Davidson principle and practice latest edition ischemia of heart notes for hkmle
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I have enough rich content to compile comprehensive HKMLE-focused notes on Ischemic Heart Disease. Let me now produce the full structured notes.
❤️ Ischaemic Heart Disease (IHD) — HKMLE Notes
Based on Braunwald's Heart Disease, Robbins & Kumar Basic Pathology, Harrison's Principles of Internal Medicine 22e
1. DEFINITION & OVERVIEW
IHD = a group of syndromes caused by an imbalance between myocardial oxygen supply and demand, almost always due to coronary atherosclerosis (>90% of cases).
Synonyms: Coronary artery disease (CAD), coronary heart disease (CHD)
Key concept: Myocardial cells depend exclusively on mitochondrial oxidative phosphorylation → strictly dependent on continuous oxygenated blood flow.
2. CLINICAL SYNDROMES
| Syndrome | Mechanism | Reversible? |
|---|---|---|
| Stable angina | Fixed stenosis → demand ↑ | Yes |
| Unstable angina | Plaque rupture + thrombus | Yes (no necrosis) |
| Prinzmetal/Variant angina | Coronary vasospasm | Yes |
| NSTEMI | Partial/subendocardial infarct | No (necrosis) |
| STEMI | Complete occlusion → transmural infarct | No (necrosis) |
| Sudden cardiac death (SCD) | Fatal ventricular arrhythmia | No |
| Chronic IHD with CHF | Accumulated ischemic damage | Progressive |
Acute Coronary Syndrome (ACS) = Umbrella term for: Unstable angina + NSTEMI + STEMI (+ SCD)
3. PATHOGENESIS
A. Fixed Atherosclerotic Stenosis
- < 70% occlusion → usually asymptomatic at rest
- ≥ 70% occlusion → exertional angina (inadequate hyperaemic response)
- ≥ 90% occlusion → symptoms at minimal exertion or rest
B. Acute Plaque Change (the critical mechanism for ACS)
Sequence in typical MI:
- Plaque erosion or rupture → exposes subendothelial collagen + necrotic plaque contents
- Platelet adhesion and aggregation → platelet plug
- Activation of coagulation cascade → fibrin-rich thrombus
- Vasospasm triggered by platelet mediators (thromboxane A2, serotonin)
- Within minutes to hours → complete occlusion → STEMI
C. Other Causes of IHD (minority)
- Coronary vasospasm (Prinzmetal; healthy vessels possible)
- Embolism from mural thrombi (AF) or valve vegetations
- Demand ischaemia: tachycardia, hypertension, hypotension, anaemia, hypoxia
- Small vessel disease: vasculitis, amyloid, sickle cell
4. ANGINA PECTORIS
Clinical Features (Harrison's)
- Typical patient: Male >50 yrs, female >60 yrs
- Character: Heaviness, pressure, squeezing, smothering (rarely "pain")
- Location: Central, substernal — patient places hand over sternum (Levine's sign = clenched fist over sternum)
- Radiation: Left arm (ulnar aspect), jaw, back, interscapular region, neck, epigastrium
- NOT above mandible, NOT below umbilicus, NOT trapezius (trapezius radiation → pericarditis)
- Duration: 2–5 minutes
- Triggers: Exertion, emotion, cold, heavy meals, sexual activity
- Relief: Rest (1–5 min), sublingual nitrates
Three Variants
| Type | Cause | ECG during attack | Treatment |
|---|---|---|---|
| Stable angina | Fixed stenosis, demand ↑ | ST depression | Nitrates, beta-blockers, CCBs |
| Prinzmetal (Variant) | Coronary vasospasm | ST elevation | Vasodilators (nitrates, CCBs) |
| Unstable angina | Plaque rupture + thrombus | ST depression / normal | ACS management (heparin, aspirin, PCI) |
Canadian Cardiovascular Society (CCS) Grading of Angina
| Class | Description |
|---|---|
| I | Angina only with strenuous activity; ordinary activity doesn't cause angina |
| II | Slight limitation — angina on walking >2 blocks on level, climbing >1 flight |
| III | Marked limitation — angina on walking 1–2 blocks, climbing 1 flight |
| IV | Inability to carry on any activity without discomfort; angina at rest |
