Overview Table

Heart Valve Disease	Mechanism	Murmur Type	Murmur Description
Aortic stenosis	Poor / obstructed flow across the aortic valve during systole (from LV to ascending aorta)	Systolic murmur	Ejection systolic murmur at right 2nd ICS Radiates to the carotids
Mitral regurgitation	Blood backflow into LA from LV (via mitral valve) during systole		Pan-systolic (aka holosystolic) murmur at the apex (left 5th ICS, mid-clavicular line) Radiates to the axilla
Aortic regurgitation	Blood backflow into LV from ascending aorta (via aortic valve) during diastole	Diastolic murmur	Early diastolic murmur  Best heard at Erb’s point (left 3rd / 4th ICS)
Mitral stenosis	Poor / obstructed blood flow across the mitral valve during diastole (from LA to LV)		Mid-diastolic murmur at the apex (left 5th ICS, mid-clavicular line)

*All the above are left-sided valve diseases, they are best heard on expiration (right-sided valve diseases are best heard on inspiration).

Aortic Stenosis

Definition

Aortic stenosis is defined as an abnormal narrowing of the aortic valve orifice, resulting in increased resistance to blood flow from the left ventricle into the aorta during systole.

Aetiology

There are 3 main causes of aortic stenosis: ^{[ref, ref]}

Cause	Description
Degenerative calcification	Leading cause in >70 y/o in developed countries Associated risk factors: Advancing age Male Hypertension Smoking Diabetes, obesity, metabolic syndrome, dyslipidaemia
Congenital bicuspid aortic valve	Leading cause in <70 y/o Bicuspid valves are prone to premature calcification and stenosis due to altered hemodynamics and genetic predisposition
Rheumatic heart disease	Significant cause in endemic regions (most commonly developing countries) Rheumatic heart disease causes commissural fusion and leaflet thickening, often in association with mitral valve disease

 

Clinical Features

Symptoms

Most patients remain asymptomatic for years. ^[ref]

If symptomatic, the classic triad of: ^{[ref, ref]}

• Exertional dyspnoea (from underlying heart failure)
• Angina (due to ↑ myocardial oxygen demand from LV hypertrophy)
• Exertional presyncope/syncope (due to fixed cardiac output from the valve stenosis)

Signs

Possible examination findings: ^{[ref, ref]}

Examination aspect	Findings
Auscultation findings	Harsh crescendo-decrescendo, ejection systolic murmur (ESM) Radiation to carotids (bilaterally) Best heard in the right 2nd ICS and on expiration Additional sounds: Early systolic ejection click Soft S2 / single S2 (or even absence of S2 in severe disease) S4 (due to LV hypertrophy)
Physical examination	Narrow pulse pressure  (<40 mmHg difference between systolic and diastolic BP) Delayed, slow-rising, low amplitude carotid pulse  (“parvus et tardus”) Heaving apex (from LV hypertrophy) Signs of heart failure are possible

 

Complications

Main complications: ^{[ref, ref]}

• Chronic heart failure (HFpEF / HFmrEF) (↑ afterload → progressive concentric remodelling → LV hypertrophy)
• Arrhythmias (esp. atrial fibrillation)
• Myocardial ischaemia (from LV hypertrophy)
• Pulmonary hypertension, secondary mitral regurgitation
• Heyde’s syndrome (triad of severe aortic stenosis + acquired type 2a von Willebrand syndrome + GI bleeding)
  • High shear stress across the aortic valve → loss of von willebrand factor → impaired platelet-mediated haemostasis → recurrent GI bleeding and anaemia (in areas of GI angiodysplasias)

Complications associated with bicuspid valves: ^[ref]

• Aortic root dilation and dissection

Investigation and Diagnosis

1st line: trans-thoracic echocardiography (TTE)

Other tests (not routinely needed):

• Trans-oesophageal echocardiography – provides better resolution of the aortic valve (e.g., if there is poor acoustic window in TTE)
• Cardiac CT – to quantify valve calcification
• Cardiac MRI – assessment of ventricular function and myocardial fibrosis

Echocardiography Severity Classification

BSE recommends using the peak aortic jet velocity (Vmax) to define AS severity:

• Mild: Vmax <3 m/s
• Moderate: Vmax 3.0-3.0 m/s
• Severe: Vmax ≥4.0 m/s

The commonly seen AS severity grading system (based on 2020 ACC/AHA guidelines):

Severity	Peak aortic jet velocity (Vmax)	Measure pressure gradient (mmHg)	Aortic valve area (cm2)
Mild	<3.0 m/s	<20	>1.5
Moderate	3.0-3.9 m/s	20-39	1.0-1.5
Severe	≥4.0 m/s	≥40	<1.0

 

Management

Pharmacological Management

This applies to ALL valvular heart diseases:

• There is no specific pharmacological management for the valve disease itself
• Pharmacological management is offered to manage heart failure if it develops (see this article)
• Optimise management of comorbidities and cardiovascular risk factors (e.g. hypertension, smoking cessation)

