DM, CKD, and thyroid disease all worsen/cause IHD |
| Cardiac biomarkers | hs-CRP, BNP | hs-CRP for inflammatory risk; BNP if heart failure suspected |
Lipoprotein(a) — A Lecture Emphasis:
Lp(a) is a subtype of LDL-C with apo(a); the major determinant of its level is genetic variation. [1] Lp(a) > 50 mg/dL is the risk threshold. [1]
In the case: Lp(a) was 150 mg/dL — markedly elevated, indicating high genetic cardiovascular risk even beyond traditional LDL-C. [1]
Case blood results: TC 6.7, LDL-C 4.8, HDL-C 1.2, FBS 5.6 — high LDL, low HDL, borderline fasting glucose — multiple risk factors. [1]
2. Stress Testing (Slides 37–42)
The purpose of stress testing is to provoke ischaemia in a controlled setting and detect it.
| Modality | Sensitivity | Specificity | Advantages | Limitations |
|---|---|---|---|---|
| Stress ECG | 50–80% | 80–95% | Simple, cheap, widely available | Conduction/repolarisation anomalies reduce interpretability |
| Myocardial perfusion scintigraphy (SPECT) | 65–90% | 90–95% | Good risk stratification, identifies hibernating myocardium | Radiation exposure |
| Stress Echo | 65–90% | 90–95% | No radiation, identifies hibernating myocardium, identifies ischaemic territory | Diagnostic images not possible in all patients (body habitus) |
| Cardiac MRI perfusion | 70–90% | 90–95% | Best identification of ischaemic territory, identifies hibernating myocardium | Claustrophobia, incompatible with some devices, expensive |
Pharmacological stress agents:
- Dobutamine — β1-agonist → increases HR, contractility, O₂ demand → mimics exercise (C/I: recent MI) [7]
- Adenosine/Dipyridamole — vasodilators → cause coronary steal phenomenon (healthy arteries dilate but diseased ones can't → differential perfusion) (C/I: asthma — adenosine causes bronchospasm) [7]
3. CT Coronary Angiogram (CTCA) (Slide 43)
Non-invasive anatomical assessment of coronary arteries. High negative predictive value — excellent for ruling OUT CAD. Used when clinical likelihood is low-to-intermediate or when stress testing is contraindicated/inconclusive.
Investigation Decision Pathway (Slide 44):
Coronary Angiogram (Slide 48)
Indications for coronary angiography: [1]
- Unacceptable angina despite medical therapy (for consideration of revascularisation)
- Non-invasive testing results with high-risk features
- Angina or risk factors for CAD in the setting of depressed LVEF
- For diagnostic purposes when non-invasive testing results are unclear
In the case (Slides 47–49): CTA showed triple vessel disease with suspected > 70% mid-LAD occlusion. Coronary angiogram showed TVD with 30–50% LAD/LCX/RCA lesions — so less severe than CTA suggested (CTA can overestimate). [1]
Management
The lecture's management section is structured around the ESC 2019 Guidelines (Slides 51–52) and concludes with the memorable ABCDE mnemonic.
- Improve prognosis (prevent MI and death)
- Relieve symptoms (improve quality of life)
1. Rule out and control aggravating conditions (non-cardiac diseases, cardiac diseases, drugs aggravating angina) 2. Smoking cessation 3. Dietary counselling for body weight and lipid control 4. Exercise prescription 5. Treat to targets: hypertension, blood lipids, diabetes [1]
Good fat diet (low saturated/trans fats, high polyunsaturated, high fish oil), good carbohydrates (low glycaemic load, high fibre), high folate, not smoking, moderate alcohol (1 drink every other day to daily), regular exercise (0.5 hr daily), BMI < 25 (optimal < 21). [1]
Pharmacological Management
| Agent | LDL-C Reduction | CVD Event Reduction Proven? | Key Notes |
|---|---|---|---|
| Statins | 18–55% | Yes | First-line; inhibit HMG-CoA reductase |
| Ezetimibe | 13–20% | Yes | Cholesterol absorption inhibitor; add-on to statin |
| PCSK9 inhibitors | 61–62% | Yes | Monoclonal antibodies (evolocumab, alirocumab); for very high risk |
| Bile-acid sequestrants | 15–30% | Yes | Older agents; GI side effects |
| Fibrates | Variable | No clear mortality benefit | Mainly for triglycerides |
| Nicotinic acid | 5–25% | No | Also lowers Lp(a) by 20–40% |
| Long-chain omega-3 | Variable | Yes (icosapent ethyl) | Mainly for triglycerides |
LDL-C targets (ESC Guideline):
- Very high risk (established CVD): LDL-C < 1.4 mmol/L AND > 50% reduction from baseline
- High risk: LDL-C < 1.8 mmol/L
- Moderate risk: LDL-C < 2.6 mmol/L
In the case: Started on Atorvastatin 40mg + Ezetimibe 10mg daily → LDL-C reduced to 1.4 mmol/L [1] — achieving the very high risk target.
