Valvular Heart Diseases

Valvular heart diseases
(Valvular heart defects)
DR DAVID ELIA SARIA

MD, MMED-IMED
Valvular heart diseases 11/05/2023 0

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Introduction
 Valvular heart diseases can take the form of stenosis, insufficiency (regurgitation), or a
combination of the two.
 These defects are typically acquired as the result of infections, underlying heart disease, or
degenerative processes. However, certain congenital conditions can also cause
valvular heart diseases.
 Acquired defects are found primarily in the left heart as a result of higher pressure and
mechanical strain on the left ventricle.

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Introduction
 Primary valvular heart disease ranks well below coronary heart disease, stroke, hypertension,
obesity, and diabetes as a major threat to the public health
 Rheumatic fever is the dominant cause of valvular heart disease in low- and middle income
countries
 Aortic stenosis (AS) and mitral regurgitation (MR) represent the most frequent aetiologies of
severe native VHD, frequently associated with congestive HF (15.5% and up to 50%,
respectively (ESE, 2022)
 Valvular stenosis leads to a greater pressure load and concentric hypertrophy, while
insufficiencies are characterized by volume overload and eccentric hypertrophy of the
preceding heart cavities.
 Diagnostic procedures typically include ECGs, chest x-ray, and echocardiograms. Management
consists of interventional or surgical procedures to reconstruct or replace valves, as well as
medical treatment of possible heart failure.
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Heart valves

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Epidemiology
• Aortic stenosis
• Most common valve defect in industrialized countries
• Mostly degenerative
• Degenerative stenosis usually becomes symptomatic after the age of 75 and is most common in
men.
• Aortic stenosis in young people is usually secondary to congenital defects (e.g., bicuspid aortic
valve).
• Aortic regurgitation
• Age of onset: 40–60 years
• Severity increases with age (AHA/ACC, 2022)

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• Mitral stenosis: symptom onset between 20 and 39 years
• Mitral regurgitation
• Overall prevalence of 0.6 to 2.4 %
• Second most common valve defect
• More common in women
• Tricuspid valve defects: occur in < 1% of the population
• Pulmonary valve defects: rare outside of congenital conditions
(AHA/ACC, 2022)

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Aortic valve stenosis
 Aortic valve stenosis (AS) is a valvular heart disease characterized by narrowing of

the aortic valve.
 Aortic valve stenosis is the most common cause of left ventricular (LV) outflow
obstruction in children and adults
 As a result, the outflow of blood from the left ventricle into the aorta is obstructed. This
leads to chronic and progressive excess load on the left ventricle and potentially left
ventricular failure
 The patient may remain asymptomatic for long periods of time; for this reason, AS is often
detected late when it first becomes symptomatic (dyspnea on exertion, angina pectoris,
or syncope).

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Risk factors for degenerative calcific
AS
1. Age – Each 10-year increase in age was associated with a twofold increased
risk.
2. Male sex – Two fold excess risk.
3. Current cigarette smoking – 35 percent increase in risk.
4. A history of hypertension – 20 percent increase in risk.

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Etiology
• Aortic valve sclerosis: calcification and fibrosis of aortic valve leaflets

• Most common cause of aortic stenosis
• Occurs at an increasing rate as patients age
• Similar pathophysiology to atherosclerosis
• Bicuspid aortic valve (BAV): fusion of two of the three aortic-valve leaflets in utero
• Most common congenital heart valve malformation , predominantly affects males (3:1) ]
• Dystrophic calcification and degeneration
• Patients present with symptoms of aortic stenosis earlier than in regular aortic valve calcification.
• Congenital aortic stenosis is rare and usually features a unicuspid or bicuspid valve
• Rheumatic fever]
• Still remains a significant cause of AS in lower-income countries, where antibiotics may be less readily available
• Stenosis is caused by commissural fusion.

