HKMLE COMPLETE STUDY NOTE
MODULE 1D: VALVULAR HEART DISEASE
Papers 1 & 2 — High-Yield, Ace-Level Reference
Date: August 2026

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TABLE OF CONTENTS
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1. Aortic Stenosis (AS)
2. Aortic Regurgitation (AR)
3. Mitral Stenosis (MS)
4. Mitral Regurgitation (MR)
5. Rheumatic Heart Disease (RHD)
6. Drug Traps Table
7. Notable Trials Table
8. Master Mnemonics Table
9. Cross-Module Links

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SECTION 1: AORTIC STENOSIS (AS)
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DEFINITION
Aortic stenosis is narrowing of the aortic valve orifice causing obstruction to
left ventricular outflow. Severe AS is defined as: valve area < 1.0 cm2,
mean gradient > 40 mmHg, or peak jet velocity > 4 m/s.

CLASSIFICATION TABLE
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Type            | Cause                   | Age group
-----------------------------------------------------------------------
Congenital      | Bicuspid aortic valve   | < 60 years (most common
                |                         | cause in younger adults)
Calcific/       | Age-related calcification| > 65 years (most common
Degenerative    | (atherosclerotic process)| overall in HK + West)
Rheumatic       | Commissural fusion      | Any age (developing world)
-----------------------------------------------------------------------

AETIOLOGY — MNEMONIC: "BAD Valves"
B — Bicuspid aortic valve (congenital, 1–2% of population)
A — Age-related calcification (degenerative; most common cause >65 yrs)
D — Disease: Rheumatic heart disease (causes commissural fusion)

PATHOPHYSIOLOGY (Step-by-Step)
Step 1: Valve leaflets narrow → increased resistance to LV outflow
Step 2: LV pressure rises to maintain cardiac output
Step 3: LV responds with CONCENTRIC HYPERTROPHY (wall thickens,
        cavity size stays normal) — this is pressure overload
Step 4: Hypertrophy increases oxygen demand → subendocardial ischaemia
Step 5: Diastolic dysfunction develops (stiff LV)
Step 6: Eventually cardiac output falls → symptoms develop
Step 7: End-stage: LV dilates → systolic dysfunction → heart failure

BEGINNER TIP: AS = PRESSURE overload → THICK (concentric hypertrophy)
             AR/MR = VOLUME overload → BIG (eccentric hypertrophy)

RISK FACTORS — MNEMONIC: "CHARM"
C — Congenital bicuspid valve
H — Hypertension, Hyperlipidaemia
A — Age (>65)
R — Rheumatic fever
M — Male sex

SYMPTOMS — MNEMONIC: "SAD" (classic triad — KNOW THIS!)
S — Syncope (on exertion — late sign, poor prognosis)
A — Angina (subendocardial ischaemia; can occur with normal coronaries)
D — Dyspnoea (exertional → rest → orthopnoea → PND)

PROGNOSIS ONCE SYMPTOMS DEVELOP:
Angina:    mean survival 5 years
Syncope:   mean survival 3 years
Dyspnoea:  mean survival 2 years
(Mnemonic: "ASD 5-3-2")

SIGNS — MNEMONIC: "SPINE of the exam"
S — Slow-rising, plateau pulse (pulsus parvus et tardus)
P — Pulse pressure NARROW (low SBP, normal/high DBP)
I — Impulse: heaving, sustained, non-displaced apex beat
N — Narrow A2 (soft/absent second heart sound)
E — Ejection systolic murmur (ESM): crescendo-decrescendo,
    radiates to carotids, best heard at right 2nd intercostal space
    with patient sitting forward

ADDITIONAL SIGNS:
- Ejection click (in bicuspid valve — disappears as valve calcifies)
- Systolic thrill at aortic area
- S4 gallop (due to stiff LV)
- Signs of heart failure (late)

MURMUR DESCRIPTION: "HERO"
H — Harsh quality
E — Ejection systolic (mid-systolic, crescendo-decrescendo)
R — Radiates to carotids ("jet stream" to neck)
O — Obliterates/softens A2

INVESTIGATIONS — MNEMONIC: "BECAM"
B — Bedside: ECG, BP both arms (rule out coarctation/dissection)
E — Echo (TTE — FIRST-LINE investigation of choice)
C — Catheterisation (gold standard if echo inconclusive or pre-op)
A — AXR/CXR (calcification in valve, post-stenotic aortic dilatation)
M — MRI cardiac (if echo windows poor)

DIAGNOSTIC ALGORITHM:
Bedside: ECG (LVH — voltage criteria, strain pattern in lateral leads)
         CXR (normal heart size in early AS; aortic knuckle prominent)
Labs:    BNP/NT-proBNP (elevated = worse prognosis/haemodynamic stress)
         FBC, U&E, LFTs pre-op
Imaging: TTE — FIRST line. Assess: valve area (AVA), gradient, LVEF
         TOE — if TTE poor quality
         Coronary angiogram — pre-operatively if age >40 or angina
         CT calcium scoring — assess aortic valve calcification burden

INVESTIGATION INTERPRETATION BOX:
Classic Echo report: "AVA 0.7 cm2, peak gradient 72 mmHg,
mean gradient 45 mmHg, LVEF 55%"
Interpretation: Severe aortic stenosis with preserved ejection fraction
(most common presentation requiring valve replacement)

ECG Findings:
- LVH: Sokolow-Lyon criteria (SV1 + RV5/V6 > 35 mm)
- Left axis deviation
- Lateral ST depression + T-wave inversion ("strain pattern")
- LBBB (late sign)

MANAGEMENT

ACUTE DECOMPENSATION (Severe AS + pulmonary oedema):
Step 1: Sit up, O2 15L via non-rebreather mask, IV access x2
Step 2: IV GTN ONLY if SBP > 110 (use with extreme caution — AS
        patients are PRELOAD dependent; vasodilators cause collapse)
Step 3: IV frusemide 40-80 mg for pulmonary oedema
Step 4: Avoid tachycardia (worsens filling) — rate control if AF
Step 5: URGENT referral to cardiology — likely valve intervention needed
Step 6: Balloon aortic valvuloplasty as BRIDGE to definitive therapy

CHRONIC MANAGEMENT:
Medical: No drug slows AS progression. Manage risk factors.
         Statins: NO proven benefit in halting calcification (SALTIRE
         and SEAS trials showed no benefit — EXAM TRAP!)
         ACEi/ARBs: Use with caution; avoid if severe AS + symptoms
         Diuretics: For symptom control only
         Beta-blockers: Avoid in severe symptomatic AS (drop HR,
         reduce CO)

Definitive Treatment — VALVE REPLACEMENT:

