---

Complete Comparison of Valvular Heart Diseases

Overview

---

Quick Reference Table

---

1. MITRAL STENOSIS (MS)

Etiology

• Rheumatic fever is the dominant cause worldwide (commissural fusion, leaflet thickening, chordal shortening)
• Rare: congenital, radiation, severe mitral annular calcification, carcinoid

Pathophysiology

• Obstruction of LV filling in diastole - LA pressure rises - pulmonary venous hypertension - pulmonary arterial hypertension
• Normal mitral valve area (MVA): 4-6 cm²
• Symptomatic when MVA < 2 cm²; severe when MVA < 1.5 cm²; critical when MVA < 1.0 cm²
• Reduced LV preload - reduced cardiac output
• Chronically elevated LA pressure triggers atrial fibrillation (in 30-40% of patients)

Symptoms

• Dyspnea on exertion (earliest), progressing to orthopnea, PND
• Fatigue (low CO)
• Hemoptysis (pulmonary venous hypertension)
• Palpitations (AF)
• Systemic emboli (LA clot, especially in AF)
• Hoarseness (Ortner's syndrome - enlarged LA compressing recurrent laryngeal nerve)

Physical Exam

• Loud S1 (delayed mitral valve closure)
• Opening snap (OS) after S2 - higher pressure gradient = shorter S2-OS interval
• Low-pitched, rumbling mid-diastolic murmur at apex, heard best in left lateral decubitus with bell of stethoscope
• Pre-systolic accentuation (if in sinus rhythm)
• Malar flush (mitral facies) - peripheral vasoconstriction with pulmonary HTN
• Signs of pulmonary HTN: loud P2, RV heave, TR murmur

ECG

• P mitrale (bifid P wave in lead II, biphasic in V1) - LA enlargement
• AF (common)
• RV hypertrophy in advanced disease

Chest X-ray

• LA enlargement (double density, splayed carina, posterior esophageal displacement)
• Pulmonary venous congestion, Kerley B lines
• Mitral valve calcification

Echocardiography (Key Investigation)

• Hockey-stick deformity of anterior mitral leaflet (restricted tip, normal base)
• Wilkins score (leaflet mobility, thickening, calcification, subvalvular involvement) - guides suitability for balloon valvuloplasty
• Doppler: pressure half-time method (MVA = 220/PHT)
• Mean gradient, planimetry of MVA

Management

• Medical: rate control (beta blockers, digoxin), diuretics, anticoagulation if AF, rheumatic fever prophylaxis
• Percutaneous mitral balloon valvuloplasty (PMBV): preferred for symptomatic MS with MVA < 1.5 cm² and favorable valve anatomy (Wilkins score ≤ 8)
• Surgery (commissurotomy or MVR): unfavorable anatomy, significant MR, or failed PMBV

---

2. MITRAL REGURGITATION (MR)

Etiology

• Primary (organic): Mitral valve prolapse (MVP, most common in developed world), rheumatic, infective endocarditis, connective tissue disease (Marfan's), chordal rupture, radiation, congenital
• Secondary (functional): Ischemic papillary muscle dysfunction, dilated cardiomyopathy (annular dilation), atrial fibrillation (atrial functional MR)

Pathophysiology

• Systolic backflow LV → LA: LA volume overload - LA dilation and increased compliance (chronic) vs. acute pulmonary edema (acute)
• LV receives both pulmonary venous return AND regurgitant volume - eccentric LV hypertrophy
• LV end-diastolic volume increases; EF initially preserved or supra-normal (misleading)
• Eventually, LV contractile dysfunction develops - EF falls - heart failure

Symptoms

• Chronic: often asymptomatic for years; then exertional dyspnea, fatigue
• Acute (chordal rupture, endocarditis, papillary muscle rupture in MI): sudden severe pulmonary edema - medical emergency

Physical Exam

• Holosystolic (pansystolic) murmur at apex, radiating to axilla/back
• Soft or absent S1
• S3 gallop (volume overload)
• Displaced, hyperdynamic apex beat (LV volume overload)
• In MVP: mid-systolic click followed by late systolic murmur (Barlow's click-murmur syndrome)