Indications: [1]
- Aspirin in the absence of contraindications (first-line)
- Clopidogrel when aspirin is contraindicated
- Aspirin + P2Y12 blocker after PCI
- Rivaroxaban 2.5 mg BD added to low-dose aspirin (81–100 mg daily) for high-risk CAD/PAD patients
Why aspirin? Irreversibly inhibits COX-1 → blocks thromboxane A2 synthesis → reduces platelet aggregation → reduces thrombotic events on atherosclerotic plaques.
Side effects: GI upset (aspirin), bleeding risk.
ACE inhibitors should be prescribed in all patients with stable IHD who also have hypertension, DM, LVEF ≤ 40%, or CKD, unless contraindicated. [1] ARBs are recommended for those intolerant of ACEIs. [1]
Why? ACEIs reduce adverse cardiac remodelling, reduce afterload, have anti-atherosclerotic effects, and reduce morbidity/mortality in high-risk patients.
Side effects: Cough (ACEI-specific, due to bradykinin accumulation), hypotension, syncope, angioedema, hyperkalaemia. Contraindication: High-grade bilateral renal artery stenosis (removes the kidney's ability to autoregulate GFR via angiotensin II). [1]
a) Beta-Blockers (Slide 62)
First-line monotherapy or in combination with CCB or nitrates to prevent or reduce frequency of angina. [1] Also indicated for systolic LV failure (EF < 40%), heart failure, prior MI, and ventricular rate control in AF. [1]
Mechanism: Block β1-receptors → ↓ heart rate, ↓ contractility, ↓ BP → ↓ myocardial O₂ demand.
Side effects: Bradycardia, syncope, hypotension, bronchospasm, impaired glucose tolerance [1] Contraindications: AV block, sinus node dysfunction, bronchial asthma, vasospastic angina, PAD, Raynaud phenomenon, depression [1]
Past Paper Alert — Beta-Blocker with Bradycardia
2022 Q35: A 65-year-old man with stable CAD, resting HR 50 bpm. Which first-line anti-anginal? Answer: A. Amlodipine — because beta-blockers are contraindicated with pre-existing bradycardia (HR 50), and non-dihydropyridine CCBs (diltiazem, verapamil) also slow HR. Amlodipine (dihydropyridine) does NOT significantly slow HR. [4]
b) Calcium Channel Blockers (Slides 63–64)
Three types:
- Phenylalkylamine (verapamil-like) — rate-limiting, negative inotropic
- Benzothiazepine (diltiazem-like) — rate-limiting, moderate negative inotropy
- Dihydropyridine (nifedipine/amlodipine-like) — predominantly vasodilating, may cause reflex tachycardia
| Property | Amlodipine (DHP) | Diltiazem (non-DHP) | Verapamil (non-DHP) |
|---|---|---|---|
| Heart rate | ↑/– | ↓ | ↓ |
| SA node | – | ↓ | ↓ |
| AV node | – | ↓ | ↓ |
| Contractility | ↓/– | ↓ | ↓↓ |
| Vascular dilation | ↑↑ | ↑ | ↑ |
| Coronary flow | ↑ | ↑ | ↑ |
Indications: Monotherapy (when beta-blockers contraindicated/intolerant) or combination; vasospastic angina; ventricular rate control in AF. [1] Side effects: Bradycardia (non-DHP), hypotension, peripheral oedema, headache, constipation. [1] Contraindications: AV block, sinus node dysfunction, and HF (non-DHP CCBs). [1]
Critical Drug Interaction
NEVER combine a non-DHP CCB (verapamil/diltiazem) with a beta-blocker — both depress SA/AV node function → risk of severe bradycardia, heart block, and cardiac arrest. Amlodipine + beta-blocker is a safe and common combination.