SURGICAL AORTIC VALVE REPLACEMENT (SAVR):
- Gold standard for low–intermediate surgical risk patients
- Preferred if age < 65 years (longevity of mechanical valve)
- Mechanical valve: needs lifelong warfarin (INR 2.5–3.5)
- Bioprosthetic valve: no anticoagulation needed, but lasts 10–15 yrs

TRANSCATHETER AORTIC VALVE IMPLANTATION (TAVI/TAVR):
- Preferred for high/prohibitive surgical risk or age > 75–80
- Via femoral artery (transfemoral — first choice) or transapical route
- Post-TAVI: dual antiplatelet (aspirin + clopidogrel) x 3–6 months,
  then aspirin alone
- Complications: stroke, vascular access complications, paravalvular
  leak, need for pacemaker (LBBB/complete heart block common)

INDICATIONS FOR INTERVENTION (ACC/AHA 2020 + ESC/EACTS 2021):
Class I (recommended):
- Symptomatic severe AS (any of SAD triad)
- Severe AS + LVEF < 50% (even if asymptomatic)
- Severe AS undergoing other cardiac surgery

Class IIa (reasonable):
- Asymptomatic severe AS + abnormal exercise test
- Asymptomatic very severe AS (Vmax > 5 m/s) at low surgical risk
- Asymptomatic severe AS + rapidly progressive disease
- BNP > 3x upper limit of normal

HA CLINICAL PATHWAY BOX:
In Hong Kong HA hospitals:
- TTE is first-line imaging for all suspected AS
- Heart team (cardiologist + cardiac surgeon) review ALL cases of
  severe AS before intervention
- TAVI programme available at QMH, PWH, and PYNEH
- Patients > 75 with high STS score referred for TAVI assessment
- Post-TAVI patients followed up at 30 days, 3 months, 1 year

HKMLE TRAP BOX 1:
Statins do NOT slow AS progression. If a question asks "which drug
slows the progression of aortic stenosis?" — the answer is NONE.
SALTIRE and SEAS trials both showed no benefit of statins.

HKMLE TRAP BOX 2:
Balloon aortic valvuloplasty is NOT a definitive treatment for
calcific AS in adults. It is only a bridge to definitive therapy or
palliation. In children with congenital AS, valvuloplasty IS
appropriate as first-line — do NOT confuse.

HKMLE TRAP BOX 3:
Nitrates and vasodilators are DANGEROUS in AS (reduced preload
causes catastrophic fall in BP). The question stem may describe a
patient with AS given sublingual GTN for "chest pain" — recognise
the trap.

COMPLICATIONS — MNEMONIC: "SAFE"
S — Syncope, Sudden cardiac death
A — Angina
F — Failure (heart failure, pulmonary oedema)
E — Endocarditis (bicuspid valves are especially at risk)
     Emboli (calcific emboli → stroke/TIA)

RED FLAGS:
- Syncope on exertion → surgery within weeks, not months
- LVEF < 50% → urgent surgery
- Rapid symptom onset in known AS → emergency review
- New LBBB in AS patient → possible complete heart block

COMMON EXAM QUESTION BOX:
Q: A 72-year-old man has exertional chest pain, dyspnoea and
syncopal episodes. Examination reveals a slow-rising pulse,
narrow pulse pressure, and an ejection systolic murmur radiating
to the carotids. What is the single most useful investigation?
A: Transthoracic echocardiography (TTE)

Q: What is the murmur of aortic stenosis?
A: Ejection systolic (crescendo-decrescendo), loudest at right
second intercostal space, radiates to carotids.

BASIC SCIENCE INTEGRATION BOX:
The Frank-Starling mechanism maintains CO initially in AS.
Concentric LVH reduces wall stress (by Laplace's Law: stress =
pressure x radius / 2 x wall thickness). As wall thickness
increases, the denominator rises and wall stress is normalised.
However, the hypertrophied myocardium has impaired diastolic
relaxation and is more susceptible to subendocardial ischaemia
due to increased oxygen demand + reduced coronary perfusion
in diastole (high LVEDP compresses subendocardial vessels).

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SECTION 2: AORTIC REGURGITATION (AR)
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DEFINITION
Aortic regurgitation (incompetence) is the backflow of blood from the
aorta into the LV during diastole, due to failure of aortic valve leaflets
to coapt completely.

CLASSIFICATION:
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Acute AR                    | Chronic AR
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Sudden valve failure        | Gradual volume overload
LV cannot compensate        | LV dilates and hypertrophies
Pulmonary oedema common     | Long asymptomatic period
Emergency surgery needed    | Surgery when LV decompensates
-----------------------------------------------------------------------

AETIOLOGY — MNEMONIC: "MARBLE"
M — Marfan syndrome (aortic root dilatation)
A — Aortic dissection (Type A — acute AR emergency)
R — Rheumatic heart disease (leaflet fusion/scarring)
B — Bicuspid aortic valve
L — Lues (syphilis — aortitis, old but classic exam answer)
E — Endocarditis (leaflet destruction)

Also: Ankylosing spondylitis, reactive arthritis (HLA-B27 diseases)

PATHOPHYSIOLOGY (Step-by-Step)

CHRONIC AR:
Step 1: Blood regurgitates back into LV in diastole
Step 2: LV receives extra volume load (regurgitant + normal filling)
Step 3: LV responds with ECCENTRIC HYPERTROPHY (cavity dilates,
        walls also thicken) — VOLUME overload
Step 4: LV compensates: increased total stroke volume maintains
        forward cardiac output
Step 5: Aortic diastolic pressure falls → wide pulse pressure
Step 6: Eventually LV cannot compensate → LVEF falls → HF symptoms

ACUTE AR:
Step 1: Sudden regurgitation into a NORMAL-SIZED LV
Step 2: LV cannot acutely dilate → LVEDP rises dramatically
Step 3: Mitral valve closes early (high LVEDP)
Step 4: Pulmonary oedema and cardiogenic shock develop rapidly
Step 5: EMERGENCY — immediate surgery required

SYMPTOMS:
Chronic (often asymptomatic for years):
- Exertional dyspnoea (most common presenting symptom)
- Orthopnoea, PND
- Palpitations (bounding, forceful heartbeat)
- Exertional angina (despite usually normal coronaries)

Acute:
- Sudden-onset severe dyspnoea/pulmonary oedema
- Hypotension, shock
- Fever (if endocarditis is cause)

SIGNS — MNEMONIC: "WWW CEDRA" (for the eponymous signs)
Pulse Signs:
W — Water-hammer (Corrigan's) pulse: bounding, collapsing
W — Wide pulse pressure (e.g. 160/40 — SBP high, DBP very low)
W — Wandering — visible carotid pulsations (Corrigan's neck sign)

