Version 1.0 — Published April 2026
Quick Answer
Rheumatic heart disease and valvular lesions contribute 3–4 direct questions per NEET PG paper. Master these 10 high-yield areas:
- Jones criteria 2015 — ARF: evidence of preceding GAS + 2 major OR 1 major + 2 minor. Major: carditis (incl. subclinical), arthritis, chorea, erythema marginatum, SC nodules. Minor: fever, ↑ESR/CRP, prolonged PR, polyarthralgia
- Mitral stenosis auscultation — Loud S1, opening snap, rumbling mid-diastolic murmur with pre-systolic accentuation (lost in AF). Best heard at apex in left lateral decubitus
- Wilkins score — MS morphology on echo: leaflet mobility + thickening + calcification + subvalvular thickening (each 1–4). <=8: favourable for BMV; >8: favour MVR
- BMV vs MVR — BMV if symptomatic severe MS (MVA <=1.5 cm²), Wilkins <=8, no LA thrombus, no moderate MR. Preferred in young / pregnancy
- Mitral regurgitation — Chronic: holosystolic murmur at apex → axilla, LV dilatation. Acute: papillary rupture post-MI, endocarditis — pulmonary oedema + soft systolic murmur
- Aortic stenosis severity — Peak velocity >=4 m/s, mean gradient >=40 mmHg, AVA <=1.0 cm². Symptom triad: angina, syncope, HF. Classic murmur: crescendo-decrescendo ejection systolic, radiating to carotids; pulsus parvus et tardus
- TAVI indications — Symptomatic severe AS at intermediate/high surgical risk; now first-line in patients >80 years (2020 ACC-AHA). SAVR in <65 years
- Aortic regurgitation (acute) — Endocarditis, dissection, blunt trauma. Short early diastolic murmur, pulmonary oedema, shock — emergency AVR
- Duke criteria — Definite IE: 2 major OR 1 major + 3 minor OR 5 minor. Major: typical organisms on blood cultures OR echo vegetation/abscess/new regurgitation
- Secondary prophylaxis — Benzathine penicillin 1.2 million U IM every 3–4 weeks. Duration: 5 yr or age 21 (no carditis); 10 yr or age 21 (carditis, no residual); lifelong (persistent valve disease / post-surgery)
Rheumatic heart disease is the most common cause of acquired valvular heart disease in India — and it sits at the heart of NEET PG cardiology questions. The student who masters Jones 2015 criteria, mitral stenosis management (BMV), aortic stenosis severity grading, and Duke criteria has covered the foundation for 3–4 marks across medicine and community medicine papers. Pair this guide with daily MCQ practice on the Medicine subject hub, cross-reference the high-yield medicine topics overview, and revise the young-woman-with-palpitations clinical case on mitral stenosis for applied reasoning.
Acute rheumatic fever — Jones 2015 revision
Acute rheumatic fever is an autoimmune post-infectious sequela of group A Streptococcus pharyngitis — and Jones 2015 is the current diagnostic framework, with important updates for high-prevalence populations like India.
Pathogenesis: Molecular mimicry between streptococcal M-protein and cardiac myosin triggers a cross-reactive Type II hypersensitivity reaction 2–4 weeks after untreated pharyngitis. Valvulitis predominantly affects mitral (70%) > aortic (25%) > tricuspid > pulmonary.
