Valvular Heart Disease

Valvular heart disease (VHD) encompasses stenotic and regurgitant lesions of the four cardiac valves. In the NEET PG context, the four "classic" lesions — mitral stenosis, mitral regurgitation, aortic stenosis and aortic regurgitation — dominate, together with rheumatic fever (the commonest cause in India) and its Jones diagnostic criteria. Mastering the murmurs, peripheral signs, echocardiographic cut-offs and timing of intervention is high-yield and repeatedly tested.

High-yield: Rheumatic heart disease (RHD) is the commonest cause of VHD in India and the developing world. The mitral valve is involved in ~90% of RHD; mitral stenosis is the most common valvular lesion of rheumatic heart disease and almost always rheumatic in origin.

Classification and overview

Valve lesions are broadly stenotic (obstruction to forward flow → pressure overload behind the valve) or regurgitant (backward leak → volume overload). The chamber that bears the burden tells you the murmur location, the pulse changes and the eventual failure pattern.

Lesion	Murmur (type & timing)	Best heard at	Radiates to	Chamber affected
Mitral stenosis (MS)	Mid-diastolic, low-pitched rumble + opening snap	Apex (left lateral, bell)	None / axilla	LA → pulmonary → RV
Mitral regurgitation (MR)	Pansystolic (holosystolic), blowing	Apex	Axilla / back	LA + LV (volume)
Aortic stenosis (AS)	Ejection systolic (crescendo-decrescendo)	Right 2nd ICS (aortic area)	Carotids	LV (pressure)
Aortic regurgitation (AR)	Early diastolic, high-pitched, decrescendo	Left sternal border (3rd–4th ICS)	—	LV (volume)

High-yield: A useful rule — diastolic murmurs are (almost) always pathological; innocent murmurs are systolic. Continuous "machinery" murmur = PDA.

Mitral stenosis

Etiology & pathophysiology

Almost always rheumatic. Other causes: congenital (parachute mitral valve, Lutembacher = ASD + MS), severe mitral annular calcification, carcinoid, SLE. Normal mitral valve area (MVA) is 4–6 cm²; symptoms begin when MVA falls below ~2 cm², and severe MS is MVA ≤ 1.5 cm² (very severe ≤ 1 cm²).

Obstruction raises left atrial pressure → pulmonary venous congestion → pulmonary hypertension → right ventricular failure. LV is typically normal/underfilled. Atrial fibrillation is common due to LA dilatation and is a major source of systemic embolism.

Flow of decompensation: Obstruction → ↑LA pressure → pulmonary venous hypertension → reactive pulmonary arterial HTN → RV hypertrophy → RV failure / tricuspid regurgitation → systemic congestion.

Clinical features

• Exertional dyspnoea (earliest), orthopnoea, PND, haemoptysis.
• Malar flush (mitral facies) from low cardiac output + pulmonary HTN.
• Palpitations (AF), systemic embolism (stroke).
• Hoarseness from left recurrent laryngeal nerve compression by enlarged LA = Ortner syndrome.

Auscultation

• Loud S1 (valve still mobile, snaps shut from a wide-open position).
• Opening snap (OS) after S2; a short A2–OS interval indicates severe MS (high LA pressure opens the valve early).
• Mid-diastolic rumble with presystolic accentuation (lost when AF develops).
• Loud P2 if pulmonary HTN.

High-yield: Severity markers in MS — (1) shorter A2–OS interval, (2) longer duration of the diastolic murmur, (3) signs of pulmonary HTN. A softer murmur in advanced disease ("silent MS") = very low flow, do not be falsely reassured.

Diagnosis

• ECG: P mitrale (broad notched P in II), RVH, AF.
• CXR: straightening of left heart border, double density (LA enlargement), splayed carina, Kerley B lines.
• Echocardiography is the investigation of choice — assesses MVA (planimetry, pressure half-time), gradient, leaflet mobility/calcification and the Wilkins score which predicts suitability for balloon valvuloplasty.

Management

• Rate control of AF (beta-blockers), diuretics for congestion, anticoagulation (warfarin) if AF/prior embolism/LA clot.
• Percutaneous balloon mitral valvotomy (PBMV) is the procedure of choice for symptomatic severe MS with pliable, non-calcified valve, no LA clot, no/mild MR (Wilkins score ≤ 8).
• Mitral valve replacement if heavily calcified, significant MR, or LA thrombus.

Mitral regurgitation

Etiology

• Primary (organic): mitral valve prolapse (commonest cause in developed world), rheumatic, infective endocarditis, ruptured chordae/papillary muscle (post-MI), connective tissue disease.
• Secondary (functional): LV dilatation tethering leaflets (dilated/ischaemic cardiomyopathy).

Acute MR (chordal/papillary rupture) → sudden severe pulmonary oedema with a normal-sized LA and LV; chronic MR allows LA/LV dilatation to compensate.

