Ischemic heart disease notes according to Davidson latest edition for Hong Kong medical license exam
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Excellent — I now have comprehensive Harrison's 22E content on IHD. Let me compile the complete notes.
Ischemic Heart Disease — Exam Notes
Based on Harrison's Principles of Internal Medicine 22E (2025) & Robbins Basic Pathology
1. DEFINITION
Ischemic heart disease (IHD) = inadequate supply of blood and oxygen to the myocardium due to imbalance between myocardial O₂ supply and demand. Most commonly caused by atherosclerotic narrowing of epicardial coronary arteries.
Synonyms in current literature: Chronic Coronary Disease (CCD) / Chronic Coronary Syndrome (CCS)
2. EPIDEMIOLOGY
- Leading cause of death and disability in the developed world
- 20.5 million people affected in the USA; ~3–4% have had an MI
- Risk factors: genetic predisposition, high-fat diet, smoking, sedentary lifestyle, obesity, insulin resistance, T2DM
- Globally: >200 million people live with IHD; shift from communicable → non-communicable disease burden
- Particularly high in men from South Asia, India, and the Middle East
- Mortality declining (~50% due to treatments; ~50% due to risk factor modification)
3. PATHOPHYSIOLOGY
Myocardial O₂ Supply vs. Demand
| Determinants of Demand (MVO₂) | Determinants of Supply |
|---|---|
| Heart rate | Hemoglobin concentration |
| Myocardial contractility | Pulmonary function / inspired O₂ |
| Wall tension (afterload/preload) | Coronary blood flow |
- Coronary flow is predominantly diastolic (~75% of resistance across R1–R3 vessels)
- R1 = large epicardial arteries; R2 = pre-arteriolar; R3 = arteriolar/capillary
- In normal vessels, R1 is trivial — resistance regulated by R2/R3 via autoregulation
- Ischemia = supply/demand mismatch → anaerobic metabolism → lactate ↑, pH ↓, ATP ↓
Mechanisms of Reduced Supply
- Fixed atherosclerotic stenosis (most common >90% of cases)
- Acute plaque change — rupture or erosion → thrombosis/vasospasm
Critical Stenosis Thresholds
| Stenosis | Effect |
|---|---|
| <70% | Typically asymptomatic |
| ≥70% | Symptoms on exertion → stable angina |
| ≥90% | Symptoms at rest → unstable angina |
4. RISK FACTORS
Non-modifiable: Age, male sex, family history (first-degree relative <55M / <65F), genetics
Modifiable:
- Dyslipidaemia (↑LDL, ↓HDL, ↑triglycerides)
- Hypertension
- Cigarette smoking
- Diabetes mellitus / insulin resistance
- Obesity (central)
- Physical inactivity
- Chronic kidney disease
- Psychosocial stress
Emerging: hs-CRP, lipoprotein(a), homocysteine, obstructive sleep apnoea
5. PATHOLOGY (Robbins)
Acute Plaque Change
- Initiating event: plaque rupture or erosion exposing subendothelial collagen and necrotic lipid core
- → Platelet adhesion → aggregation → thrombus formation
- → ± vasospasm (via TXA₂, serotonin from platelets; endothelin > NO imbalance)
- Plaques vulnerable to rupture: large lipid core, thin fibrous cap, rich in macrophages (foam cells)
Coronary Artery Distribution
- LAD: first several cm from takeoff — supplies anterior LV, anterior septum
- LCX: obtuse marginal branches — lateral LV
- RCA: along entire length — inferior LV, SA/AV nodes (right-dominant in 80%)
Collateral Circulation
- Develops with gradual occlusion (weeks–months) → protective against MI
- No time for collaterals with acute occlusion → infarction
6. CLINICAL SYNDROMES
A. Stable Angina (Chronic Coronary Syndrome)
Characteristics:
- Predictable chest discomfort precipitated by exertion, emotion, cold, meals
- Relieved within minutes by rest or sublingual GTN
- Substernal pressure/tightness; may radiate to left arm, jaw, neck, back
- Women more often have atypical symptoms: dyspnoea, fatigue, nausea