Jones 2015 criteria:
Evidence of preceding group A streptococcal infection (required):
- Elevated or rising anti-streptolysin O (ASO) titre (>200 IU/mL adults, >320 IU/mL children)
- Positive throat culture or rapid antigen detection test
- Anti-DNase B antibodies
- Recent scarlet fever
Major criteria:
| Criterion | High-risk populations (India) | Moderate/low-risk |
|---|
| Carditis | Clinical and/or subclinical (echo) | Clinical and/or subclinical |
| Arthritis | Monoarthritis, polyarthritis, or polyarthralgia | Polyarthritis only |
| Chorea | Sydenham chorea (6 months after infection) | Same |
| Erythema marginatum | Pink, non-pruritic, trunk / proximal extremities, evanescent | Same |
| Subcutaneous nodules | 0.5–2 cm, firm, extensor surfaces | Same |
Minor criteria:
| Criterion | High-risk | Moderate / low-risk |
|---|
| Fever | >=38.0 °C | >=38.5 °C |
| Polyarthralgia | — (counted as major) | Counted here |
| Monoarthralgia | Counted here | — |
| ESR / CRP | ESR >=30 mm/h or CRP >=3 mg/dL | ESR >=60 or CRP >=3 |
| Prolonged PR interval | Age-adjusted | Age-adjusted |
Diagnosis of ARF:
- Initial attack: 2 major OR 1 major + 2 minor
- Recurrent attack: 2 major, OR 1 major + 2 minor, OR 3 minor (in established RHD)
Key 2015 updates:
- Recognises subclinical carditis on echocardiography (Doppler evidence of valvulitis) — a major criterion in high-risk populations
- Adds monoarthritis / polyarthralgia as a major criterion in high-risk populations (accounts for early NSAID masking)
- India classified as a high-risk population (incidence >=2 per 100,000 school-age children per year)
Treatment of acute ARF:
- Bed rest until inflammatory markers normalise
- Eradicate GAS: single IM benzathine penicillin 1.2 million U (or oral penicillin V 500 mg BD × 10 days)
- Arthritis: naproxen or aspirin (aspirin 80–100 mg/kg/day, monitor salicylism)
- Carditis: corticosteroids (prednisolone 1–2 mg/kg/day tapered over 4–6 weeks) for moderate-severe carditis
- Chorea: haloperidol, valproate, or carbamazepine; resolves spontaneously in 6 weeks–6 months
Mitral stenosis — auscultation, Wilkins score, and BMV
Mitral stenosis is narrowing of the mitral valve orifice, most commonly from rheumatic heart disease in India — and its management algorithm is classic NEET PG material.
Rheumatic MS pathology:
- Commissural fusion → fish-mouth valve appearance
- Chordal thickening / fusion
- Calcification (in older / longstanding disease)
- Normal MV area 4–6 cm²; symptoms typically at <1.5 cm²
Severity (MVA):
- Mild MS: 1.5–2.0 cm²
- Moderate MS: 1.0–1.5 cm²
- Severe MS: <=1.0 cm² (recent ACC-AHA now uses 1.5 cm² as symptomatic-severe cutoff for intervention)
Classic auscultation (apex, left lateral decubitus, bell):
- Loud S1 (valve leaflets still pliable)
- Opening snap after S2 (closer to S2 = more severe MS)
- Low-pitched rumbling mid-diastolic murmur with pre-systolic accentuation (lost when atrial fibrillation develops)
- Duration of murmur correlates with severity (longer = more severe), not intensity
Symptoms: Exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, haemoptysis (pink frothy sputum from rupture of bronchial-pulmonary anastomoses), atrial fibrillation, systemic embolism, right heart failure.
Complications / signs:
- Atrial fibrillation in ~30–40%
- Left atrial thrombus → systemic embolism
- Ortner syndrome: hoarseness from left recurrent laryngeal nerve compression by enlarged LA / pulmonary artery
- Mitral facies: malar flush
- Pulmonary hypertension with loud P2, right ventricular heave
Investigations:
- ECG: P mitrale (broad notched P in lead II >120 ms), AF, RVH
- CXR: Straightening of left heart border, double right heart border (LA enlargement), splaying of carina, pulmonary venous congestion
- Echo: The diagnostic modality. Measures MVA (planimetry, pressure half-time), mean gradient, pulmonary artery pressure
Wilkins score (4 components, each scored 1–4; total 4–16):
| Component | Score 1 | Score 2 | Score 3 | Score 4 |
|---|
| Leaflet mobility | Highly mobile | Mid + base mobile | Movement forward in diastole (mainly at base) | No / minimal movement |
| Leaflet thickening | Normal (4–5 mm) | Normal mid with thickened margins | Thickened throughout (5–8 mm) | Markedly thickened (>8–10 mm) |
| Calcification | Single area of increased brightness | Scattered brightness confined to margins | Extending to mid-leaflet | Extensive throughout |
| Subvalvular thickening | Minimal | Thickening up to 1/3 of chordal length | Extending to distal 1/3 | Extensive to papillary muscles |
Wilkins <=8 → favourable for balloon mitral valvuloplasty (BMV). Wilkins >8 → MVR preferred.