Eponymous Signs (high-yield for MCQ):
C — Corrigan's: visible pulsation in neck/carotid
E — de Musset's: head nodding with each heartbeat
D — Duroziez's: systolic + diastolic murmurs over femoral artery
    with compression
R — Rosenbach's: liver pulsation
A — Austin Flint murmur: mid-diastolic murmur at apex (regurgitant
    jet pushes against anterior mitral leaflet, simulating MS)
    Quincke's: capillary pulsation in nail beds

Cardiac Examination:
- Apex beat: displaced laterally and inferiorly (dilated LV)
- Apex character: THRUSTING/HYPERDYNAMIC (volume overload)
- Murmur: EARLY DIASTOLIC, high-pitched, blowing, decrescendo,
  best heard at left sternal edge (3rd-4th ICS), with patient
  sitting forward and breath held in expiration
- Soft S1 (early mitral valve closure)
- S3 gallop (volume overload, dilated LV)

INVESTIGATIONS — MNEMONIC: "CLUE"
C — CXR (cardiomegaly, aortic root dilatation, pulmonary oedema)
L — LV function on Echo (most important investigation)
U — Ultrasound (TTE/TOE) — grade severity, assess root
E — ECG (LVH, left axis deviation)

Specific Echo findings:
- Dilated LV (LVIDd > 70 mm = severe dilatation)
- Fluttering of anterior mitral leaflet (Austin Flint mechanism)
- Holodiastolic flow reversal in descending aorta
- Colour Doppler: regurgitant jet width/LVOT ratio grades severity

MANAGEMENT

ACUTE AR (Emergency):
Step 1: Resuscitate — O2, IV access, monitor
Step 2: IV vasodilators (sodium nitroprusside) + inotropes if shocked
Step 3: Do NOT use intra-aortic balloon pump (IABP inflates in
        diastole — CONTRAINDICATED in AR as it WORSENS regurgitation)
Step 4: URGENT cardiac surgery (emergency AVR)
Step 5: If infective endocarditis: start antibiotics first, then surgery

CHRONIC AR (Medical):
- Vasodilators (ACEi, amlodipine) if LVEF impaired or hypertension
- Beta-blockers for Marfan syndrome (reduce aortic root expansion)
- Serial Echo monitoring: every 1–2 years (mild-moderate),
  6–12 months (severe asymptomatic)

INDICATIONS FOR SURGERY (ACC/AHA 2020):
Class I:
- Symptomatic severe AR
- Severe AR + LVEF < 55%
- Severe AR undergoing other cardiac surgery

Class IIa:
- Asymptomatic severe AR + LVEF 55–60% (progressive LV dilatation)
- Asymptomatic + LVIDd > 65 mm (or > 50 mm/m2 BSA)
- Aortic root > 55 mm (Marfan: > 50 mm; bicuspid: > 55 mm)

Type of surgery:
- Valve repair (if anatomy suitable) or replacement
- Bentall procedure: composite valve + root replacement (if root disease)

HKMLE TRAP BOX:
IABP is CONTRAINDICATED in AR. It is also contraindicated in
aortic dissection and severe aortic regurgitation. Do not confuse
with cardiogenic shock from other causes where IABP may help.

HKMLE TRAP BOX 2:
The Austin Flint murmur of AR mimics mitral stenosis (both are
mid-diastolic murmurs at the apex). Differentiating features:
- Austin Flint: NO opening snap, WIDE pulse pressure, collapsing
  pulse, early diastolic murmur also present
- True MS: opening snap present, narrow pulse pressure,
  slow-rising pulse (not collapsing)

COMPLICATIONS — MNEMONIC: "FHE"
F — Failure (LV systolic dysfunction, heart failure)
H — Heart block, infective endocarditis
E — Emboli, aortic root complications (Marfan aneurysm rupture)

COMMON EXAM QUESTION BOX:
Q: A young man with tall stature, long arms, pectus excavatum and
arachnodactyly presents with an early diastolic murmur. What is
the diagnosis and most appropriate next investigation?
A: Marfan syndrome with aortic regurgitation.
Investigation: TTE (Echo) to assess aortic root diameter and AR severity.

Q: Which peripheral sign of AR involves head nodding?
A: de Musset's sign

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SECTION 3: MITRAL STENOSIS (MS)
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DEFINITION
Mitral stenosis is narrowing of the mitral valve orifice, obstructing
diastolic flow from the left atrium to the left ventricle.
Normal mitral valve area (MVA): 4–6 cm2
Mild MS: MVA > 1.5 cm2
Moderate MS: MVA 1.0–1.5 cm2
Severe MS: MVA < 1.0 cm2 (or mean gradient > 10 mmHg)

CLASSIFICATION:
-----------------------------------------------------------------------
Severity    | MVA (cm2) | Mean Gradient | PHT (ms)
-----------------------------------------------------------------------
Mild        | > 1.5     | < 5 mmHg      | < 100
Moderate    | 1.0–1.5   | 5–10 mmHg     | 100–150
Severe      | < 1.0     | > 10 mmHg     | > 150
-----------------------------------------------------------------------

AETIOLOGY — MNEMONIC: "RACE"
R — Rheumatic heart disease (most common cause — 99% in HK/Asia)
A — Age-related calcification (rare, elderly)
C — Congenital (rare, parachute mitral valve)
E — Endocarditis (rare cause of MS)

LOCAL EPIDEMIOLOGY VARIANT BOX:
In Hong Kong, rheumatic heart disease remains the dominant cause
of mitral stenosis. While prevalence has declined with improved
living standards and antibiotic access, MS is STILL significantly
more common in Hong Kong and Asia compared to Western Europe/USA.
Many patients presenting with MS in HK are immigrants from mainland
China, South/Southeast Asia where rheumatic fever remains endemic.
This is a HIGH-YIELD HK-specific fact for your exam.