Canadian Cardiovascular Society (CCS) Grading:
| Class | Description |
|---|---|
| I | Angina only with strenuous activity |
| II | Slight limitation — angina on walking >2 blocks or climbing >1 flight of stairs |
| III | Marked limitation — angina walking 1–2 blocks or 1 flight of stairs |
| IV | Inability to carry on any activity without angina; angina at rest |
ECG during angina: ST depression ± T-wave changes (horizontal or downsloping)
Investigations:
- Resting ECG (may be normal between episodes)
- Exercise stress test (Bruce protocol) — evidence of ischaemia: ≥1 mm horizontal/downsloping ST depression
- Stress echocardiography / myocardial perfusion imaging (if resting ECG abnormal or non-interpretable)
- CT coronary angiography (CTCA) — preferred non-invasive anatomical test for intermediate pre-test probability
- Invasive coronary angiography (ICA) — gold standard; indicated if high probability, failed medical therapy, or prior to revascularisation
Medical Management:
- Anti-anginal drugs:
- Short-acting nitrates (GTN SL) — acute relief
- Beta-blockers (1st line): ↓HR and contractility → ↓MVO₂; also reduce mortality post-MI
- Calcium channel blockers (CCBs): Amlodipine/diltiazem — vasodilation; use if beta-blockers contraindicated
- Long-acting nitrates (isosorbide mononitrate) — add as 2nd line; nitrate-free interval required
- Ranolazine — late Na⁺ channel inhibitor; 3rd line add-on
- Ivabradine — If-channel blocker; reduces HR when beta-blockers not tolerated
- Antiplatelet: Aspirin 75–100 mg daily (all patients unless contraindicated)
- Statin: High-intensity (atorvastatin 40–80 mg) — pleiotropic and LDL-lowering effects
- ACE inhibitor/ARB: If coexistent HF, hypertension, or diabetes
- Risk factor modification: smoking cessation, diet, exercise, weight loss, DM/HTN/lipid control
Revascularisation:
- PCI (percutaneous coronary intervention): preferred for single/double vessel disease
- CABG (coronary artery bypass grafting): preferred for left main disease, triple vessel disease, LV dysfunction (EF <35%), or diabetes with multivessel disease
- ISCHEMIA trial (2020): In stable CCS with moderate–severe ischaemia, initial invasive strategy did not reduce major events vs. optimal medical therapy → medical therapy first approach supported
B. Acute Coronary Syndromes (ACS)
ACS spectrum: Unstable Angina (UA) → NSTEMI → STEMI
Common pathophysiology: Plaque rupture/erosion → thrombus → sudden reduction in coronary flow
Unstable Angina (UA)
- Rest angina, new-onset severe angina, or crescendo angina
- No myocardial necrosis (troponin negative)
- ECG: ST depression or T-wave inversion (or normal)
NSTEMI (Non-ST-Elevation MI)
- Same presentation as UA
- Troponin positive (myocardial necrosis)
- No ST elevation or new LBBB on ECG
- ECG: ST depression, T-wave inversion, or non-specific changes
STEMI (ST-Elevation MI)
- Complete occlusion of epicardial coronary artery
- ECG: ≥1 mm ST elevation in ≥2 contiguous limb leads OR ≥2 mm in ≥2 contiguous precordial leads OR new LBBB
- Troponin positive
- Requires immediate reperfusion
7. MYOCARDIAL INFARCTION — DETAILED
Biomarkers
| Marker | Rises | Peaks | Returns to normal |
|---|---|---|---|
| Troponin I/T (high-sens.) | 1–3 h | 24–48 h | 7–14 days |
| CK-MB | 4–6 h | 12–24 h | 48–72 h |
| Myoglobin | 1–2 h | 4–8 h | 24 h |
- High-sensitivity troponin (hs-cTn): preferred — detect at 0 h, 1–2 h (ESC 0/1h or 0/2h algorithm)
- STEMI: treat without waiting for troponin result
ECG Evolution in STEMI
| Time | Changes |
|---|---|
| Minutes–hours | Hyperacute T waves → ST elevation |
| Hours | Q waves develop (transmural necrosis) |
| Days | ST normalisation, T-wave inversion |
| Weeks–months | Persistent Q waves (>0.04 s, >25% of R height) |
Territories of Infarction