ECG

• LA enlargement (P mitrale)
• LV hypertrophy
• AF (common in chronic disease)

Echocardiography

• Identifies mechanism (Carpentier classification: Type I normal motion, II prolapse/flail, III restricted)
• Color Doppler quantifies regurgitation (jet area, vena contracta, PISA method)
• LV size and function (EF <60% or LVESD >40 mm = surgery threshold)
• Reparability assessment

Management

• Medical: vasodilators (nifedipine, ACEi) in symptomatic or hypertensive patients; heart failure therapy for secondary MR
• Surgery: First-line for primary severe MR. Mitral valve repair preferred over replacement (lower mortality, better LV preservation, no anticoagulation needed)
  • Indicated: symptomatic severe primary MR, OR asymptomatic with EF <60%, LVESD >40 mm, new AF, or PA systolic pressure >50 mmHg
• MitraClip (transcatheter edge-to-edge repair): for high surgical risk patients; approved for both primary and secondary MR (EVEREST II trial)

---

3. AORTIC STENOSIS (AS)

Etiology

• Calcific (degenerative): Most common cause in adults >65 years; progressive calcification of normal tricuspid valve (presents at 70-80 years) or bicuspid aortic valve (presents earlier, 50-60 years; present in 1-2% of population)
• Rheumatic: now rare in developed countries
• Congenital (unicuspid, bicuspid, hypoplastic annulus)

Pathophysiology

• Obstruction to LV outflow in systole - LV pressure overload - concentric LV hypertrophy (compensatory, increases wall stress)
• Cardiac output preserved for years while LV hypertrophies
• Classic symptom triad appears when compensation fails: Angina, Syncope, Dyspnea (HF)
• Once symptoms appear, prognosis is poor without intervention: 5-year survival ~15-50%
  • Angina: mean survival 5 years
  • Syncope: mean survival 3 years
  • Heart failure: mean survival 1-2 years

Severity (Doppler Echo Criteria)

Symptoms

• Angina (demand ischemia - subendocardial ischemia from hypertrophy + reduced coronary perfusion pressure)
• Syncope (exertional - failure of CO to increase, peripheral vasodilation)
• Dyspnea/Heart failure (diastolic dysfunction first, then systolic failure)

Physical Exam

• Harsh, crescendo-decrescendo (diamond-shaped) systolic ejection murmur at right 2nd intercostal space, radiating to carotids
• Parvus et tardus pulse (slow-rising, low-amplitude carotid pulse) - unreliable in elderly with stiff arteries
• Sustained, forceful apex beat (pressure overload)
• Diminished or absent A2 (calcification)
• S4 gallop (stiff, hypertrophied LV)
• Heaving, undisplaced apical impulse

ECG

• LV hypertrophy with strain pattern (ST depression, T-wave inversion in I, aVL, V4-V6)
• LBBB (advanced disease)

Echocardiography

• Heavily calcified, restricted leaflets (tricuspid or bicuspid)
• LV wall thickness increased
• Doppler gradients and continuity equation for AVA

Management

• Medical: No medication slows progression; treat comorbidities (hypertension, HF)
• Aortic Valve Replacement (AVR): Only definitive treatment
  • SAVR (surgical): Standard for low/intermediate risk, younger patients (<65 years prefer mechanical)
  • TAVR (transcatheter): Initially for high-risk/inoperable; now recommended even for low-risk; preferred >80 years; bioprosthetic
  • Indications: Symptomatic severe AS (Class I); Asymptomatic severe AS with EF <50% (Class I); Very severe AS (Class IIa)
• No role for balloon valvuloplasty in adults (high restenosis rate) - only as bridge to AVR

---

4. AORTIC REGURGITATION (AR)

Etiology

• Valve leaflet disease: Bicuspid aortic valve, infective endocarditis, rheumatic fever, myxomatous degeneration, radiation
• Aortic root/annular disease: Hypertensive aortic root dilation (most common in elderly), Marfan syndrome, aortic dissection, syphilitic aortitis, ankylosing spondylitis
• Acute AR: Aortic dissection, infective endocarditis - surgical emergency