c) Nitrates (Slide 65)
Mechanism: Release NO → activate guanylate cyclase → ↑ cGMP → smooth muscle relaxation → venodilatation (reduces preload) + coronary vasodilatation [1]
Short-acting nitrates: Relieve acute anginal pain; use prophylactically before exertion. [1] Long-acting nitrates: Prevent angina as monotherapy or combination. [1] Side effects: Hypotension, syncope, tachycardia, headache, facial flushing. Less common: methaemoglobinaemia. [1] Contraindications: HOCM (reduces preload → worsens dynamic LVOT obstruction), concomitant PDE-5 inhibitors (sildenafil, tadalafil, vardenafil) — catastrophic hypotension, SBP < 90 mmHg. [1]
Nitrate tolerance: Continuous use leads to reduced efficacy. Managed by providing a nitrate-free interval (usually overnight).
d) Novel Anti-Ischaemic Agents (Slides 66–68)
| Agent | Mechanism | Key Side Effects |
|---|---|---|
| Ivabradine | Selectively inhibits If current in SA node → ↓ HR without affecting contractility or BP | Phosphenes (visual flashes), bradycardia, AF |
| Ranolazine | Inhibits late inward Na⁺ current → reduces intracellular Ca²⁺ overload during ischaemia | QT prolongation, nausea, headache, dizziness, constipation. C/I: liver and renal failure |
| Trimetazidine | Shifts myocardial metabolism from fatty acid oxidation to glucose oxidation (more O₂-efficient) | Nausea, vomiting, fatigue, dizziness, myalgia. May induce/worsen Parkinsonism |
| Nicorandil | ATP-sensitive K⁺ channel opener + nitrate-like arteriolar dilation; may have ischaemic preconditioning effect | Caution with corticosteroids (GI perforation risk). Sulfonylureas may antagonise its effects |
Why trimetazidine works: During ischaemia, the heart switches to fatty acid oxidation which requires MORE oxygen per ATP generated. Trimetazidine forces the metabolism back to glucose oxidation, which is more oxygen-efficient.
| Class | Mortality Benefit |
|---|---|
| Beta-blockers | Decrease mortality |
| Nitrates | No mortality benefit |
| CCBs | No clear mortality benefit; short-acting nifedipine alone increases reinfarction |
| Ranolazine | Decreases recurrent ischaemia and arrhythmias |
| Trimetazidine | Decreases short-term mortality |
| Nicorandil | Decreases arrhythmias and transient ischaemia |
Percutaneous Coronary Intervention (PCI):
- Balloon angioplasty + drug-eluting stent (DES)
- Requires dual antiplatelet therapy (DAPT: aspirin + P2Y12 inhibitor) post-procedure
Coronary Artery Bypass Grafting (CABG):
- Uses arterial conduits (internal mammary artery — best long-term patency) or saphenous vein grafts
CABG is preferable to PCI for revascularisation to improve survival in: [1]
- Unprotected left main disease
- Three-vessel disease
- Two-vessel disease with a proximal LAD lesion
Why? These represent the highest-risk anatomical patterns. The left main supplies ~75% of myocardium (or > 75% if right-dominant). Proximal LAD supplies the anterior wall and septum. CABG provides more complete revascularisation and long-term patency (especially LIMA-to-LAD graft) in these scenarios.
Treatment: [1]
- Diet advice and smoking cessation
- Aspirin 100mg daily
- Betaloc (metoprolol) 25mg daily
- Atorvastatin 40mg + Ezetimibe 10mg daily → LDL-C dropped to 1.4 mmol/L
No revascularisation was performed because coronary angiogram showed only 30–50% lesions (< 70% threshold for haemodynamically significant stenosis in non-left-main vessels). Medical therapy was appropriate.