PATHOPHYSIOLOGY (Step-by-Step)
Step 1: Rheumatic fever → immune-mediated inflammation of mitral leaflets
Step 2: Leaflet thickening, commissural fusion, chordal shortening/fusion
Step 3: Mitral orifice narrows → obstruction to LV filling
Step 4: Left atrial pressure rises → left atrial dilatation
Step 5: Raised LA pressure → pulmonary venous hypertension →
        pulmonary oedema (dyspnoea, orthopnoea)
Step 6: Pulmonary arterial hypertension develops (reactive vasoconstriction)
Step 7: Right heart failure (RVH, tricuspid regurgitation)
Step 8: Left atrial dilatation → atrial fibrillation → thrombus → stroke
Step 9: LV is PROTECTED (MVA limits filling) — LV is actually SMALL
        and may have NORMAL or LOW function

SYMPTOMS — MNEMONIC: "DOHH"
D — Dyspnoea (exertional → rest; hallmark symptom)
O — Orthopnoea and PND (raised PAWP)
H — Haemoptysis (from pulmonary venous hypertension — pink frothy
    sputum or frank haemoptysis from bronchial vein rupture)
H — Hoarseness (Ortner's syndrome: enlarged LA compresses left
    recurrent laryngeal nerve)

Also: Palpitations (AF), systemic emboli/stroke (from LA thrombus),
right heart failure symptoms (oedema, ascites)

BEGINNER TIP on Ortner's Syndrome:
The LEFT recurrent laryngeal nerve hooks under the aortic arch.
An enlarged left atrium can compress this nerve causing hoarseness.
This is PATHOGNOMONIC of severe mitral stenosis in exams.

SIGNS — MNEMONIC: "MOST" + extras
M — Malar flush (mitral facies — bilateral bluish-red patches on cheeks
    due to low CO and peripheral vasoconstriction)
O — Opening snap (OS) — high-pitched early diastolic sound after S2;
    reflects valve opening; shorter S2-OS interval = more severe MS
S — Signs of AF (irregularly irregular pulse)
T — Tapping apex beat (non-displaced; palpable S1 due to stiff, loud MV)

Also:
- Mid-diastolic murmur at the apex: LOW-PITCHED, rumbling, best
  heard with patient in left lateral decubitus position, with the
  bell of the stethoscope; may have PRESYSTOLIC ACCENTUATION
  (if in sinus rhythm, due to atrial contraction)
- LOUD S1 (due to wide-open leaflets being shut forcefully)
- Parasternal heave (RV hypertrophy)
- Elevated JVP (pulmonary hypertension/RV failure)
- Signs of right heart failure

MURMUR DETAILS:
Position: Apex (left lateral decubitus)
Character: Low-pitched, rumbling
Timing: Mid-diastolic (after opening snap)
Accentuation: Presystolic accentuation (if sinus rhythm — lost in AF)
Bell > Diaphragm (low frequency)
Increases with: Exercise, left lateral position, expiration

INVESTIGATIONS — MNEMONIC: "ECCL"
E — ECG (P mitrale — bifid P waves; RVH if pulm HT; AF)
C — CXR (see below)
C — Colour Doppler TTE (diagnostic, grades severity by MVA and PHT)
L — Left heart catheterisation (if echo inconclusive or pre-procedure)

CXR Findings:
- Straightening of left heart border (enlarged LA appendage)
- Double density right heart border (enlarged LA behind RA)
- Splaying of carina (enlarged LA pushes up left main bronchus)
- Pulmonary oedema features (Kerley B lines, upper lobe diversion)
- Calcification of mitral valve (in chronic disease)

INVESTIGATION INTERPRETATION BOX:
Echo: "MVA 0.9 cm2 by PHT (220 ms), mean gradient 12 mmHg,
moderate-severe pulmonary hypertension with RVSP 55 mmHg,
LA diameter 55 mm"
Interpretation: Severe rheumatic mitral stenosis with pulmonary
hypertension and left atrial dilatation — indication for intervention.

MANAGEMENT

ACUTE DECOMPENSATION (MS + AF with fast ventricular rate):
Step 1: O2, monitoring, IV access
Step 2: Rate control FIRST: IV metoprolol 2.5–5 mg or IV digoxin
        (rate control slows heart → more time for LV filling)
Step 3: IV frusemide if pulmonary oedema
Step 4: Anticoagulate if AF (high stroke risk) — heparin then warfarin
Step 5: Consider electrical cardioversion if haemodynamically unstable

CHRONIC MANAGEMENT:

Rate control in AF:
- Beta-blockers (metoprolol) — first choice
- Rate-limiting calcium channel blockers (verapamil, diltiazem)
- Digoxin (third line or addition)

Anticoagulation:
- Warfarin (target INR 2–3) for AF or prior emboli
- NOACs (direct oral anticoagulants) are NOT recommended in
  rheumatic MS (valvular AF) — WARFARIN remains the standard
  (HKMLE TRAP: NOACs are for non-valvular AF only!)

Beta-blockers: Reduce exertional symptoms by reducing heart rate

Intervention (definitive):
PERCUTANEOUS MITRAL BALLOON COMMISSUROTOMY (PMBC/PBMV):
- Preferred if:
  * Pliable, non-calcified valve (Wilkins score < 8)
  * No significant MR
  * No LA thrombus (TOE to exclude)
  * No severe subvalvular disease
- Technique: Balloon inflated across stenotic mitral valve via
  transseptal approach
- Excellent results: MVA doubles, symptoms improve dramatically

MITRAL VALVE REPLACEMENT:
- If valve unsuitable for PBMV (calcified, heavily fused, MR present)
- Mechanical valve preferred in young patients with AF
  (already need anticoagulation)
- Bioprosthetic if anticoagulation contraindicated

HA CLINICAL PATHWAY BOX:
In HK HA hospitals:
- All new MS referred to cardiologist for TTE assessment
- TOE mandatory before PBMV to exclude LA thrombus
- Wilkins echocardiographic score used to select PBMV candidates
- Anti-rheumatic prophylaxis (penicillin) continued per guidelines
- Warfarin (NOT NOACs) for AF + MS

HKMLE TRAP BOX 1:
NOACs (rivaroxaban, apixaban, dabigatran) are CONTRAINDICATED
in rheumatic (valvular) AF with mitral stenosis. This has been
specifically studied — ENGAGE AF-TIMI 48, RE-LY, ROCKET-AF all
excluded valvular AF. Use WARFARIN for rheumatic MS with AF.

HKMLE TRAP BOX 2:
The presystolic accentuation of the MS murmur DISAPPEARS when
AF develops (because there is no atrial contraction in AF).
This is a classic exam distinction.

HKMLE TRAP BOX 3:
The opening snap (OS) of MS: shorter S2-OS interval = MORE severe
(higher LA pressure closes valve more rapidly, OS comes earlier).
Do NOT confuse: "closer = more severe."

COMPLICATIONS — MNEMONIC: "SAFE PAH"
S — Stroke (LA thrombus → embolism, most common in AF)
A — AF (most common arrhythmia)
F — Failure (pulmonary oedema, right heart failure)
E — Embolism (systemic)
P — Pulmonary Arterial Hypertension
A — Aortic/laryngeal compression (Ortner's)
H — Haemoptysis

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SECTION 4: MITRAL REGURGITATION (MR)
================================================================================

DEFINITION
Mitral regurgitation is backward flow of blood from the LV into the LA
during systole due to failure of mitral valve leaflet coaptation.