| ECG Leads | Territory | Artery |
|---|---|---|
| V1–V4 | Anterior | LAD |
| V1–V2 (tall R) | Posterior | RCA/LCX |
| II, III, aVF | Inferior | RCA (80%), LCX (20%) |
| I, aVL, V5–V6 | Lateral | LCX/diagonal |
| V1–V6 + I, aVL | Extensive anterior | LAD (proximal) |
Immediate Management of STEMI
MONA+ BASH mnemonic:
- Morphine (caution — may mask symptoms, use for refractory pain)
- Oxygen (only if SpO₂ <94%)
- Nitrates (SL GTN — avoid if hypotension, RV infarct, PDE5i use)
- Aspirin 300 mg loading dose
- Beta-blocker (oral, when haemodynamically stable)
- Anticoagulation (UFH/enoxaparin/bivalirudin)
- Statin (high-intensity)
- Heparin + P2Y12 inhibitor (ticagrelor 180 mg or clopidogrel 300–600 mg)
Reperfusion Strategy
| Strategy | Timing | Indication |
|---|---|---|
| Primary PCI (pPCI) | Door-to-balloon ≤90 min | Preferred if available |
| Thrombolysis (fibrinolysis) | Door-to-needle ≤30 min | If pPCI not available within 120 min of diagnosis |
| Rescue PCI | After failed thrombolysis | If <50% ST resolution at 60–90 min |
Contraindications to thrombolysis (absolute): Previous haemorrhagic stroke, ischaemic stroke <3 months, active internal bleeding, known intracranial neoplasm, suspected aortic dissection, significant head trauma <3 months
P2Y12 inhibitors:
- Ticagrelor 180 mg load then 90 mg BD — preferred (reversible, faster onset)
- Prasugrel 60 mg load then 10 mg OD — avoid if prior stroke/TIA, age ≥75, weight <60 kg
- Clopidogrel 600 mg load then 75 mg OD — if others unavailable or contraindicated
NSTEMI/UA Management
Risk stratification: GRACE score (preferred), TIMI score
Timing of invasive strategy:
| Risk | Timing |
|---|---|
| Immediate (<2 h) | Haemodynamic instability, refractory angina, life-threatening arrhythmia |
| Early (<24 h) | GRACE >140, dynamic ECG changes, troponin rise |
| Selective invasive | Low-risk (GRACE <109, no troponin rise) |
Anticoagulation: Fondaparinux preferred (OASIS-5); UFH if PCI planned; LMWH alternative
8. COMPLICATIONS OF MI
| Complication | Timing | Features |
|---|---|---|
| Arrhythmias | Immediate/early | VF most common cause of early death; AF common |
| Cardiogenic shock | Hours–days | BP <90 mmHg, cool peripheries; worst prognosis; IABP/Impella/ECMO |
| Acute HF / pulmonary oedema | Early | Killip class II–IV |
| RV infarction | With inferior STEMI | Hypotension + clear lungs + raised JVP; do NOT give nitrates |
| Pericarditis (early) | 1–3 days | Pleuritic chest pain, friction rub, diffuse ST elevation |
| Free wall rupture | 3–5 days | Sudden haemodynamic collapse → haemopericardium/tamponade |
| VSD (ventricular septal defect) | 3–7 days | New harsh pansystolic murmur + haemodynamic deterioration |
| Acute mitral regurgitation | 2–7 days | Papillary muscle rupture → pulmonary oedema; soft murmur |
| LV thrombus | Days–weeks | Anterior STEMI; risk of systemic embolism; anticoagulate |
| Dressler's syndrome | 2–10 weeks | Immune-mediated pericarditis; fever, pleurisy; treat with NSAIDs/colchicine |
| Ventricular aneurysm | Weeks–months | Persistent ST elevation; paradoxical pulsation |
Killip Classification (STEMI)
| Class | Description | Mortality |
|---|---|---|
| I | No HF | ~6% |
| II | Mild HF (S3, basal crackles) | ~17% |
| III | Pulmonary oedema | ~38% |
| IV | Cardiogenic shock | ~81% |
9. SECONDARY PREVENTION POST-MI
| Drug | Duration | Target |
|---|---|---|
| Aspirin 75–100 mg | Lifelong | Antiplatelet |
| P2Y12 inhibitor (ticagrelor/clopidogrel) | 12 months | Dual antiplatelet therapy (DAPT) |
| High-intensity statin (atorvastatin 80 mg) | Lifelong | LDL <1.4 mmol/L (<55 mg/dL), ≥50% reduction |
| Beta-blocker | ≥1 year (lifelong if HF/EF↓) | ↓Mortality, ↓sudden death |
| ACE inhibitor/ARB | Lifelong if EF ↓, HTN, DM, CKD | ↓Remodelling, ↓mortality |