Pathophysiology

• Diastolic backflow Ao → LV - LV volume overload - eccentric LV hypertrophy
• Wide pulse pressure (high systolic from increased stroke volume, low diastolic from regurgitation)
• LV can compensate for years with eccentric hypertrophy
• Eventually, LV contractile dysfunction - irreversible if surgery delayed too long
• Acute AR: LV not dilated - sudden high diastolic pressure - acute pulmonary edema - emergency

Symptoms

• Chronic: often asymptomatic for decades; early symptom is awareness of forceful heartbeat/pulsations, exertional dyspnea
• Exertional dyspnea, orthopnea, PND (LV decompensation)
• Angina (less common than AS)
• Acute AR: sudden severe dyspnea, pulmonary edema, shock

Physical Exam - Classic Signs (Wide Pulse Pressure Phenomena)

• Early diastolic murmur at left sternal border (3rd-4th ICS), best heard with patient sitting forward, in held expiration
• Austin Flint murmur: mid-diastolic rumble at apex (AR jet causes functional MS of anterior mitral leaflet)
• Corrigan's pulse (water-hammer pulse) - rapid rise and collapse of carotid pulse
• De Musset's sign - head bobbing with heartbeat
• Quincke's sign - visible capillary pulsations in nailbeds
• Duroziez's sign - femoral systolic/diastolic murmur
• Hill's sign - popliteal BP >20 mmHg higher than brachial BP
• Displaced, hyperdynamic apex beat (LV dilation)
• Soft A2

Management

• Medical: Vasodilators (ACEi, ARB, amlodipine, nifedipine) if hypertensive or symptoms present; no benefit in normotensive asymptomatic patients
• Surgery (AVR):
  • Symptomatic severe AR (Class I)
  • Asymptomatic severe AR with EF <50% (Class I)
  • Asymptomatic with severe LV dilation (LVESD >50 mm or LVEDD >65 mm) (Class IIa)
  • Acute severe AR (emergency surgery)

---

5. TRICUSPID STENOSIS (TS)

Etiology

• Almost exclusively rheumatic fever (rarely occurs in isolation; almost always associated with MS)
• More common in women
• Rare causes: carcinoid syndrome, congenital, right atrial myxoma, lupus

Pathophysiology

• Diastolic pressure gradient RA > RV
• Mean gradient of 4 mmHg sufficient to cause systemic venous congestion
• Elevated RA pressure - systemic venous HTN - hepatomegaly, ascites, peripheral edema
• Cardiac output is depressed and fails to rise with exercise
• TS can mask coexisting MS by reducing CO, thereby reducing pulmonary pressures
• In sinus rhythm: giant "a" wave in JVP; prolonged y descent

Symptoms

• Relatively little dyspnea for the degree of systemic congestion (because pulmonary circulation is protected by low CO)
• Fatigue (low CO)
• Hepatomegaly, abdominal discomfort, ascites
• Peripheral edema (often massive)
• Anasarca

Physical Exam

• Opening snap (after S2, but heard at lower left sternal border vs. apex for MS)
• Mid-diastolic murmur at lower left sternal border, louder on inspiration (Carvallo's sign - increases with inspiration due to increased venous return to right heart)
• Elevated JVP with prominent "a" wave, slow "y" descent
• Hepatomegaly, ascites, peripheral edema

ECG

• RA enlargement (tall, peaked P waves in II and V1 - P pulmonale)
• No RV hypertrophy (RV protected by stenosis)

Management

• Diuretics (reduce systemic congestion)
• Salt restriction
• Percutaneous balloon valvuloplasty (less effective than for MS due to valve calcification)
• Tricuspid valve repair or replacement - usually performed at same time as mitral valve surgery
• Tricuspid replacement usually uses a bioprosthesis (high thrombosis rate with mechanical valves in tricuspid position due to lower right-sided pressures)