CLASSIFICATION TABLE:
-----------------------------------------------------------------------
Type        | Mechanism       | Causes
-----------------------------------------------------------------------
Primary (   | Leaflet/chordal | Myxomatous degeneration (MVP),
organic)    | abnormality     | rheumatic, endocarditis, radiation
Secondary   | Annular/LV      | Ischaemic MR, dilated CMP, HFrEF
(functional)| remodelling     | (any cause of LV dilatation)
Acute MR    | Sudden rupture  | Papillary muscle rupture (post-MI),
            |                 | chordal rupture, endocarditis
-----------------------------------------------------------------------

AETIOLOGY — MNEMONIC: "PRIME"
P — Prolapse (mitral valve prolapse/myxomatous — most common in West)
R — Rheumatic heart disease (most common in HK/Asia)
I — Ischaemic (papillary muscle dysfunction or rupture post-MI)
M — Myxomatous degeneration (Marfan, connective tissue disease)
E — Endocarditis (leaflet destruction)

LOCAL EPIDEMIOLOGY VARIANT BOX:
In HK, rheumatic MR remains more prevalent than in the West, where
myxomatous/mitral valve prolapse is the predominant cause. When the
exam scenario involves a young Asian patient — rheumatic is more likely.
When scenario involves older Western patient — MVP more likely.

PATHOPHYSIOLOGY

CHRONIC MR (Step-by-Step):
Step 1: Mitral valve incompetent → blood regurgitates into LA in systole
Step 2: LA receives extra volume → LA pressure rises → LA dilates
Step 3: LV empties into low-resistance LA → initially LV feels "unloaded"
Step 4: Total LV stroke volume increases (forward + regurgitant)
Step 5: LV undergoes ECCENTRIC HYPERTROPHY (volume overload → dilates)
Step 6: LVEF may appear falsely normal (ejecting into low-resistance LA)
Step 7: When LV finally decompensates, LVEF falls to "abnormal" levels
        (TRAP: LVEF < 60% in MR is already significant dysfunction!)
Step 8: Pulmonary hypertension → right heart failure

ACUTE MR (Step-by-Step):
Step 1: Sudden large regurgitation into NORMAL-SIZED LA
Step 2: LA cannot dilate acutely → LA pressure spikes dramatically
Step 3: Pulmonary venous pressure rises → flash pulmonary oedema
Step 4: Forward CO falls → cardiogenic shock
Step 5: Loud murmur may be SOFT or absent in severe acute MR
        (pressure equalises between LV and LA quickly)
Step 6: EMERGENCY — urgent surgery required

SYMPTOMS:
Chronic (asymptomatic for years):
- Exertional dyspnoea (most common)
- Fatigue (reduced forward CO)
- Palpitations (AF from LA dilatation)
- Orthopnoea, PND (when LA pressure rises)

Acute:
- Sudden severe dyspnoea, orthopnoea
- Signs of cardiogenic shock (post-MI papillary muscle rupture —
  typically day 2–7 post inferior MI)

SIGNS — MNEMONIC: "PALM"
P — Pansystolic murmur at apex, radiates to axilla
    (harsh, blowing; in MVP — mid-late systolic click + murmur)
A — Apex: displaced inferolaterally, HYPERDYNAMIC (thrusting)
L — Loud P2 (pulmonary hypertension sign)
M — Mitral click (in MVP — mid-systolic click)

Cardiac Examination Details:
- Pulse: normal or fast (AF)
- JVP elevated if RV failure
- Pansystolic murmur:
  * Best at apex with diaphragm
  * Radiates to axilla (and sometimes to back)
  * Increases with squatting (increases preload/afterload)
  * Decreases with Valsalva or standing (reduces preload)
  * Grade 3–6/6 in significant MR
- S3 (volume overload — very important sign of severity)
- Soft S1 (leaflets don't close properly)

INVESTIGATIONS — MNEMONIC: "FEEL"
F — Function (LV): LVEF on Echo — critical (< 60% = already severe)
E — Echo (TTE + colour Doppler — definitive investigation)
E — ECG (P mitrale, LVH, AF)
L — Left heart cath + coronary angiogram (pre-op, rule out ischaemia)

Echo Parameters for Severe MR:
- Vena contracta > 7 mm
- Regurgitant volume > 60 mL
- ERO (effective regurgitant orifice) > 0.40 cm2
- LA dilatation, LV dilatation

MANAGEMENT

ACUTE MR (Emergency — e.g. papillary muscle rupture post-MI):
Step 1: O2, IV access, monitoring, call cardiac team
Step 2: IV vasodilators (sodium nitroprusside) — reduce afterload,
        increase forward CO
Step 3: Intra-aortic balloon pump (IABP) — INDICATED in acute MR
        (unlike in AR — reduces afterload, improves forward CO)
Step 4: Urgent echo to confirm diagnosis
Step 5: Emergency mitral valve surgery (repair or replacement)
Step 6: Treat underlying MI with PCI/thrombolysis first if possible

CHRONIC MR (Medical — for secondary/functional MR):
- ACEi/ARBs: reduce afterload, helpful in functional MR
- Beta-blockers, diuretics: for HF symptoms
- Aldosterone antagonist if HFrEF features
- Anticoagulation: if AF develops (warfarin if rheumatic)
- GDMT (guideline-directed medical therapy): for functional MR

Transcatheter MitraClip:
- Percutaneous edge-to-edge mitral valve repair
- For patients with severe primary MR who are high surgical risk
- COAPT trial (2018): in functional MR, MitraClip significantly
  reduced hospitalisations and mortality

INDICATIONS FOR SURGERY (ACC/AHA 2020):
Class I:
- Symptomatic severe primary MR (LVEF > 30%)
- Asymptomatic severe primary MR + LVEF < 60% or LVESD > 40 mm

Class IIa:
- Asymptomatic severe MR + AF or pulmonary hypertension
- Rheumatic MR amenable to repair (highly durable in expert centres)

Type of Surgery:
- Mitral valve REPAIR preferred over replacement when possible
  (preserves LV function, no anticoagulation needed for repair)
- If repair not feasible: valve replacement
- Mechanical valve: younger patients, already in AF needing warfarin
- Bioprosthetic: older patients or anticoagulation contraindicated

HKMLE TRAP BOX 1:
LVEF of 55–60% in MR is already ABNORMAL. In MR, the LV ejects
into the low-resistance LA, so LVEF appears artificially elevated.
A "normal" LVEF of 55% in someone with severe MR is actually a sign
of LV dysfunction. Surgery should be considered at LVEF < 60%.