| Eplerenone/spironolactone (MRA) | If EF <40% + HF or DM | ↓Mortality post-MI with LV dysfunction |
PCSK9 inhibitors (evolocumab/alirocumab): If LDL target not met on max statin + ezetimibe
Cardiac rehabilitation: Exercise training + education + psychological support — reduces mortality ~25%
10. SPECIAL FORMS OF ANGINA
Vasospastic (Prinzmetal / Variant) Angina
- Transient coronary spasm → ST elevation during attacks (unlike stable angina)
- Often occurs at rest, early morning; may not be associated with significant atherosclerosis
- Triggered by smoking, cocaine, cold, hyperventilation
- Treatment: Calcium channel blockers (first-line) + long-acting nitrates; avoid beta-blockers
- Diagnosis: Provocation testing with ergonovine or acetylcholine during angiography
Microvascular Angina (Cardiac Syndrome X / INOCA)
- Angina + positive stress test but normal coronary angiogram
- Abnormal coronary microvascular function (increased resistance R3)
- More common in women; associated with oestrogen deficiency
- Treatment: Beta-blockers, CCBs, ranolazine; ACE inhibitors
11. SILENT ISCHAEMIA
- Objective evidence of ischaemia without angina
- Common in elderly, diabetics (autonomic neuropathy blunts pain perception)
- Detected on Holter monitoring or stress testing
- Same prognostic significance as symptomatic ischaemia
- Treat as per stable IHD guidelines
12. INVESTIGATIONS SUMMARY
| Test | Use |
|---|---|
| 12-lead ECG | ST/T changes, Q waves, LBBB; compare serial ECGs |
| hs-Troponin | Diagnosis/exclusion of MI; 0/1h or 0/2h ESC algorithm |
| CXR | Pulmonary oedema, cardiomegaly |
| Echocardiography | RWMA, EF, pericardial effusion, valve pathology, complications |
| Exercise ETT | Diagnosis, risk stratification in stable angina |
| Stress echo / MPI | If abnormal resting ECG or functional assessment needed |
| CTCA | Non-invasive anatomical; intermediate pre-test probability |
| Invasive angiography | Gold standard; defines anatomy pre-revascularisation |
| Cardiac MRI | Viability, infarct size, myocarditis distinction |
| BNP/NT-proBNP | Risk stratification; elevated if concurrent HF |
13. HIGH-YIELD EXAM POINTS (HK License Exam)
- STEMI = immediate pPCI (door-to-balloon ≤90 min); thrombolyse if pPCI delay >120 min
- NSTEMI troponin positive, no ST elevation — risk stratify with GRACE score
- RV infarction (inferior STEMI): raised JVP + hypotension + clear lungs → fluids, NO nitrates
- Aspirin + ticagrelor = preferred DAPT in ACS (unless high bleeding risk or prior stroke)
- Vasospastic angina = calcium channel blockers, avoid beta-blockers
- Cardiac syndrome X / microvascular = normal angiogram + angina symptoms + positive stress test
- Dressler's syndrome = late pericarditis (2–10 weeks post-MI), treat with NSAIDs + colchicine
- Free wall rupture (3–5 days), VSD (3–7 days), MR (2–7 days) — all present with haemodynamic collapse ± new murmur
- Statin LDL target post-ACS: <1.4 mmol/L AND ≥50% reduction from baseline
- Beta-blockers contraindicated in vasospastic angina, severe bradycardia, high-degree AV block, decompensated HF (acute phase)
- CABG preferred over PCI for: left main disease, 3-vessel CAD + DM, 3-vessel CAD + LV dysfunction
- Colchicine post-MI (COLCOT trial): reduces recurrent cardiovascular events
- Ranolazine: late Na⁺ channel blocker — anti-anginal only, no mortality benefit
- Ivabradine: reduces heart rate without affecting BP — useful in sinus tachycardia when beta-blockers not tolerated
- Silent ischaemia most common in diabetics — same treatment principles as symptomatic IHD
Sources: Harrison's Principles of Internal Medicine 22E (2025); Robbins & Kumar Basic Pathology; Braunwald's Heart Disease
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