5. MYOCARDIAL INFARCTION
Definition (2018 Universal Definition)
"Acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischaemia"
Risk Factors
- Age (10% MI <40 yrs; 45% MI <65 yrs)
- Male sex (women protected pre-menopause; post-menopausal risk equalises)
- Hypertension, diabetes, dyslipidaemia, smoking, obesity, family history
Coronary Artery Territory
| Artery | Territory Supplied | ECG Leads |
|---|---|---|
| LAD | Anterior LV, anterior 2/3 septum, apex | V1–V4 |
| RCA | Posterior LV, posterior septum, SA node, AV node | II, III, aVF |
| LCx | Lateral wall LV | I, aVL, V5–V6 |
Pathological Changes (Robbins)
| Time | Gross | Microscopy |
|---|---|---|
| 0–30 min | None | None (reversible injury) |
| 30 min–4 hrs | None | None visible |
| 4–12 hrs | Dark mottling (early) | Coagulative necrosis begins, wavy fibres |
| 12–24 hrs | Dark mottling | Coagulative necrosis + oedema |
| 1–3 days | Mottling with yellow-tan centre | Neutrophil infiltration (peak 1–3 days) |
| 3–7 days | Hyperaemic border | Neutrophil degradation; macrophages arrive |
| 7–10 days | Yellow-tan, soft centre | Macrophage phagocytosis of necrotic debris |
| 10–14 days | Red-grey margins | Granulation tissue + new capillaries |
| 2–8 weeks | Grey-white scar forming | Fibrosis progresses |
| >2 months | Dense white scar | Complete fibrous scar |
STEMI vs NSTEMI
| Feature | STEMI | NSTEMI |
|---|---|---|
| Mechanism | Complete occlusion | Partial occlusion or reperfusion |
| ECG | ST elevation + Q waves | ST depression / T-wave changes |
| Troponin | Markedly elevated | Elevated (lower) |
| Infarct type | Transmural | Subendocardial |
| Management | Immediate reperfusion (PCI/thrombolysis) | Medical ± PCI |
Cardiac Biomarkers
| Marker | Rises | Peaks | Returns to normal |
|---|---|---|---|
| Troponin I/T | 3–6 hrs | 24–48 hrs | 7–10 days |
| CK-MB | 3–6 hrs | 24 hrs | 48–72 hrs |
| Myoglobin | 1–3 hrs | 6–9 hrs | 24 hrs |
| LDH | 24–48 hrs | 3–6 days | 8–14 days |
HKMLE key: Troponin = most specific; Myoglobin = earliest to rise; CK-MB = best for re-infarction (returns to normal fastest → rise again indicates new event)
Clinical Features of MI
- Severe, crushing substernal chest pain — lasting hours (not relieved by nitrates or rest)
- Radiation to jaw, neck, left arm, epigastrium
- Diaphoresis, nausea, vomiting (especially posterior wall MI)
- Dyspnoea (LV dysfunction → pulmonary oedema)
- Rapid, weak pulse
- Silent MI in ~25%: especially in diabetics (autonomic neuropathy) and elderly
- With >40% LV loss → cardiogenic shock
6. REPERFUSION INJURY
When blood flow is restored after ischaemia, additional injury occurs:
- Free radical generation (O₂⁻, H₂O₂, •OH, peroxynitrite) within minutes → membrane damage
- Calcium overload → contraction band necrosis (intense eosinophilic bands = hypercontracted sarcomeres; diagnostic of reperfusion)
- Leukocyte aggregation → "no-reflow" phenomenon (microvascular occlusion)
- Platelet + complement activation → endothelial swelling + inflammation
Morphological hallmark of reperfusion injury: Contraction band necrosis (vs. coagulative necrosis in non-reperfused MI)
7. COMPLICATIONS OF MI
| Complication | Timing | Mechanism |
|---|---|---|
| Arrhythmias (VF, VT) | Hours–days | Ischaemia of conduction tissue |
| LV failure / Pulmonary oedema | Hours–days | Loss of contractile mass |
| Cardiogenic shock | Hours–days | >40% LV involvement |
| Pericarditis (Dressler's syndrome) | 1–8 weeks | Autoimmune (anti-myocardial Abs) |
| Papillary muscle rupture | 3–5 days | Necrosis → acute mitral regurgitation |
| Ventricular free wall rupture | 3–7 days | Necrosis → haemopericardium/tamponade |
| IV septal rupture | 3–7 days | Necrosis → VSD + sudden L→R shunt |
| Mural thrombus | Days–weeks | Stasis over infarcted endocardium → embolism |