HKMLE TRAP BOX 2:
IABP is INDICATED in acute MR (reduces afterload) but CONTRAINDICATED
in acute AR. Know both — this distinction is a frequent MCQ trap.

HKMLE TRAP BOX 3:
Acute MR post-MI classically presents on day 2–7 with SUDDEN onset
severe dyspnoea and a NEW pansystolic murmur. It is due to posterior
papillary muscle rupture (supplied only by posterior descending artery —
less collateral supply than anterior papillary muscle).

COMPLICATIONS — MNEMONIC: "AFSHE"
A — Atrial fibrillation (LA dilatation)
F — Failure (pulmonary oedema, right heart failure)
S — Stroke (AF + LA thrombus)
H — Heart failure (LV decompensation)
E — Endocarditis

COMMON EXAM QUESTION BOX:
Q: A 58-year-old man presents on day 4 after an inferior MI with sudden
severe dyspnoea and a loud pansystolic murmur. What is the diagnosis
and immediate management?
A: Acute MR due to posterior papillary muscle rupture.
Immediate: O2, IV nitroprusside, IABP, urgent echo, emergency MVR.

Q: What is the murmur of MR?
A: Pansystolic, blowing, best at apex, radiates to axilla,
louder with squatting, softer with Valsalva.

================================================================================
SECTION 5: RHEUMATIC HEART DISEASE (RHD)
================================================================================

DEFINITION
Rheumatic heart disease is the chronic cardiac sequela of acute rheumatic
fever (ARF), an inflammatory condition triggered by Group A Streptococcal
(GAS) pharyngitis. It results in progressive valve damage, most commonly
affecting the mitral valve.

AETIOLOGY — MNEMONIC: "SGAS"
S — Streptococcus pyogenes (Group A beta-haemolytic Strep)
G — Group A: throat infection (NOT skin infection — important!)
A — Antibody cross-reactivity (molecular mimicry)
S — Susceptible host + repeated infections = cumulative valve damage

Pathogenesis:
GAS pharyngitis → host produces anti-streptococcal antibodies →
antibodies cross-react with cardiac myosin, valvular collagen,
neuronal antigens → inflammation of heart, joints, brain, skin

VALVE INVOLVEMENT IN RHEUMATIC HEART DISEASE (in order of frequency):
1. Mitral valve (most common — 65–70% of cases)
2. Aortic valve (30–40%)
3. Tricuspid valve (rarely significant)
4. Pulmonary valve (extremely rare — "relatively immune")
Mnemonic: "Mitral Most, Aortic And, Tricuspid Trickle, Pulmonary
Practically Protected" = MATP

ACUTE RHEUMATIC FEVER — JONES CRITERIA (2015 Revised)

DIAGNOSIS: 2 Major + 1 Minor OR 1 Major + 2 Minor criteria
(plus evidence of preceding GAS infection)

MAJOR CRITERIA — MNEMONIC: "JONES"
J — (no J — mnemonic only)
O — (Oedema of joints) — Arthritis (migratory polyarthritis —
    most common manifestation)
N — Nodules (subcutaneous — firm, painless, over bony prominences)
E — Erythema marginatum (skin: pink rings with clear centres,
    trunk + proximal limbs)
S — Sydenham's chorea (involuntary movements, emotional lability)
+ Carditis (pancarditis affecting pericardium, myocardium, endocardium)

ACTUAL MAJOR CRITERIA (5):
1. Carditis (clinical or subclinical — subclinical = echo only)
2. Arthritis — migratory polyarthritis (large joints)
   In high-prevalence settings (like HK/Asia): monoarthritis also counts
3. Chorea (Sydenham's) — delayed manifestation, after strep has cleared
4. Erythema marginatum (rare)
5. Subcutaneous nodules (rare)

MINOR CRITERIA:
1. Fever (> 38.5°C)
2. Elevated ESR or CRP
3. Prolonged PR interval on ECG
4. Arthralgia (ONLY if arthritis is NOT already a major criterion)

EVIDENCE OF PRIOR GAS INFECTION REQUIRED:
- Elevated ASO titre (anti-streptolysin O) > 200 IU/mL
- Elevated anti-DNase B
- Positive throat culture for GAS
- Rapid streptococcal antigen test

LOCAL EPIDEMIOLOGY VARIANT BOX:
In Hong Kong:
- ARF incidence has declined dramatically since the 1970s with
  improved housing, antibiotics and living standards
- However, RHD remains present in elderly HK residents and recent
  immigrants from high-prevalence areas
- Carditis with subclinical valvular disease (echocardiographic only)
  is increasingly recognised and is a major criterion in 2015 guidelines
- The 2015 AHA/WHF revised Jones criteria recommend echo for ALL
  suspected ARF cases — a change from older guidelines

INVESTIGATIONS IN ARF:
- Throat swab + culture
- ASO titre (repeat at 2 weeks if initially normal)
- Anti-DNase B
- ESR, CRP, WBC, FBC
- ECG (PR interval, arrhythmias)
- CXR (cardiac size)
- ECHOCARDIOGRAM — now recommended in ALL cases (2015 revision)

MANAGEMENT OF ACUTE RHEUMATIC FEVER:

Step 1: Eradicate GAS — Benzylpenicillin 1.2 million units IM
        single dose OR amoxicillin 500 mg TDS x 10 days
        (If penicillin allergic: azithromycin or cephalexin)
Step 2: Anti-inflammatory:
        - Arthritis: aspirin 80–100 mg/kg/day (children)
          OR naproxen (better tolerated)
        - Carditis (mild-moderate): NSAIDs
        - Carditis (severe — cardiac failure): oral prednisolone
          2 mg/kg/day x 2 weeks then taper
Step 3: Heart failure management: diuretics, ACEi, bed rest
Step 4: Chorea: haloperidol or valproate if severe
Step 5: Secondary prophylaxis: START IMMEDIATELY after acute episode

SECONDARY PROPHYLAXIS (PREVENTION OF RECURRENT ARF):
Goal: Prevent recurrent GAS pharyngitis → prevent further valve damage

DRUG OF CHOICE: Benzathine penicillin G (BPG)
- Dose: 1.2 million units IM every 4 weeks (every 3 weeks if high risk)
- Duration depends on risk (see below)

DURATION TABLE:
-----------------------------------------------------------------------
Category                              | Duration
-----------------------------------------------------------------------
ARF without carditis                  | 5 years or until age 21
                                      | (whichever is longer)
ARF with carditis, no residual VHD   | 10 years or until age 21
ARF with carditis + residual VHD     | Minimum 10 years or until
                                      | age 40 (whichever longer)
Severe VHD or post-valve surgery     | Lifelong prophylaxis
-----------------------------------------------------------------------

HA CLINICAL PATHWAY BOX:
HK HA protocol for secondary prophylaxis:
- Benzathine penicillin G 1.2 million units IM 4-weekly
- Patients enrolled in a dedicated rheumatic fever registry
  (primarily paediatric cardiology service)
- Oral penicillin V 250 mg BD is an alternative but less reliable
- Duration as per WHO/AHA guidelines above
- Annual echocardiography to monitor valve disease progression

CHP STATUTORY NOTIFICATION BOX:
Acute Rheumatic Fever (ARF) is NOT a statutory notifiable disease
in Hong Kong under Cap. 599B Infectious Disease Regulations.
However, it is a condition of public health significance and is
monitored by HA surveillance systems.
Group A Streptococcal invasive disease (iGAS) IS notifiable.