BMV vs MVR decision
Balloon mitral valvuloplasty (Inoue balloon):
- Indications: Symptomatic (NYHA II–IV) severe MS + favourable anatomy (Wilkins <=8) + absence of contraindications
- Contraindications: Left atrial thrombus, moderate / severe MR, active endocarditis
- Preferred in young patients and pregnancy — preserves native valve, no anticoagulation needed post-procedure
- Re-intervention rate 10–15% at 10 years; restenosis in 30–40% at 15 years
Mitral valve replacement:
- For heavily calcified / fibrosed valves (Wilkins >8), combined MS/MR, failed BMV
- Mechanical valve (lifelong warfarin, INR 2.5–3.5) preferred in <65 years
- Bioprosthetic valve (no long-term anticoagulation) in >65 years or contraindication to warfarin
Pregnancy considerations: Severe symptomatic MS in pregnancy should be managed with bed rest, beta-blockers (atenolol / metoprolol), diuretics. BMV in 2nd trimester is the preferred intervention if refractory symptoms; surgery carries high fetal loss risk.
Mitral regurgitation — acute vs chronic
Mitral regurgitation is incompetence of the mitral valve causing systolic backflow from LV to LA, with sharply different haemodynamics in acute vs chronic disease.
Causes by mechanism (Carpentier classification):
| Type | Leaflet motion | Causes |
|---|
| I | Normal | Annular dilatation (dilated CM), leaflet perforation (endocarditis) |
| II | Excessive | Mitral valve prolapse, papillary muscle rupture, chordal rupture |
| IIIa | Restricted (diastole) | Rheumatic, post-inflammatory |
| IIIb | Restricted (systole) | Ischemic MR, dilated CM (tethered leaflets) |
Chronic MR:
- Dyspnoea on exertion, fatigue; LV gradually dilates and eccentrically hypertrophies
- Holosystolic murmur at apex radiating to axilla; S3 in severe MR; soft or absent S1
- Echo: LV function, regurgitant volume, effective regurgitant orifice area (EROA); severe MR has EROA >=0.40 cm² or regurgitant fraction >=50%
- Surgery indicated when symptomatic OR asymptomatic with LVEF <60% or LVESD >40 mm
- Mitral valve repair preferred over replacement when feasible (better long-term outcomes)
Acute MR (emergency):
- Papillary muscle rupture post-MI (most often inferior MI, posteromedial papillary muscle with single blood supply from PDA)
- Endocarditis with leaflet destruction
- Chordal rupture (spontaneous in myxomatous disease, trauma)
- Presentation: flash pulmonary oedema, cardiogenic shock
- Auscultation: soft early systolic murmur (normal-sized LA cannot accommodate regurgitant volume, so gradient equalises rapidly)
- Urgent echo; emergency mitral valve repair / replacement; IABP as bridge
Aortic stenosis — severity grading and TAVI
Aortic stenosis is narrowing of the aortic valve orifice restricting LV outflow, most often from calcific degeneration in the elderly and from bicuspid aortic valve in younger patients.