| LV aneurysm | Weeks–months | Paradoxical bulge, refractory heart failure |
| Sudden cardiac death | Any time | VF |
Papillary muscle most at risk: Posteromedial papillary (single blood supply from RCA/LCx) vs anterolateral (dual supply from LAD + LCx)
8. INVESTIGATIONS
ECG Changes
- Hyperacute T waves → ST elevation → Q waves (transmural necrosis) → T-wave inversion
- LBBB (new onset) = STEMI equivalent
Imaging
- Echo: Wall motion abnormalities, EF, complications (MR, VSD, effusion)
- Stress testing (TMT / stress echo / stress nuclear): For stable angina workup
- Coronary CT Angiography (CCTA): Intermediate pre-test probability, young (<65 yrs)
- Agatston score (calcium scoring) — measures coronary calcification burden
- Invasive coronary angiography (ICA): Gold standard for stenosis; guides revascularisation
- Note: Does NOT image arterial wall → can miss non-stenotic plaques
9. MANAGEMENT SUMMARY
Stable Angina
- Lifestyle: Smoking cessation, weight loss, exercise, diet
- Antiplatelet: Aspirin 75–100 mg OD (or clopidogrel if intolerant)
- Antianginals: Beta-blockers (1st line), nitrates (sublingual for acute; long-acting for prophylaxis), CCBs (especially amlodipine), ivabradine (rate control if BB contraindicated)
- Statins: All patients (plaque stabilisation + lipid lowering)
- ACE inhibitors: If diabetes, LV dysfunction, hypertension
- Revascularisation (PCI/CABG): If refractory to medical therapy or high-risk anatomy
- ISCHEMIA trial: Revascularisation ≠ reduced MI/death vs medical therapy in stable IHD with EF >35%; but better angina relief
ACS / STEMI / NSTEMI
- MONA (mnemonic for acute): Morphine (pain), Oxygen (if SpO₂ <94%), Nitrates, Aspirin
- Dual antiplatelet: Aspirin + P2Y12 inhibitor (ticagrelor preferred > clopidogrel)
- Anticoagulation: LMWH (enoxaparin) or UFH
- STEMI: Primary PCI within 90 min (door-to-balloon) — gold standard; thrombolysis if PCI unavailable within 120 min
- NSTEMI: PCI within 24–72 hrs based on risk score (GRACE, TIMI)
- Beta-blockers: Start within 24 hrs if no cardiogenic shock
- ACE inhibitor/ARB: Start within 24 hrs, especially anterior MI / reduced EF
- Statin: High-intensity (atorvastatin 80 mg or rosuvastatin 40 mg)
10. HKMLE HIGH-YIELD POINTS ⭐
| Topic | Key Fact |
|---|---|
| Most common cause of IHD | Atherosclerosis (>90%) |
| Most common cause of MI | Plaque rupture + acute thrombosis |
| Most common cause of death before hospitalisation | Ventricular fibrillation |
| Most specific marker for MI | Troponin I/T |
| Earliest marker | Myoglobin |
| Best for re-infarction | CK-MB |
| Silent MI most common in | Diabetics (autonomic neuropathy) + elderly |
| Reperfusion injury hallmark | Contraction band necrosis |
| Free wall rupture timing | 3–7 days post-MI (most dangerous week) |
| Dressler's syndrome | Weeks post-MI, autoimmune pericarditis |
| Prinzmetal angina ECG | ST elevation at rest (not depression) |
| Levine's sign | Clenched fist over sternum (typical angina descriptor) |
| CCS Class IV | Angina at rest |
| LAD occlusion | Anterior + septal infarct (V1–V4) |
| RCA occlusion | Inferior infarct + SA/AV node involvement (heart block risk) |
| ISCHEMIA trial finding | PCI ≠ mortality benefit over medical therapy in stable IHD with EF >35% |
| Posteromedial papillary rupture | Single blood supply → more vulnerable to necrosis |
| No-reflow phenomenon | Microvascular occlusion by leukocytes after reperfusion |
| Most common complication in first hour | Arrhythmia (VF/VT) |
| Cardiogenic shock threshold | >40% LV myocardium infarcted |
Sources: Robbins & Kumar Basic Pathology (9e), Harrison's Principles of Internal Medicine (22e, 2025), Braunwald's Heart Disease (11e)
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