HKMLE TRAP BOX 1:
Secondary prophylaxis is benzathine penicillin IM — NOT daily oral
penicillin (oral has poor compliance and lower efficacy). The exam
will test the CORRECT drug and route.

HKMLE TRAP BOX 2:
Steroids in ARF: Only used for SEVERE carditis with heart failure.
They do NOT prevent the development of RHD (multiple trials showed
this). NSAIDs are first choice for arthritis. This is a classic trap.

HKMLE TRAP BOX 3:
ARF follows THROAT infection with GAS — NOT skin infection.
Streptococcal skin infections (impetigo) can cause glomerulonephritis
but NOT rheumatic fever. Know the distinction.

HKMLE TRAP BOX 4:
Chorea (Sydenham's) can appear MONTHS after the initial strep
infection — it is a DELAYED manifestation. The ASO titre may have
returned to normal by the time chorea develops. Do NOT dismiss the
diagnosis because ASO is normal if chorea is present.

Jones CRITERIA REVISION NOTE (2015):
The 2015 revision introduced SUBCLINICAL CARDITIS (echo only, no
auscultatory findings) as a major criterion. This was NOT in older
versions of Jones criteria. The HK exam may test the updated criteria.

CROSS-REFERENCE: For prophylaxis — see also Module Infections

================================================================================
SECTION 6: DRUG TRAPS TABLE
================================================================================

Drug / Class        | Trap / Pitfall                    | Correct Answer
--------------------+-----------------------------------+--------------------
Statins (all)       | Do NOT slow AS progression        | No drug slows AS
                    | (SALTIRE/SEAS trials)             |
Nitrates/GTN        | DANGEROUS in severe AS —          | Avoid in severe
                    | causes collapse (preload drop)    | symptomatic AS
ACEi/ARBs           | Can be used in AR (vasodilate)   | CONTRAINDICATED
                    | but CAUTION in severe AS          | in severe AS
NOACs               | NOT for rheumatic (valvular) AF   | Use WARFARIN
(rivaroxaban etc)   | with MS — excluded from trials   |
IABP                | CONTRAINDICATED in AR            | USE in acute MR
                    | (worsens regurgitation)           | (reduces afterload)
Beta-blockers       | AVOID in severe symptomatic AS    | Use in HCM, AR
                    | (reduce CO further)               | post-MI, HF
Verapamil/Diltiazem | AVOID in heart failure/LVEF <40  | Can use for rate
                    | Can use for rate control in AF+MS | control in MS/AF
Digoxin             | NOT first-line rate control in    | Use BB or RLCCBs
                    | MS with sinus rhythm              | first
Benzathine pen G    | Route = IM (NOT oral)            | 1.2 MU IM q4 weeks
Steroids in ARF     | Do NOT prevent RHD development   | Only for severe
                    |                                   | carditis + HF

================================================================================
SECTION 7: NOTABLE TRIALS TABLE
================================================================================

Trial Name      | Year | Topic           | Key Finding
----------------+------+-----------------+-----------------------------
PARTNER 1       | 2010 | TAVI vs medical | TAVI reduced mortality in
                |      | therapy (insurg) | inoperable severe AS (20%
                |      |                 | absolute risk reduction at
                |      |                 | 1 year)
PARTNER 2       | 2016 | TAVI vs SAVR    | TAVI non-inferior to SAVR
                |      | (intermed risk) | in intermediate-risk AS
PARTNER 3       | 2019 | TAVI vs SAVR    | TAVI superior at 1 year
                |      | (low risk)      | (lower death/stroke/rehospital)
EVOLUT Low Risk | 2019 | TAVI vs SAVR    | TAVI non-inferior to SAVR
                |      | (low risk)      | in low surgical risk pts
SALTIRE         | 2005 | Statins in AS   | Atorvastatin did NOT slow
                |      |                 | progression of calcific AS
SEAS            | 2008 | Ezetimibe +     | Combined statin/ezetimibe
                |      | simvastatin AS  | did NOT slow AS progression
AVATAR          | 2022 | Early vs delayed| Early AVR superior to
                |      | surgery in      | watchful waiting in
                |      | asymptomatic AS | asymptomatic very severe AS
COAPT           | 2018 | MitraClip vs    | MitraClip reduced HF
                |      | medical in fxn  | hospitalisations and
                |      | MR (HFrEF)      | all-cause mortality
MITRA-FR        | 2018 | MitraClip vs    | MitraClip did NOT improve
                |      | medical (fxn MR)| outcomes — conflicting
                |      |                 | with COAPT
EXPLORER-HCM    | 2020 | Mavacamten in   | Mavacamten improved LVOT
                |      | obstructive HCM | gradient and symptoms (new
                |      |                 | cardiac myosin inhibitor)
CORP-2          | 2014 | Colchicine      | Colchicine halved rate of
                |      | recurrent       | recurrent pericarditis
                |      | pericarditis    |

================================================================================
SECTION 8: MASTER MNEMONICS TABLE
================================================================================