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Pathophysiology
• Narrowed opening area of the aortic valve during systole → obstruction of blood flow
from left ventricle (LV) → increased LV pressure → left ventricular concentric
hypertrophy, which leads to:
• Increased LV oxygen demand
• Impaired ventricular filling during diastole → left heart failure
• Reduced coronary flow reserve
• Initially, cardiac output (CO) can be maintained
• Later, the decreased distensibility of the left ventricle reduces cardiac output and may
then cause backflow into the pulmonary
veins and capillaries → higher afterload (pulmonic pressure) on the right heart → right
heart failure
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Clinical features
 AS may remain asymptomatic for years, particularly with mild or moderate stenosis, The classic clinical manifestations of
AS are heart failure (HF), syncope, and angina And Symptoms usually start to develop when the disease progresses to
severe AS, and may present at rest or on exertion.
• Signs and symptoms
• Dyspnea (typically exertional)
• Angina pectoris
• Dizziness and syncope
• Additional signs specific to infants: wheezing and difficulty feeding
• Physical examination
• Small blood pressure amplitude, decreased pulse pressure
• Weak and delayed distal pulse (pulsus parvus et tardus)
• Palpable systolic thrill over the bifurcation of the carotids and the aorta

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• Auscultation
• Harsh crescendo-decrescendo (diamond-shaped), late systolic ejection murmur that radiates bilaterally to
the carotids
• Best heard in the 2nd right intercostal space
• Handgrip decreases the intensity of the murmur.
• Valsalva and standing from squatting decreases or does not change the intensity of the murmur (in contrast to hypertrophic
cardiomyopathy).
• Soft S2
• S4 is best heard at the apex.
• Early systolic ejection click
• The murmur may also radiate to the apex of the heart, where it may have a different quality (musical due
to high frequency vibrations) and may be louder, suggesting that the patient also has mitral regurgitation.
• This is known as the Gallavardin phenomenon.

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Classification
AHA/ACC staging for aortic valve stenosis
Mean aortic
Stage Definition AVA Transaortic velocity Symptoms
pressure gradient
Stage A aortic valve

At risk of AS 3–4 cm2 < 2.0 m/second < 10 mm Hg None
stenosis
Mild: 1.5–2.9 cm2 2.0– 2.9 m/second 10–19 mm Hg None

Stage B aortic valve
Progressive AS
stenosis Moderate: 1.0–1.4
3.0–3.9 m/second 20–39 mm Hg None
cm2
Asymptomatic
Stage C1 aortic
severe AS (LVEF nor
valve stenosis None
mal)
Exercise testing is
reasoble to confirm
Asymptomatic symptom status
Stage C2 aortic
severe AS (LVEF < ≤ 1.0 cm2 ≥ 4.0 m/second ≥ 40 mm Hg
valve stenosis
50%)
HF
Stage D aortic valve Symptomatic Angina
stenosis severe AS Syncope or
presyncope
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Diagnostics
Echocardiography
• Indication: Assessment of aortic valve structure, function, and stenosis severity, left
ventricle and other heart valves (see valvular heart diseases)
• Supportive findings
• Calcification and narrowing of the aortic valve
• Increased mean aortic pressure gradient and transvalvular velocity
• Signs of cardiac remodeling, e.g., concentric hypertrophy

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 Continuous wave (CW) Doppler in aortic valvular
stenosis
 Echocardiography (transthoracic; apical five-
chamber view; with CW Doppler)
 The aortic valve is hyperechoic due to calcification
and fibrosis of the valve leaflets.Transaortic
velocity measures 4.01 m/s and the mean aortic
pressure gradient measures 42.2 mmHg. From
these measurements, the aortic valve stenosis
would be classified as stage C2.

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Other
• Laboratory studies: usually nonspecific and
therefore not routinely indicated;
• BNP/NT-proBNP
• Troponin T/I
• ECG
• ECG signs of LVH (e.g., positive Sokolow-Lyon
index)
• Nonspecific ST-segment and T-wave abnormalities
• Chest x-ray: Used to assess for pulmonary
edema and Visible calcifications within the aortic
valve .
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Additional evaluation
 Low-dose dobutamine stress testing

• Indication: stage D AS with LVEF < 50% to determine the true anatomic severity of the
stenosis
• Typical findings
• Severe AS: valve area, transaortic velocity, and mean aortic pressure gradient stay fixed.
• Moderate AS: valve area will increase as the stroke volume increases in response to dobutamine.