Causes by age:
- <30 years: Unicuspid valve, rheumatic (usually with MS)
- 30–65 years: Bicuspid aortic valve
- >65 years: Senile calcific (tricuspid) AS
Severity grading (all three must align for pure severe AS):
| Parameter | Mild | Moderate | Severe | Very severe |
|---|
| Peak velocity (m/s) | <3.0 | 3.0–4.0 | >=4.0 | >5.0 |
| Mean gradient (mmHg) | <20 | 20–40 | >=40 | >60 |
| AVA (cm²) | >1.5 | 1.0–1.5 | <=1.0 | <=0.6 |
| Indexed AVA (cm²/m²) | — | — | <=0.6 | — |
Low-flow low-gradient AS: AVA <=1.0 cm² but mean gradient <40 mmHg. Subtypes:
- Classical LFLG: Reduced LVEF → dobutamine stress echo to distinguish true severe AS (AVA stays small, gradient rises) from pseudo-severe AS (AVA opens up)
- Paradoxical LFLG: Preserved LVEF but reduced stroke volume (small, hypertrophied LV)
Symptoms (Harrison's triad — appear only with severe AS):
- Angina: mean survival 5 years
- Syncope (exertional): mean survival 3 years
- Heart failure: mean survival 2 years
Physical exam:
- Mid-to-late peaking crescendo-decrescendo ejection systolic murmur at right 2nd intercostal space, radiating to carotids
- Pulsus parvus et tardus (small, delayed carotid upstroke)
- Soft S2 / absent A2 in severe AS
- Gallavardin phenomenon: high-frequency component radiating to apex (mimics MR)
- S4 gallop (LV hypertrophy)
- Narrow pulse pressure
Investigations:
- Echo (diagnosis and severity)
- CT coronary angiography before intervention (exclude CAD)
- BNP for symptom correlation
Management — SAVR vs TAVI (2020 ACC-AHA):
| Patient profile | Preferred intervention |
|---|
| <65 years | SAVR (surgical aortic valve replacement), mechanical valve |
| 65–80 years, low surgical risk | Shared decision — SAVR or TAVI |
| 65–80 years, intermediate risk | TAVI |
| >80 years | TAVI first-line |
| High surgical risk or prohibitive risk | TAVI |
| Bicuspid valve, heavy calcification, young | SAVR |
| Concomitant CABG / aortic root surgery | SAVR |
TAVI landmark trials:
- PARTNER 3 (2019) — TAVI non-inferior to SAVR in low-risk patients at 1 year
- Evolut Low Risk (2019) — self-expanding TAVI non-inferior to SAVR at 2 years
- PARTNER 2 (2016) — TAVI equivalent to SAVR in intermediate-risk
Do not: Give vasodilators (ACE inhibitors, nitrates) in severe symptomatic AS — can precipitate catastrophic hypotension.
Aortic regurgitation — chronic vs acute emergency
Aortic regurgitation is incompetence of the aortic valve causing diastolic backflow from aorta to LV, with a distinct haemodynamic picture in acute vs chronic disease.
Causes:
| Category | Examples |
|---|
| Valve disease (chronic) | Bicuspid aortic valve, rheumatic, calcific, myxomatous, prior endocarditis |
| Aortic root disease (chronic) | Marfan syndrome, Ehlers-Danlos, ankylosing spondylitis, syphilitic aortitis, hypertension, aortic root aneurysm |
| Acute | Infective endocarditis (most common), aortic dissection (Stanford A), blunt chest trauma |
Chronic AR:
- Asymptomatic for years; LV eccentric hypertrophy + dilation compensate
- Eventually: dyspnoea, angina, palpitations
- Early diastolic decrescendo murmur at left sternal border, sitting up, leaning forward, held expiration
- Wide pulse pressure (systolic-diastolic gap >=60 mmHg)
- Peripheral signs: Corrigan (water-hammer) pulse, de Musset (head bobbing), Quincke (capillary pulsations), Müller (uvular pulsations), Traube (pistol-shot femoral), Duroziez (to-and-fro femoral murmur)
- Austin Flint murmur: mid-diastolic rumble at apex (regurgitant jet striking anterior mitral leaflet, mimics MS)
Acute AR (emergency):
- LV has no time to dilate → markedly elevated end-diastolic pressure → pulmonary oedema, shock
- Short soft early diastolic murmur (LV and aortic pressures equalise quickly)
- No wide pulse pressure (LVEDP rises rapidly)
- Premature mitral valve closure on echo
- Emergency surgery is lifesaving; IV nitroprusside + inotropes as bridge
Surgery indications (chronic AR):
- Symptomatic severe AR regardless of LV function
- Asymptomatic severe AR with LVEF <=55% or LVESD >50 mm (>=25 mm/m² indexed)
- Concomitant aortic surgery for root >=5.5 cm (lower threshold in Marfan, bicuspid valve)
Tricuspid regurgitation and other valvular lesions
Tricuspid regurgitation is most often functional — secondary to RV / annular dilatation from pulmonary hypertension or left-sided heart disease — rather than primary valve disease.