Surgical Management

Indications

Offer intervention if there is symptomatic, severe aortic stenosis

Consider referring asymptomatic, severe AS for intervention if ANY of the following:

• LVEF <55%
• Symptoms unmasked on exercise testing
• BNP/ NT-proBNP >2x upper limit of normal
• Echo measurements
  • Vmax >5 m/s (very severe AS)
  • Aortic valve area <0.6 cm² (very severe AS)

Choice of Intervention

• 1st line: surgical aortic valve replacement (SAVR) (by median sternotomy or minimally invasive surgery)

 

• 2nd line (if high surgical risk): transcatheter aortic valve implantation (TAVI)

 

• If unfit for TAVI: balloon valvuloplasty

Surveilllance

Echo surveillance is recommended in AS, depending on severity:

• Mild → every 3-5 years
• Asymptomatic severe (intervention not currently needed) → every 6-12 months

Aortic Sclerosis

Definition

Aortic sclerosis is defined as focal thickening and calcification of the aortic valve with NO significant restriction of leaflet motion and NO hemodynamically significant left ventricular outflow obstruction. ^[ref]

NOT the same as aortic stenosis, but it is considered a precursor to aortic stenosis.

Aetiology

Multifactorial, mainly shared risk factors with atherosclerosis: ^[ref]

• Advancing age
• Male
• Hypertension
• Smoking
• Diabetes, obesity, metabolic syndrome, dyslipidaemia

Clinical Features

Aortic sclerosis is typically asymptomatic. ^{[ref, ref]}

Possible examination findings: ^{[ref, ref]}

• Soft ejection systolic murmur
• With NO radiation to the carotids

Complications

Main complications are: ^{[ref, ref]}

• Progression to aortic stenosis
• Increased risk of cardiovascular events (aortic sclerosis is a marker of systemic endothelial dysfunction)

Investigation and Diagnosis

1st line: trans-thoracic echocardiography (TTE)

Echocardiography criteria:

• Leaflet thickening and calcification
• Peak aortic jet velocity (Vmax) <2.5 m/s (no evidence of haemodynamic obstruction)

 

Management

There is no specific management for aortic sclerosis:

• Optimise management of comorbidities and cardiovascular risk factors (e.g. hypertension, smoking cessation)
• No routine echocardiography surveillance is needed

Aortic Regurgitation (AR)

Definition

Aortic regurgitation is defined as the backflow of blood from the aorta into the left ventricle during diastole due to incompetent closure of the aortic valve. ^[ref]

Aetiology

Causes of AR can be largely classified into acute vs chronic: ^[ref]

Category	Common causes
Acute AR	Infective endocarditis (esp. bacterial) Aortic dissection Blunt chest trauma
Chronic AR (more common)	Ascending aorta / aortic root dilation causes Age-related generation Hypertension Bicuspid aortic valve Connective tissue disorders (e.g. Marfan syndrome, Ehlers-Danlos syndrome) Aortitis (e.g. Takayasu arteritis, giant cell arteritis, cardiac syphilis) Rheumatic heart disease

Clinical Features

Symptoms

Acute AR tends to have acute heart failure features and those of the underlying cause​​​​​. ^[ref]

Chronic AR features: ^[ref]

• Asymptomatic during the compensated phase (for many years)
• Chronic heart failure features
• Palpitations
• Angina

Signs

Possible examination findings: ^[ref]

Examination aspect	Findings
Auscultation findings	High-pitched, blowing, early decrescendo diastolic murmur Best heard at the Erb’s point (left 3rd/4rth ICS by the sternal border), while leaning forward in a sitting position, and on expiration Additional sounds: S3 (from volume overload) Austin flint murmur (regurgitant flow obstructing the anterior mitral leaflet → mitral stenosis-like murmur)
Physical examination	Wide pulse pressure (>60mmHg difference between systolic and diastolic BP) Colapsing (water hammer) pulse  Displaced, hyperdynamic apex (from volume overload and LV dilation) Some additional signs (common in exams): De Musset’s sign – head nodding with each heartbeat Quincke’s sign – visible capillary pulsations Corrigan’s pulse – visible bounding carotid pulse Muller’s sign – visible pulsation of the uvula Traube’s sign – pistol shot sound over the femoral artery (on auscultation with gentle compression of the femoral artery)

Complications

Main complications of chronic AR are: ^[ref]

• Heart failure (from LV dilation) – most common
• Arrhythmias (from chamber dilation and fibrosis)
• Aortic root dilation can lead to aortic dissection or rupture

Investigation and Diagnosis

1st line: trans-thoracic echocardiography (TTE)

Management

Pharmacological Management

This applies to ALL valvular heart diseases:

• There is no specific pharmacological management for the valve disease itself
• Pharmacological management is offered to manage heart failure if it develops (see this article)
• Optimise management of comorbidities and cardiovascular risk factors (e.g. hypertension, smoking cessation)

Surgical Management

Indications

Offer intervention if there is symptomatic, severe AR

Considering referring asymptomatic, severe AR for intervention if ANY of the following:

• LVEF <55%
• ESD >50mm or ESDI >24mm/m²

Choice of Intervention

• 1st line: surgery
  • Surgical aortic valve replacement (SAVR) – standard procedure for most patients
  • Aortic valve repair – preferred in selected patients with favourable valve anatomy

 

• 2nd line (if high surgical risk): transcatheter aortic valve implantation (TAVI)

Mitral Stenosis (MS)

Definition

Mitral stenosis is defined as an abnormal narrowing of the mitral valve orifice, obstructing blood flow from the left atrium to the left ventricle.