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Exercise stress testing
• Indication: stage C1 AS and stage C2 AS to provoke possible exertional symptoms
• Findings:
• Typical symptoms, e.g., angina, excessive dyspnea, or dizziness
• Arrhythmia or ST-segment depression
• Hypotension or insufficient rise in blood pressure (< 20 mm Hg)
 Cardiac CT
• Used in select patients to rule out concomitant CAD if pretest probability is low
• Can quantify valve calcification
 Cardiac MRI
• Provides precise information on anatomy and hemodynamics
• Can be helpful in evaluating severity of AS but is not always available
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Cardiac catheterization
• Diagnostic hemodynamic cardiac catheterization: an accurate diagnostic test for the
evaluation of aortic valve area, cardiac output, and mean aortic pressure gradient.
Coronary angiography
• Indication: Preoperative cardiac risk stratification for patients with angina, reduced LVEF, signs
of ischemia, or other CAD risk factors
• Findings: signs of CAD (e.g., coronary stenosis)

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General principles
• Aortic valve stenosis is a progressive condition and definitive management requires valve
replacement.
• Urgency of valve repair/replacement depends on staging.
• Symptomatic and/or severe AS: aortic valve replacement usually indicated
• Asymptomatic or mild-moderate AS: management of medical comorbidities and
monitoring echocardiography; some may benefit from early valve replacement
• Management of acute complications requires individualized and specialized care.

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Management of medical comorbidities
• Hypertension
• Hyperlipidemia
• Diabetes mellitus
• Atrial fibrillation
Management of acute complications
 Acute decompensated heart failure:
 Cardiogenic shock
 Atrial fibrillation

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Monitoring and prophylactic antibiotics
• Echocardiography
• Regular follow-up imaging is indicated for asymptomatic patients with:
• Mild stage B AS: every 3–5 years
• Moderate stage B AS: every 1–2 years
• Any stage C AS: every 6–12 month
• On-demand imaging is indicated for patients with:

• Any change in signs or symptoms
• Conditions that have high hemodynamic/metabolic demands

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Aortic valve replacement (AVR) and repair
 Indications
• Symptomatic patients with severe, high-gradient AS (stage D AS)
• Asymptomatic patients with severe AS and:
• Significantly ↓ LVEF (stage C2 AS)
• Undergoing cardiac surgery for other indications (stage C AS or stage D AS)
• AVR can also be beneficial for certain patients with moderate (stage B AS) to severe (stage
D AS) with specific characteristics
 The presence of exertional symptoms (dyspnea on exertion, angina pectoris, syncope) is an
indication for surgery.

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Complications of aortic valve replacement
• Vascular complications, thromboembolism/stroke

• Major bleeding
• Renal failure
• Arrhythmias: atrioventricular block, atrial fibrillation
• Aortic regurgitation/paravalvular leak
• Infection: endocarditis

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Antithrombotic therapy after aortic valve replacement
Antithrombotic therapy for patients with prosthetic aortic valves [8][14]
Choice of agent Target INR Duration of therapy
Mechanical valve and no risk

•2.5 (range 2.0–3.0)
factors for thromboembolism
•Combination antiplatelet
agent and VKA is recommended, e.g., •Lifelong
Mechanical valve and ≥ 1 risk ASA PLUS warfarin
factor for thromboembolism
•3.0 (range 2.5–3.5)
OR older generation mechanical
valves
•Antiplatelet agents: lifelong

•Antiplatelet agent is reasonable, e.g., •VKAs
Bioprosthetic valve with low risk of ASA • 3–6 months after surgical
•2.5 (range 2.0–3.0)
bleeding •Addition of a VKA is reasonable, AVR
e.g., warfarin • At least 3 months post-
TAVR

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Prognosis
• Asymptomatic patients: Mortality rate is < 1% in a given year.
• Symptomatic patients: Mortality rate in the first 2 years is > 50% if left untreated.