Causes of TR:
- Functional (80%): Left-sided valve disease (MS, MR, AS), pulmonary hypertension, RV infarction, RV cardiomyopathy
- Primary: Rheumatic, Ebstein anomaly, carcinoid syndrome (right-sided), endocarditis in IV drug users (S. aureus), pacemaker / ICD lead, trauma
Auscultation:
- Pansystolic murmur at left lower sternal border, increases with inspiration (Carvallo sign)
- Large V wave in JVP (CV wave)
- Pulsatile liver, peripheral oedema, ascites
Ebstein anomaly: Apical displacement of the septal and posterior tricuspid leaflets → atrialisation of RV. Often with ASD and Wolff-Parkinson-White syndrome. Associated with maternal lithium exposure.
Carcinoid heart disease: Serotonin-induced fibrosis of right-sided valves → TR + pulmonary stenosis. Left-sided valves protected by pulmonary metabolism (unless patent foramen ovale).
Pulmonary stenosis: Congenital; systolic ejection click, ejection systolic murmur at left 2nd ICS. Severe PS → balloon valvuloplasty.
Infective endocarditis — Duke criteria and management
Infective endocarditis is microbial infection of the endocardial surface, most often affecting heart valves, diagnosed by the modified Duke criteria.
Risk factors:
- Prosthetic valves, prior IE
- Rheumatic heart disease, congenital heart disease (especially bicuspid AV, VSD)
- IV drug use (tricuspid valve, S. aureus)
- Degenerative valve disease in elderly
- Indwelling catheters, haemodialysis, immunosuppression
Common organisms:
| Setting | Predominant organisms |
|---|
| Native valve, community-acquired | Streptococcus viridans (dental), Staph aureus, Streptococcus gallolyticus (formerly bovis — associated with colon Ca) |
| IV drug users | Staph aureus (right-sided, tricuspid) |
| Prosthetic valve, <2 months | Staph epidermidis, Staph aureus, Candida |
| Prosthetic valve, >12 months | Same as native valve (Strep viridans, Staph aureus) |
| Culture-negative (5–10%) | HACEK group (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella), Bartonella, Coxiella, fungi |
Modified Duke criteria (definite IE = 2 major OR 1 major + 3 minor OR 5 minor):
Major criteria:
- Typical organisms on 2 separate blood cultures (Strep viridans, Strep gallolyticus, HACEK, community-acquired Staph aureus or enterococci without primary focus), OR
- Persistently positive blood cultures (≥2 cultures >12 hours apart, or majority positive), OR
- Single positive culture for Coxiella burnetii or anti-phase 1 IgG titre >=1:800
- Evidence of endocardial involvement: echo showing vegetation, abscess, or new dehiscence of prosthetic valve, OR new valvular regurgitation (increased murmur alone is insufficient)
Minor criteria:
- Predisposing condition (valve disease, IVDU)
- Fever >=38 °C
- Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions (non-tender macules on palms / soles)
- Immunologic phenomena: glomerulonephritis, Osler nodes (tender nodules on finger/toe pads), Roth spots (retinal haemorrhages with pale centre), rheumatoid factor
- Microbiological evidence not meeting major criteria
Empiric antibiotics (start after 3 sets of blood cultures):
| Setting | Regimen | Duration |
|---|
| Native valve (community) | Ampicillin-sulbactam + gentamicin, OR vancomycin + gentamicin (allergy / MRSA risk) | 4–6 weeks |
| Native valve, severe sepsis | Vancomycin + ceftriaxone (+ gentamicin for enterococci) | 4–6 weeks |
| Prosthetic valve | Vancomycin + gentamicin + rifampicin | 6 weeks (rifampicin for prosthetic material) |
| Right-sided IE in IVDU (uncomplicated Staph) | Nafcillin / cefazolin | 2–4 weeks |
Surgical indications:
- Heart failure (severe valve dysfunction, most common indication)
- Uncontrolled infection (persistent bacteremia >5–7 days despite appropriate antibiotics, perivalvular abscess, fistula)
- Systemic embolism or high embolic risk (>10 mm mobile vegetation)
- Fungal or multidrug-resistant organism
- Early prosthetic valve endocarditis
Prophylaxis (only for highest-risk patients):
- Prosthetic valve, prior IE, congenital cyanotic heart disease, heart transplant with valvulopathy
- Dental procedures manipulating gingiva / apex: amoxicillin 2 g PO 30–60 minutes before
Secondary prophylaxis for RHD
Secondary prophylaxis is long-term antibiotic administration to prevent recurrent group A streptococcus infection in patients with established RHD, and is the highest-impact intervention in Indian RHD management.