Mnemonic     | Stands For                        | Topic
-------------+-----------------------------------+---------------------------
SAD          | Syncope, Angina, Dyspnoea         | AS symptoms
ASD 5-3-2   | Angina 5yr, Syncope 3yr,          | AS prognosis after
             | Dyspnoea 2yr survival             | symptoms develop
HERO         | Harsh, Ejection systolic,          | AS murmur character
             | Radiates to carotids,             |
             | Obliterates A2                    |
BECAM        | Bedside ECG, Echo, Cath,          | AS investigations
             | AXR, MRI                          |
MARBLE       | Marfan, Aortic dissection,        | AR causes
             | Rheumatic, Bicuspid,              |
             | Lues, Endocarditis                |
WWW CEDRA   | Water-hammer, Wide PP,            | AR peripheral signs
             | Wandering carotids; Corrigan,     |
             | de Musset, Duroziez,             |
             | Rosenbach, Austin Flint           |
RACE         | Rheumatic, Age-related,           | MS causes
             | Congenital, Endocarditis          |
DOHH         | Dyspnoea, Orthopnoea,            | MS symptoms
             | Haemoptysis, Hoarseness          |
MOST         | Malar flush, Opening snap,        | MS signs
             | Sinus AF, Tapping apex            |
ECCL         | ECG, CXR, Colour echo, L-cath     | MS investigations
SAFE PAH     | Stroke, AF, Failure, Emboli,      | MS complications
             | PAH, Airway/Ortner, Haemoptysis   |
PRIME        | Prolapse, Rheumatic,              | MR causes
             | Ischaemic, Myxomatous,            |
             | Endocarditis                      |
PALM         | Pansystolic murmur, Apex          | MR signs
             | displaced, Loud P2, Mitral click  |
FEEL         | Function, Echo, ECG, L-cath       | MR investigations
AFSHE        | AF, Failure, Stroke, HF, Endo     | MR complications
MATP         | Mitral, Aortic, Tricuspid,        | RHD valve involvement
             | Pulmonary (in decreasing freq)    | order
JONES        | Joints, Oh (subcutaneous          | Major Jones criteria
             | nOdules), Nodules, Erythema,      | mnemonic aid
             | Sydenham, Carditis                |
SGAS         | Streptococcus Group A, Antibody,  | RHD aetiology
             | Susceptible host                  |
FHE          | Failure, Heart block/IE, Emboli   | AR complications
CHARM        | Congenital bicuspid, HTN,         | AS risk factors
             | Age, Rheumatic, Male             |

================================================================================
SECTION 9: CROSS-MODULE LINKS
================================================================================

This Module Links To...

MODULE 1A (Heart Failure):
- All valvular disease can cause HF (pressure and volume overload)
- AS causes HFpEF (stiff LV) then HFrEF (dilated failing LV)
- AR and MR cause HFrEF (volume overload, LV dilatation)
- GDMT for HF applies to secondary (functional) MR

MODULE 1B (Arrhythmias):
- MS is the classic cause of AF — enlarged LA is the substrate
- AF in MS: always anticoagulate with WARFARIN (not NOACs)
- Prolonged PR interval = minor Jones criterion
- AF with fast ventricular rate worsens MS (less time for LV filling)

MODULE 1C (Ischaemic Heart Disease):
- Acute papillary muscle rupture post-MI → acute MR
  (inferior MI → posterior papillary muscle → posterior leaflet MR)
- Ischaemic functional MR from LV remodelling post-MI
- Pre-operative coronary angiogram required before valve surgery

MODULE 1D (This module):
- RHD causes MS, MR, AR, TR (in decreasing frequency)
- Endocarditis complicates all valvular disease

MODULE 1E (Infective Endocarditis — same module):
- Bicuspid aortic valve + MVP = highest risk structural lesions for IE
- Endocarditis causes: AR (leaflet destruction), MR (perforation),
  MS (rare), TR (IVDU)
- IE prophylaxis indicated before dental procedures in HIGH-risk
  structural heart disease

MODULE 2 (Respiratory):
- Severe MS with pulmonary venous hypertension mimics LVF
- Haemoptysis in MS can mimic pulmonary TB or bronchiectasis
  (important differential in HK where TB remains endemic)

MODULE 3 (Rheumatology):
- Rheumatic fever (GAS) — see ARF and Jones criteria above
- Ankylosing spondylitis, reactive arthritis → AR (HLA-B27 diseases)
- Marfan syndrome → AR + aortic root dilatation
- SLE → Libman-Sacks endocarditis (sterile vegetations on both
  surfaces of mitral valve — distinct from infective endocarditis)

MODULE 4 (Pharmacology):
- Warfarin monitoring: INR 2–3 for AF in valvular disease;
  INR 2.5–3.5 for mechanical mitral valve
- Penicillin allergy for prophylaxis → use azithromycin or doxycycline

LEGAL/ETHICAL ORDINANCE BOX:
Rheumatic fever prophylaxis for CHILDREN in HK:
- Under Cap. 382 Public Health and Medical Services Ordinance,
  the HA has an obligation to provide preventive healthcare services
- Consent for ongoing IM penicillin injections in minors:
  parental consent required; Gillick competence applies for
  adolescents with capacity
- Cap. 136 Mental Health Ordinance: relevant if patient with RHD
  lacks capacity to consent to valve surgery

================================================================================
KEY TAKEAWAYS FOR THE EXAM
================================================================================

1. AS: SAD symptoms, ESM radiating to carotids, slow-rising pulse,
   narrow PP. TAVI for high risk/elderly. SAVR for young/low risk.
   No drug slows progression.

2. AR: MARBLE causes. Wide PP, collapsing pulse, early diastolic murmur
   at LSE. IABP CONTRAINDICATED. Acute AR = emergency surgery.

3. MS: Rheumatic. "MOST" signs + mid-diastolic murmur. Warfarin (NOT
   NOACs) for AF. PBMV if pliable valve. Short S2-OS = more severe.

4. MR: PRIME causes. Pansystolic murmur at apex to axilla. LVEF < 60%
   already abnormal in MR. Acute (papillary rupture) = emergency. IABP
   INDICATED in acute MR.

5. RHD: Jones criteria 2015. GAS throat infection (not skin). Secondary
   prophylaxis = benzathine penicillin G IM q4 weeks. Duration depends
   on valve damage. Steroids do NOT prevent RHD.

================================================================================
SOURCES
================================================================================
- Braunwald's Heart Disease, 12th/13th Edition
- Fuster and Hurst's The Heart, 15th Edition
- Bailey and Love's Short Practice of Surgery, 28th Edition
- ACC/AHA 2020 Guideline for Management of Valvular Heart Disease
- ESC/EACTS 2021 Guidelines on Valvular Heart Disease
- 2025 ESC/EACTS Guidelines on VHD (Lancellotti et al, Rev Med Liege)
- 2024 AHA/ACC Guideline for Hypertrophic Cardiomyopathy
- AHA 2015 Revised Jones Criteria for ARF
- PubMed: PARTNER 3, COAPT, EXPLORER-HCM, AVATAR trials
- Hong Kong Hospital Authority Clinical Guidelines
- WHO/WHF Guidelines on Rheumatic Fever Prophylaxis

================================================================================
END OF MODULE 1D: VALVULAR HEART DISEASE
HKMLE High-Yield Study Note | August 2026
================================================================================