---

6. TRICUSPID REGURGITATION (TR)

Etiology

• Secondary (functional) - most common (>85%):
  • RV dilation from any cause (pulmonary HTN, left-sided heart disease, mitral valve disease, cardiomyopathy, RV MI)
  • Atrial functional TR (dilated tricuspid annulus from AF without RV dilation)
  • Cardiac implantable electronic device (CIED) lead-related injury
• Primary (organic):
  • Rheumatic fever, infective endocarditis (IV drug users), carcinoid syndrome, myxomatous (TVP), radiation, Ebstein's anomaly (displacement of septal leaflet toward apex), trauma

Pathophysiology

• Systolic backflow RV → RA - RA volume overload - RA dilation and elevated RA pressure
• Systemic venous congestion (JVD, hepatic congestion, ascites, edema)
• Hepatic vein systolic flow reversal on Doppler (severe TR)
• Reduced forward cardiac output
• Secondary hyperaldosteronism from hepatic congestion

Symptoms

• Fatigue, weakness (low CO)
• Right upper quadrant pain (hepatic congestion)
• Ascites, peripheral edema
• Pulsatile sensation in neck (systolic hepatic pulsation)
• Anorexia, nausea (hepatic/GI congestion)

Physical Exam

• Holosystolic murmur at lower left sternal border, louder on inspiration (Carvallo's sign)
• Prominent "c-v" wave in JVP with rapid "y" descent (systolic wave = regurgitant flow into RA)
• Pulsatile enlarged liver
• Positive hepatojugular reflux
• Peripheral edema, ascites

ECG

• RV hypertrophy or RBBB (if primary cause related)
• RA enlargement (P pulmonale - tall P waves)
• AF common

Management

• Treat underlying cause (reduce pulmonary HTN, treat left-sided disease)
• Diuretics (aldosterone antagonist particularly useful - secondary hyperaldosteronism)
• Tricuspid valve repair/annuloplasty: recommended for severe TR at time of left-sided valve surgery; also for moderate TR with annular dilation (>40 mm)
• Tricuspid valve replacement: for non-reparable valves (carcinoid, Ebstein's severe)
• Transcatheter edge-to-edge repair (TEER): FDA approved (2024) for high surgical risk patients - reduces TR severity and improves QoL; mortality benefit not yet established
• Isolated tricuspid surgery has high perioperative mortality (~8-9%) due to advanced RV dysfunction

---

7. PULMONARY STENOSIS (PS)

Etiology

• Congenital - most common cause (~90%); isolated or part of tetralogy of Fallot
• Carcinoid syndrome - fibrous plaques on RV side of pulmonary and tricuspid valves
• Rare: rheumatic, post-radiation

Pathophysiology

• Obstruction to RV outflow in systole - RV pressure overload - RV hypertrophy (concentric)
• Severity classified by peak systolic gradient:
  • Mild: < 36 mmHg (peak velocity < 3 m/s)
  • Moderate: 36-64 mmHg
  • Severe: > 64 mmHg (peak velocity > 4 m/s)
• Right-to-left shunt if patent foramen ovale (PFO) is present with elevated RV pressures - cyanosis

Symptoms

• Often asymptomatic (mild-moderate cases)
• Severe: exertional dyspnea, fatigue
• Advanced: right heart failure (edema, ascites), exertional syncope
• Cyanosis if associated ASD/PFO with right-to-left shunting

Physical Exam

• Ejection click (early systolic, decreases with inspiration - unique to pulmonary stenosis among right-sided lesions)
• Harsh systolic ejection murmur at upper left sternal border (2nd ICS), radiates to left shoulder/clavicle
• Loud P2 in mild PS; soft/absent P2 in severe PS
• RV heave (pressure overload)
• Wide split S2 (delayed pulmonic closure)
• Rarely: signs of RV failure (elevated JVP, edema)

ECG

• RV hypertrophy (tall R in V1, deep S in V6)
• RA enlargement (P pulmonale) in severe disease
• RBBB pattern

Management

• Mild PS: No intervention needed; observation
• Percutaneous balloon pulmonary valvuloplasty (BPVP): treatment of choice for symptomatic or severe congenital PS (gradient > 50 mmHg) - excellent long-term results
• Surgical valvotomy/valvuloplasty: if balloon not feasible (dysplastic valve in Noonan syndrome)
• Carcinoid PS: valve replacement (fibrous/rigid valves not amenable to balloon)