ABCDE Approach Rx for IHD: [1]
- A → Anti-platelet agents, Anti-anginal agents & ACEI/ARB, Angioplasty
- B → Beta-blocker, BP control & Bypass
- C → Cholesterol-lowering agents, Cigarette cessation & Calcium channel blockers
- D → Diabetes & Diet management
- E → Education & Exercise
High Yield Summary
IHD is caused by myocardial oxygen supply-demand mismatch, predominantly due to coronary atherosclerosis. Stable angina presents as predictable exertional chest pain (SOCRATES; 4 Es) relieved by rest/NTG in < 10 minutes. Physical exam is often normal but look for risk factor signs (xanthelasma, corneal arcus, Frank sign) and IHD complications (CHF, MR). Investigation strategy depends on pre-test probability — exercise ECG for interpretable baseline, stress imaging if not, CTCA or invasive angiography for high-risk features. Management follows ABCDE: Aspirin + Anti-anginals (beta-blockers first-line) + ACEI; Beta-blockers + BP control + Bypass; Cholesterol lowering (statin ± ezetimibe ± PCSK9i to LDL < 1.4 for very high risk) + Cessation of smoking + CCBs; Diabetes/Diet; Education/Exercise. CABG preferred over PCI for left main, 3-vessel disease, and 2-vessel with proximal LAD. 10–20% of stable angina patients progress to ACS within 12 months. Remember Prinzmetal variant (rest angina, ST elevation, coronary spasm, treat with CCB ± nitrate, NOT beta-blockers) and cardiac syndrome X (ischaemia without obstructive CAD, microvascular dysfunction).
Special Entities
Occurs at rest, common after cold exposure. Cyclical in nature. ECG: episodic ST-segment elevations. Caused by coronary artery spasm ± superimposed CAD. Patients are more likely to develop ventricular arrhythmias. Rx: CCBs ± Nitrate. [1]
Why NOT beta-blockers? Beta-blockers block β2-mediated vasodilation → unopposed α-mediated vasoconstriction → can WORSEN coronary vasospasm. This is a classic exam discriminator.
Angina in patients with evidence of myocardial ischaemia and NO obstructive coronary artery disease. [1] Management: Traditional antianginal/anti-ischaemic medications, enhanced external counterpulsation, cognitive behavioural therapy, tricyclic medication, and neurostimulation. [1]
Likely involves microvascular coronary dysfunction — small vessels that don't show up on angiography but cannot adequately increase flow during demand.
Account for 6–17% of sudden death in athletes. Symptoms: chest pain, exertional syncope, sudden cardiac death. P/E and ECG: NAD. Diagnosis: CT coronary angiogram, MRI, or coronary angiogram. Avoid competitive sport; consider surgical intervention if positive for myocardial ischaemia. [1]
Based on past papers (2021–2025) and lecture content:
- EMQ: Epigastric pain with exertional dyspnoea relieved by rest → IHD (not dyspepsia/GERD) [6]
- MCQ: % of stable angina progressing to ACS within 12 months → 10–20% [4]
- MCQ: First-line anti-anginal in a patient with resting bradycardia → Amlodipine (not beta-blocker, not non-DHP CCB) [4]
- SAQ: List the ABCDE approach to IHD management → full mnemonic with examples
- SAQ: Describe the SOCRATES features of typical angina pectoris
- MCQ: Contraindication to nitrates → HOCM, PDE-5 inhibitors, SBP < 90
- MCQ: When is CABG preferred over PCI? → Left main, 3-vessel, 2-vessel with proximal LAD
- SAQ/Viva: What physical exam findings would you look for in a patient with suspected IHD? → Three categories (risk factors, complications, other causes)
- MCQ: Lp(a) risk threshold → > 50 mg/dL
- MCQ/EMQ: Prinzmetal angina features and treatment → rest pain, ST elevation, CCB ± nitrate
Active Recall - Lecture Notes
[1] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf (slides 1–86) [2] Senior notes: Block A - Accelerating chest pain_ Acute Coronary Syndromes.pdf (p1 — same patient reference) [3] Senior notes: Ryan Ho Cardiology.pdf (pp. 54–57, 115 — CCS grading, angina equivalents, clinical approach) [4] Past papers: 2022 Fourth Summative MCQ.pdf (Q34, Q35) [5] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (pp. 11, 13, 15, 19) [6] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Q11) [7] Senior notes: Maksim Medicine Notes.pdf (p7 — stress testing methods, pharmacological agents)
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