Aetiology

Leading cause: rheumatic heart disease (often presents decades after initial rheumatic episode). ^[ref]

Calcific degeneration is increasingly recognised as a cause in developed countries. ^[ref]

Clinical Features

Symptoms

Most patients remain asymptomatic initially.

When they become symptomatic:

• Most commonly presents as heart failure ^[ref]
• Haemoptysis is possible due to ruptured bronchial veins from elevated pulmonary venous pressure.

Signs

Possible examination findings: ^[ref]

Examination aspect	Findings
Auscultation findings	Low-pitch, rumbling, mid-to-late diastolic murmur Best heard at the apex with the bell of the stethoscope with the patient in the left lateral decubitus position and on expiration Additional sounds: Loud S1 Opening snap following S2
Physical examination	Malar flush Signs of atrial fibrillation are common (e.g., irregularly irregular pulse) Signs of pulmonary hypertension: Loud P2 Parasternal heave (from RV hypertrophy) Raised JVP Peripheral oedema

 

Complications

Important complications: ^[ref]

• Atrial fibrillation (from left atrial dilation) – notable association
• Right-sided heart failure and pulmonary hypertension
• Infective endocarditis

Investigation and Diagnosis

1st line: trans-thoracic echocardiography (TTE)

Management

Pharmacological Management

This applies to ALL valvular heart diseases:

• There is no specific pharmacological management for the valve disease itself
• Pharmacological management is offered to manage heart failure if it develops (see this article)
• Optimise management of comorbidities and cardiovascular risk factors (e.g. hypertension, smoking cessation)

Surgical Management

Indications

Offer intervention if there is symptomatic, severe MS

ESC guidelines also recommend considering intervention if:

• Asymptomatic severe MS, and
• ↑ Pulmonary artery pressure (>50 mmHg)

Choice of Intervention

• 1st line: transcatheter valvotomy (also called balloon valvuloplasty)
• 2nd line: surgical mitral valve replacement

Mitral Regurgitation (MR)

Definition

Mitral regurgitation is defined as the backflow of blood from the left ventricle into the left atrium during systole due to incompetent closure of the mitral valve.

Aetiology

Primary causes:

• Mitral valve prolapse
• Degenerative changes
• Rheumatic heart disease
• Infective endocarditis
• Connective tissue disorder (e.g. Marfan syndrome, Ehlers-Danlos syndrome)

Secondary (functional) causes:

• Ischaemic mitral regurgitation (post-MI complication from anterior papillary muscle rupture)
• Left ventricular dilation (e.g. chronic volume overload, dilated cardiomyopathy)
• Atrial dilation (common in atrial fibrillation)
• HCM / HOCM (causes abnormal papillary muscle/leaflet movement)

Clinical Features

Symptoms

Most patients remain asymptomatic initially.

When they become symptomatic:

• Most commonly present as heart failure ^[ref]
• Features of the underlying cause

Signs

Possible examination findings: ^[ref]

Examination aspect	Findings
Auscultation findings	High-pitch, blowing, pansystolic murmur (PSM) Radiation to left axilla Best heard at the apex with the bell of the stethoscope with the patient in the left lateral decubitus position and on expiration Additional sounds: Soft S1  In severe MR Widely split S2  S3
Physical examination	Displaced hyperdynamic apex beat (from LV overload) Signs of pulmonary hypertension: Loud P2 Parasternal heave (from RV hypertrophy) Raised JVP Peripheral oedema

 

Complications

Important complications: ^[ref]

• Atrial fibrillation (from left atrial dilation) – notable association
• Right-sided heart failure and pulmonary hypertension

Investigation and Diagnosis

1st line: trans-thoracic echocardiography (TTE)

Management

Pharmacological Management

This applies to ALL valvular heart diseases:

• There is no specific pharmacological management for the valve disease itself
• Pharmacological management is offered to manage heart failure if it develops (see this article)
• Optimise management of comorbidities and cardiovascular risk factors (e.g. hypertension, smoking cessation)

Surgical Management

Indications

Offer intervention if there is symptomatic, severe MR

Considering referring asymptomatic, severe AR for intervention if ANY of the following:

• LVEF <60%
• ↑ Systolic pulmonary artery pressure on exercise testing (>60 mmHg)
• ESD >45mm or ESDI >22mm/m²

Choice of Intervention

• 1st line: surgical mitral valve repair (by median sternotomy or minimally invasive surgery)

 

• 2nd line: surgical mitral valve replacement

 

• 3rd line (if unfit for surgery): transcatheter edge-to-edge repair (e.g., using MitraClip device)
  • Device used to approximate the mitral valve leaflets, reducing regurgitation

References