---

8. PULMONARY REGURGITATION (PR)

Etiology

• Iatrogenic - most common: following repair of tetralogy of Fallot (pulmonary valvotomy/homograft)
• Secondary/Functional: pulmonary arterial hypertension (annular dilation from dilated pulmonary root) - "Graham Steell murmur" context
• Primary: infective endocarditis (IV drug users), carcinoid, rheumatic (rare), congenital (absent pulmonary valve)
• Post-balloon valvuloplasty for PS

Pathophysiology

• Diastolic backflow PA → RV - RV volume overload - RV dilation and eccentric hypertrophy
• RV initially tolerates volume overload well
• Progressive RV dilation leads to:
  • TR (annular dilation)
  • RV systolic dysfunction
  • Right heart failure
  • Reduced exercise capacity
• Usually well-tolerated for years unless severe and from high PA pressures

Symptoms

• Often asymptomatic for decades (especially post-ToF repair)
• Reduced exercise tolerance
• Progressive RV dilation/dysfunction - right heart failure (edema, ascites)
• Palpitations (arrhythmias from RV dilation - ventricular tachycardia in post-ToF patients)
• Sudden cardiac death (in post-ToF patients with severe PR + RV dilation)

Physical Exam

• Early diastolic murmur at upper left sternal border (2nd-3rd ICS)
• Graham Steell murmur: high-pitched early diastolic murmur from pulmonary HTN-related PR (similar to AR murmur but at upper left sternal border)
• RV heave (volume overload)
• Wide split S2
• Loud P2 if PA HTN is underlying cause
• Signs of RV failure in advanced disease

ECG

• RV volume overload: RBBB (rsR' pattern in V1)
• RV hypertrophy if pulmonary HTN is cause
• RA enlargement

Management

• Mild PR with normal RV: observation only
• PR with pulmonary HTN: treat underlying cause
• Pulmonary valve replacement (PVR): Indicated for symptomatic severe PR, or asymptomatic with RV dilation (RVEDV index > 150-160 mL/m²) or declining RV systolic function
  • Particularly important in post-ToF patients: PVR improves exercise capacity and may reduce arrhythmia risk and SCD risk
  • Transcatheter pulmonary valve replacement (TPVR/Melody valve, SAPIEN valve): FDA approved for patients with a suitable conduit or dilated RVOT (becoming first-line in appropriate anatomy)
  • Bioprosthetic valves preferred (no anticoagulation, lower-pressure right side)

---

Comparative Summary by Key Features

Etiology at a Glance

---

Murmur Comparison

---

Hemodynamic Consequences

---

Key Investigations

---

Treatment Summary

---

Inspiration vs. Expiration Effect on Murmurs (Clinical Pearl)

• Right-sided murmurs increase with inspiration (Carvallo's sign): TS, TR, PS, PR - all increase with inspiration as venous return to right heart increases
• Left-sided murmurs generally unaffected by respiration (or may decrease slightly with inspiration)

Pregnancy Considerations

• MS: Poorly tolerated in pregnancy - increased heart rate in pregnancy reduces diastolic filling time, dramatically raising LA pressure; PMBV can be done during pregnancy
• AS: High-risk, particularly severe AS
• MR/AR: Better tolerated (reduced afterload in pregnancy is beneficial)
• TR/PR: Usually tolerated if right heart function preserved

---

• 8 individual sections - one per valvular lesion (MS, MR, AS, AR, TS, TR, PS, PR), each covering etiology, pathophysiology, symptoms, physical exam, investigations, and management
• 5 comparative summary tables:
  • Table A: Etiology at a glance
  • Table B: Murmur comparison (type, location, radiation, key features)
  • Table C: Hemodynamic consequences
  • Table D: Key investigations (Echo, ECG, CXR)
  • Table E: Management summary
• 8 clinical pearls section at the end
• Color-coded layout with navy/blue theme, sourced from Braunwald's Heart Disease 11e, Harrison's 22e, and Grainger & Allison's