Regimen:
| Option | Dose / schedule | Notes |
|---|
| Benzathine penicillin G (IM, preferred) | 1.2 million U every 3–4 weeks (600,000 U if weight <27 kg) | Skin test first; adrenaline on hand; every 3 weeks in high-risk areas |
| Penicillin V (oral) | 250 mg BD | Less effective; reserve for IM-refusers |
| Sulfadiazine | 1 g daily (0.5 g if <27 kg) | Penicillin allergic |
| Erythromycin | 250 mg BD | Penicillin + sulfa allergic |
Duration (WHO / AHA):
| Clinical scenario | Duration |
|---|
| Rheumatic fever without carditis | 5 years after last attack or until age 21 (whichever is longer) |
| Rheumatic fever with carditis, no residual valve disease | 10 years after last attack or until age 21 (whichever is longer) |
| Carditis with persistent valvular disease, or post-valve surgery | Lifelong (or until at least age 40) |
India-specific considerations (RHD control programme):
- 3-weekly benzathine penicillin preferred in endemic areas (vs 4-weekly globally)
- National Rheumatic Heart Disease Control Programme (1993) integrated with general health services
- Echocardiographic screening of school-age children in high-burden districts
Primary prevention: Treat all sore throats compatible with GAS pharyngitis promptly. A single dose of benzathine penicillin 1.2 million U IM after GAS pharyngitis prevents ARF in the vast majority of cases.
Sources and references
- American Heart Association / American College of Cardiology — 2020 Guideline for the Management of Patients with Valvular Heart Disease (Otto et al., Circulation 2021; 143:e72-e227) — global reference for SAVR / TAVI cutoffs.
- Gewitz MH et al. — Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography. Circulation 2015; 131:1806-1818.
- Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo et al., 2022) — Chapters on Rheumatic Fever and Valvular Heart Disease.
- Li JS et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clinical Infectious Diseases 2000; 30:633-638 (modified Duke).
- World Health Organization — Technical Report Series on Rheumatic Fever and Rheumatic Heart Disease (2004), updated WHO global RHD strategy.
- API Textbook of Medicine, 11th Edition (Munjal et al., 2019) — Indian perspective on RHD management and benzathine penicillin prophylaxis.
Frequently asked questions
How many RHD and valvular questions appear in NEET PG?
Rheumatic heart disease and valvular lesions contribute 3-4 direct questions per NEET PG paper across medicine, cardiology, and community medicine. Jones criteria 2015, mitral stenosis auscultation and BMV eligibility (Wilkins score), Duke criteria for infective endocarditis, and benzathine penicillin prophylaxis are the most tested subtopics based on 2019-2025 pattern analysis.
What are the Jones criteria 2015 for acute rheumatic fever?
Jones criteria 2015 require evidence of preceding group A streptococcal infection plus two major criteria OR one major and two minor criteria. Major (high-risk populations): carditis (including subclinical), arthritis (polyarthritis or monoarthritis or polyarthralgia), chorea, erythema marginatum, subcutaneous nodules. Minor: fever, elevated ESR or CRP, prolonged PR interval, polyarthralgia (moderate-risk populations). The 2015 revision recognises subclinical carditis on echo and lowers the bar in high-risk populations.