Clinical features & auscultation

• Fatigue, dyspnoea, AF.
• Apex: displaced, hyperdynamic; soft S1, wide split S2, S3 (volume overload).
• Pansystolic murmur at apex radiating to the axilla.
• MVP: mid-systolic click followed by a late systolic murmur; manoeuvres that decrease LV volume (standing, Valsalva) move the click earlier.

High-yield: Distinguishing MR from AS murmur dynamics — squatting/handgrip (↑afterload) increases MR (and AR) murmurs but decreases AS murmur. Valsalva/standing decreases most murmurs except HOCM and MVP, which increase/lengthen.

Investigation & management

• Echocardiography quantifies severity (regurgitant volume, regurgitant orifice area, vena contracta).
• Vasodilators/ACE inhibitors and diuretics for symptoms.
• Surgery (repair preferred over replacement) for severe MR with symptoms, OR asymptomatic with LVEF 30–60% or LV end-systolic diameter ≥ 40 mm, new AF, or pulmonary HTN. MitraClip for selected high-risk/secondary MR.

Aortic stenosis

Etiology by age

Age group	Commonest cause
< 30 yrs	Congenital (unicuspid)
30–70 yrs	Bicuspid aortic valve (calcified)
> 70 yrs	Senile degenerative calcification

Rheumatic AS is almost always accompanied by mitral involvement.

Pathophysiology & clinical features

Fixed obstruction → concentric LV hypertrophy → diastolic dysfunction, then systolic failure. The classic triad (poor prognosis once present):

Angina → Syncope (exertional) → Dyspnoea / heart failure (mnemonic "ASD" / SAD). Median survival after symptom onset: angina ~5 yr, syncope ~3 yr, heart failure ~2 yr.

• Pulsus parvus et tardus (small-volume, slow-rising carotid pulse).
• Narrow pulse pressure.
• Ejection systolic murmur radiating to carotids; soft/absent A2 and reversed (paradoxical) splitting in severe disease.
• Gallavardin phenomenon — the high-frequency component radiates to apex, mimicking MR.

High-yield: Severe AS criteria — aortic valve area ≤ 1.0 cm², mean gradient ≥ 40 mmHg, peak jet velocity ≥ 4 m/s. A later peaking and softer murmur with a single S2 paradoxically indicates more severe AS (low flow across a tight valve).

Diagnosis & management

• Echocardiography is investigation of choice (gradient, valve area, LV function). Dobutamine stress echo for low-flow low-gradient AS.
• No medical therapy improves survival. Avoid vasodilators/nitrates in severe AS (risk of syncope). Diuretics cautiously.
• Aortic valve replacement (AVR) for symptomatic severe AS, or asymptomatic severe AS with LVEF < 50% or undergoing other cardiac surgery. TAVR/TAVI for high/intermediate (and now selected low) surgical-risk patients.

Aortic regurgitation

Etiology

• Valvular: rheumatic, bicuspid valve, infective endocarditis.
• Aortic root disease: Marfan, syphilitic aortitis, ankylosing spondylitis, aortic dissection (acute AR), hypertension.

Acute AR (endocarditis, dissection) → catastrophic LV volume overload with little dilatation → cardiogenic shock; chronic AR allows massive LV dilatation ("cor bovinum").

The peripheral signs (very high-yield eponyms)

Wide pulse pressure produces a parade of named signs:

• Corrigan pulse / water-hammer pulse — collapsing carotid/radial pulse.
• de Musset sign — head bobbing with each beat.
• Quincke sign — capillary pulsation in nail beds.
• Müller sign — pulsation of the uvula.
• Traube sign — "pistol-shot" femoral sounds.
• Duroziez sign — to-and-fro femoral murmur on compression.
• Hill sign — popliteal systolic BP exceeds brachial by > 60 mmHg (most sensitive).
• Becker sign — visible retinal artery pulsation.

High-yield: Austin Flint murmur — a low-pitched mid/late diastolic rumble at the apex in severe AR, caused by the regurgitant jet striking the anterior mitral leaflet (functional MS); there is no opening snap and no loud S1, distinguishing it from true MS.

Auscultation & management

• Early diastolic, high-pitched, decrescendo murmur at left sternal border, best heard sitting up, leaning forward, in expiration.
• A systolic flow murmur is common (high stroke volume).
• Echocardiography is investigation of choice.
• Vasodilators (ACE inhibitors, dihydropyridines) for symptomatic patients/hypertension.
• AVR for symptomatic severe AR, OR asymptomatic with LVEF ≤ 55% or LV end-systolic diameter > 50 mm (or > 25 mm/m²). Acute severe AR is a surgical emergency.

Rheumatic fever and the Jones criteria

Rheumatic fever follows group A streptococcal (Streptococcus pyogenes) pharyngitis (not skin infection) after a latent period of ~2–4 weeks, via molecular mimicry (antibodies to M protein cross-react with cardiac myosin/laminin).

Diagnosis uses the Revised Jones Criteria (2015) — evidence of preceding strep infection (raised ASO titre, positive throat culture/rapid antigen) plus either 2 major, or 1 major + 2 minor criteria.

