Ch16: Valvular Heart Disease

Preparatory Mindset

Valvular heart disease is a physical-examination-driven topic: each lesion has a signature murmur, a pressure/volume consequence, and a surgical threshold. The exam skills: (1) recognise the murmur and its timing (systolic: aortic stenosis, MR; diastolic: aortic regurgitation, mitral stenosis), (2) know the echocardiographic severity cut-offs (e.g., aortic valve area: severe <1.0 cm²; MR/AR jet quantification), (3) link the pathophysiology to symptoms (AS → syncope/angina/heart failure; MS → atrial fibrillation + pulmonary congestion; AR → wide pulse pressure), and (4) commit the surgical indications (symptomatic severe AS → valve replacement regardless of EF; endocarditis prophylaxis in highest-risk patients). Rheumatic disease remains the leading cause in China; the HKHA handbook links valvular disease to heart-failure and IE-prophylaxis sections.

Core Concepts

Aortic stenosis (AS)

• Definition: narrowing of the aortic valve orifice (deformity in 0.5–2% of people; prevalence ~2% >65 y, ~4% >85 y).
• Etiology: calcific/degenerative (most common — elderly), congenital bicuspid valve, rheumatic (China — often with MS).
• Pathophysiology: LV outflow obstruction → concentric LV hypertrophy → ↑ myocardial O₂ demand + ↓ coronary perfusion → angina, syncope, heart failure (classic triad); sudden death.
• Diagnosis: crescendo-decrescendo systolic ejection murmur at right upper sternal border, radiating to carotids; delayed/weak carotid upstroke (pulsus parvus et tardus); S4; echo — AVA: mild >1.5 cm², moderate 1.0–1.5, severe <1.0 cm²; mean gradient (severe ≥40 mmHg), jet velocity (severe ≥4 m/s).
• Treatment: symptomatic severe AS → aortic valve replacement (TAVI or SAVR) — the only effective therapy; no medical therapy reverses it; avoid vasodilators/nitrates (hypotension); IE prophylaxis if highest-risk category.
• Heyde syndrome: AS + GI bleeding (angiodysplasia, acquired von Willebrand syndrome) — prevalence 1.5–3%.

Aortic regurgitation (AR)

• Etiology: rheumatic, endocarditis, aortic dissection, bicuspid valve, connective tissue (Marfan, Ehlers-Danlos), syphilis, hypertension, trauma.
• Pathophysiology: diastolic backflow → LV volume overload → eccentric LV dilatation/hypertrophy → heart failure; low diastolic pressure → ↓ coronary perfusion.
• Diagnosis: early diastolic decrescendo murmur (left sternal border, leaning forward, end-expiration); wide pulse pressure, water-hammer pulse (Corrigan), bounding pulses, head-bobbing (de Musset), pistol-shot femorals; echo — regurgitant jet width/vena contracta: mild <25% LVOT, moderate 25–65%, severe >65%; regurgitant fraction <30% / 30–49% / ≥50%.
• Treatment: acute severe AR — surgical emergency (endocarditis/dissection → urgent AVR); chronic severe with symptoms or LV dilatation (LVESD >50 mm / LVEDD >65 mm, or declining EF) → surgery; vasodilators (nifedipine/ACEi) can slow progression in chronic asymptomatic severe AR with hypertension; treat endocarditis.

Mitral stenosis (MS)

• Etiology: rheumatic (almost always — China/HK), congenital, severe annular calcification.
• Pathophysiology: obstructed LA emptying → LA enlargement → atrial fibrillation, pulmonary congestion/pulmonary hypertension → right heart failure; reduced cardiac output.
• Diagnosis: mid-diastolic rumbling murmur at apex (bell, left lateral decubitus), opening snap; loud S1; signs of pulmonary hypertension; echo — mitral valve area (severe <1.0 cm²), mean gradient, pressure half-time; CXR — straight left heart border, LA enlargement, pulmonary congestion.
• Complications: AF (embolic stroke risk — CHA₂DS₂-VASc), pulmonary oedema (pregnancy, fever, AF), infective endocarditis, haemoptysis.
• Treatment: rate control in AF (β-blocker/CCB, digoxin) + anticoagulation (valvular AF — warfarin, NOT DOAC); diuretics for congestion; percutaneous mitral balloon valvuloplasty (PMBV) for suitable pliable non-calcified valves; valve replacement for severe symptoms/calcified valves; surgical commissurotomy.

Mitral regurgitation (MR)

• Etiology: rheumatic, mitral valve prolapse (MVP), ischaemic (papillary muscle dysfunction/rupture — post-MI), endocarditis, annular dilatation (LV failure), myxomatous.
• Pathophysiology: LV volume overload → LA + LV dilatation → pulmonary congestion; acute MR (papillary rupture) → sudden cardiogenic shock + pulmonary oedema.
• Diagnosis: pansystolic murmur at apex radiating to axilla; S3; echo — jet area/vena contracta, regurgitant fraction, LV size/EF; LV dysfunction (EF <60%) is the trigger for surgery in chronic severe MR.
• Treatment: acute severe MR → urgent surgery (papillary muscle rupture); chronic severe symptomatic → mitral repair (preferred) or replacement; medical — vasodilators, diuretics, afterload reduction; MVP — β-blocker for palpitations/pain, IE prophylaxis if highest risk.

Valvular disease & heart failure / IE links

• Any severe lesion → heart failure (see heart-failure chapter: GDMT applies to the LV dysfunction; acute severe AR/MR are surgical emergencies).
• IE prophylaxis: highest-risk patients only (prosthetic valve, previous IE, cyanotic/repaired CHD ≤6 months, transplant valvulopathy) — dental procedures (see IE chapter).
• Multiple valve disease (involvement of ≥2 valves) — commonly rheumatic (MS + AR); surgical planning complex.

High-Yield Points

• AS: crescendo-decrescendo systolic murmur → carotids; angina, syncope, HF triad; AVA severe <1.0 cm²; surgery for symptomatic severe AS.
• AR: early diastolic murmur (L sternal border, lean forward); wide pulse pressure, water-hammer pulse; acute severe = emergency.
• MS: rheumatic, apical mid-diastolic rumble + opening snap; AF + thromboembolism (warfarin); PMBV for suitable valves.
• MR: pansystolic apical murmur → axilla; EF <60% → surgery; acute (papillary rupture) = emergency.
• Heyde syndrome: AS + angiodysplasia GI bleeding.
• Valvular AF → warfarin (DOACs not indicated).
• IE prophylaxis: highest-risk only, dental procedures.

Topic Summary

Valvular heart disease is diagnosed at the bedside by murmur pattern and timing, quantified by echocardiography (AVA, gradients, jet measurements, regurgitant fraction), and managed surgically when severe and symptomatic. AS presents with the angina-syncope-HF triad and is treated by valve replacement; AR and MR cause LV volume overload with surgery at EF <60% or LV dilatation (acute severe forms are emergencies); MS is rheumatic, complicated by AF and thromboembolism (warfarin), with PMBV for suitable valves. Rheumatic heart disease remains common in China; the HKHA links valvular management to the heart-failure algorithm and restricts IE prophylaxis to highest-risk patients — both LMCHK priorities.