What is the Wilkins score and its cutoff for BMV?
The Wilkins score grades mitral valve morphology on echocardiography across 4 components: leaflet mobility, leaflet thickening, valvular calcification, and subvalvular thickening — each scored 1 to 4 for a total of 16. A Wilkins score of 8 or less indicates favourable anatomy for balloon mitral valvuloplasty (BMV), with high success and low restenosis rates. Scores above 8 generally favour surgical mitral valve replacement.
What are the indications for BMV in mitral stenosis?
Balloon mitral valvuloplasty is indicated in symptomatic (NYHA class II-IV) patients with severe mitral stenosis (valve area less than or equal to 1.5 cm2) and favourable anatomy (Wilkins score less than or equal to 8, no left atrial thrombus, no moderate-severe MR). Absolute contraindications are left atrial thrombus and moderate-to-severe mitral regurgitation. BMV is preferred over MVR in young patients and pregnancy because it preserves the native valve.
What are the severity criteria for aortic stenosis?
Severe aortic stenosis is defined by any of: peak aortic jet velocity greater than or equal to 4 m/s, mean transvalvular gradient greater than or equal to 40 mmHg, or aortic valve area less than or equal to 1.0 cm2 (indexed AVA less than or equal to 0.6 cm2/m2). Very severe is peak velocity greater than 5 m/s or mean gradient greater than 60 mmHg. Low-flow low-gradient severe AS requires dobutamine stress echo to confirm.
When is TAVI preferred over SAVR?
TAVI (transcatheter aortic valve implantation) is preferred in elderly patients with symptomatic severe aortic stenosis at intermediate or high surgical risk (STS score greater than 4). The 2020 ACC-AHA guidelines now recommend TAVI as first-line in patients above 80 years of age. SAVR is preferred in patients under 65 and in those with aortic pathology requiring concomitant surgery (e.g., aortic root aneurysm or coronary bypass).
What causes acute severe aortic regurgitation?
Acute severe aortic regurgitation is caused by infective endocarditis (destruction of leaflets), aortic dissection (loss of commissural support), or blunt chest trauma. Presentation is pulmonary oedema and cardiogenic shock — the left ventricle is unprepared for the volume load. Auscultation shows a short early diastolic murmur (not the long murmur of chronic AR). Emergency surgical valve replacement is lifesaving; medical therapy is a bridge.
What are the Duke criteria for infective endocarditis?
Duke criteria diagnose infective endocarditis. Definite IE requires 2 major, or 1 major plus 3 minor, or 5 minor criteria. Major: typical organisms on 2 separate blood cultures (Strep viridans, Strep gallolyticus, HACEK, Staph aureus, enterococci) OR echo evidence of vegetation, abscess, or new valvular regurgitation. Minor: predisposition, fever greater than 38 degrees C, vascular phenomena (Janeway lesions, septic emboli), immunologic phenomena (Osler nodes, Roth spots, glomerulonephritis), microbiologic evidence not meeting major.
What is the empiric antibiotic regimen for infective endocarditis?
Empiric IE therapy covers likely organisms pending blood culture results. Native valve: ampicillin-sulbactam plus gentamicin (or vancomycin plus gentamicin in penicillin allergy, MRSA risk). Prosthetic valve: vancomycin plus gentamicin plus rifampicin. Therapy duration is 4-6 weeks (2 weeks for uncomplicated right-sided Staph IE in IV drug users). Blood cultures should be drawn (3 sets from different sites) before antibiotic start if patient is stable.
What is secondary prophylaxis for RHD in India?
Secondary prophylaxis against recurrent acute rheumatic fever uses benzathine penicillin G 1.2 million units IM every 3-4 weeks (600,000 units if weight under 27 kg). Duration: 5 years after the last attack OR until age 21 if no carditis; 10 years after attack OR until age 21 (whichever is longer) if carditis without residual valve disease; lifelong if carditis with persistent valvular disease or after valve surgery. Skin test before injection; have adrenaline ready for anaphylaxis.
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: April 2026
This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.