Major (mnemonic JONES / ♥CASES)	Minor (mnemonic FRAPP / CAFE PAL)
J – Joints (migratory polyarthritis)	Fever
♥/O – Carditis (pancarditis)	Arthralgia
N – Nodules (subcutaneous)	Raised ESR/CRP
E – Erythema marginatum	Prolonged PR interval
S – Sydenham chorea	Previous RF (history)

High-yield: Carditis is the only manifestation that causes permanent damage (chronic RHD). Sydenham chorea and indolent carditis are "stand-alone" major criteria that can establish the diagnosis even alone in some settings. Arthritis as a major criterion cannot also count arthralgia as a minor.

The 2015 revision allows separate thresholds for low-risk vs moderate/high-risk populations (India = high risk) — e.g. monoarthritis/polyarthralgia counts as major in high-risk groups.

Treatment & prophylaxis

• Acute: benzathine penicillin to eradicate strep; aspirin/NSAIDs for arthritis; corticosteroids for severe carditis; valproate/carbamazepine for chorea.
• Secondary prophylaxis: benzathine penicillin G IM every 3–4 weeks. Duration: RF without carditis = 5 yr or until age 21; with carditis but no residual disease = 10 yr or until 21; with residual valvular disease = 10 yr or until age 40 (often lifelong).

Complications across lesions

• Atrial fibrillation & systemic embolism (esp. MS, MR).
• Pulmonary hypertension and right heart failure (MS).
• Infective endocarditis (regurgitant lesions, bicuspid valve > stenotic).
• Sudden cardiac death (severe AS).
• Haemoptysis and Ortner syndrome (MS).
• LV systolic dysfunction (chronic MR, AR, AS).

Key differentials

• MS vs Austin Flint murmur of AR: both apical diastolic rumbles — MS has loud S1 + opening snap; Austin Flint does not, and AR signs (collapsing pulse) are present.
• AS vs HOCM: AS murmur radiates to carotids and decreases with Valsalva; HOCM murmur increases with Valsalva/standing and has no carotid radiation, with normal/jerky pulse.
• MR vs tricuspid regurgitation: TR murmur increases with inspiration (Carvallo sign), prominent v waves, pulsatile liver.
• MR vs AS at apex (Gallavardin): distinguish by carotid radiation and pulse character.

Recently asked / exam angle

• A young woman with malar flush, AF and a loud S1 with mid-diastolic rumble → mitral stenosis; investigation of choice = echocardiography; intervention of choice for pliable valve = PBMV.
• "Shortest A2–OS interval indicates..." → severe MS.
• Collapsing pulse + early diastolic murmur + head nodding → chronic AR (name the signs: Corrigan, de Musset, Quincke, Duroziez, Hill).
• Elderly man, exertional syncope, slow-rising pulse, ESM to carotids → aortic stenosis; severe AS cut-offs (AVA ≤ 1 cm², mean gradient ≥ 40, V ≥ 4 m/s).
• Manoeuvre questions: handgrip/squatting ↑ MR & AR, ↓ AS & HOCM; Valsalva ↑ HOCM & MVP.
• Jones criteria: identify major vs minor; carditis = only manifestation with lasting damage; secondary prophylaxis drug and duration.
• "Austin Flint murmur is due to" → regurgitant AR jet on anterior mitral leaflet (functional MS).
• Lutembacher syndrome = ASD + mitral stenosis.
• Most common cause of AS in a 40–60 year old = bicuspid aortic valve.

Rapid revision

1. MS = most common rheumatic valve lesion; severe MVA ≤ 1.5 cm².
2. Loud S1 + opening snap + mid-diastolic rumble = MS; short A2–OS interval = severe.
3. Echocardiography is the investigation of choice for all valve lesions.
4. PBMV needs a pliable, non-calcified valve, Wilkins ≤ 8, no LA clot, no significant MR.
5. MR = pansystolic murmur at apex → axilla; operate before LVEF < 60% or LVESD ≥ 40 mm.
6. Severe AS: AVA ≤ 1 cm², mean gradient ≥ 40 mmHg, jet velocity ≥ 4 m/s; no drug improves survival, AVR/TAVR is definitive.
7. AS triad Angina → Syncope → Dyspnoea; heart failure carries the worst prognosis (~2 yr).
8. Chronic AR = wide pulse pressure → Corrigan, de Musset, Quincke, Müller, Duroziez, Hill, Traube signs.
9. Austin Flint murmur = apical diastolic rumble of severe AR (no OS, no loud S1).
10. Handgrip/squatting ↑ MR & AR murmurs, ↓ AS & HOCM; Valsalva ↑ HOCM & MVP.
11. Jones: 2 major OR 1 major + 2 minor + evidence of preceding strep; carditis = only permanent damage.
12. Secondary prophylaxis = benzathine penicillin G every 3–4 weeks; with residual RHD up to age 40 / lifelong.