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Aortic regurgitation
(Aortic insufficiency)
 Aortic regurgitation (AR) is a valvular heart disease characterized by incomplete closure of
the aortic valve leading to the reflux of blood from the aorta into the left ventricle (LV)
during diastole.
 Aortic regurgitation can be acute (primarily caused by bacterial endocarditis or aortic

dissection) or chronic (e.g., due to a congenital bicuspid valve or rheumatic fever) and may
be caused by a valvular defect or an abnormality of the aorta.
 AR is most often due to aortic root dilation, congenital bicuspid aortic valve,
and calcific valve disease

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Pathophysiology
• General
• Regurgitation of blood from the aorta into the left ventricle (LV) leads to:
• Increased systolic blood pressure and decreased diastolic pressure
• Widened pulse pressure → water hammer pulse
• Acute AR
• Because LV cannot sufficiently dilate in response to regurgitant blood, LV end-diastolic pressure increases
rapidly → pressure transmits backwards into pulmonary circulation → pulmonary edema and dyspnea
• Decreased cardiac output if severe → cardiogenic shock and myocardial ischemia
• Chronic AR
• Initially, a compensatory increase in stroke volume can maintain adequate cardiac output despite regurgitation
(compensated heart failure)
• Over time, increased left ventricular end-diastolic volume → LV enlargement and eccentric
hypertrophy of myocardium → left ventricular systolic dysfunction → decompensated heart failure

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Clinical features
Acute aortic regurgitation

 Signs and symptoms
• Sudden, severe dyspnea
• Rapid cardiac decompensation secondary to heart failure
• Pulmonary edema
• Symptoms related to underlying disease (e.g., fever due to endocarditis, chest pain due to aortic
dissection)
 Auscultation
• Soft S1
• Soft and short early diastolic murmur

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Chronic aortic regurgitation
 Signs and symptoms
• May be asymptomatic for up to decades despite progressive LV dilation
• Palpitations
• Symptoms of high pulse pressure
• Water hammer pulse of peripheral arteries characterized by rapid upstroke and
downstroke
• Pulsing of carotid arteries with rapid upstroke and downstroke
• Quincke sign: visible capillary pulse when pressure is applied to the tip of a fingernail
• De Musset sign: rhythmic nodding or bobbing of the head in synchrony with
heartbeats
• Point of maximal impulse (PMI): diffuse, hyperdynamic, and displaced inferolaterally

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• Symptoms of left heart failure
• Exertional dyspnea
• Angina
• Orthopnea
• Easy fatigability
• Syncope
Auscultation
• S3
• High-pitched, blowing, decrescendo early diastolic murmur (Austin Flint
murmur)
• Rumbling, low-pitched, middiastolic or presystolic murmur heard best at the apex
• Caused by regurgitant blood striking the anterior leaflet of the mitral valve, which leads
to premature closure of the mitral leaflets
• In more severe stages, possiblyValvular
a harsh, crescendo-decrescendo midsystolic
heart diseases 11/05/2023 0
murmur that resembles the ejection murmur heard in aortic stenosis 5:00 PM
American Heart Association (AHA)/American College of
Cardiology (ACC) staging system for chronic AR
Diagnostics
Approach
• Transthoracic echocardiography (TTE) is the primary diagnostic tool to diagnose AR and
assess the severity of disease.
• Acute AR is an emergency that must be diagnosed and treated immediately.
• CTA Chest (or TEE) is the preferred diagnostic tool if aortic dissection is suspected.
• Additional diagnostics depend on patient stability and the suspected underlying condition
(e.g., blood cultures for endocarditis).
• In chronic AR, TEE, CMR, or cardiac catheterization can be used to confirm the diagnosis
if TTE findings are inconclusive.

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Supportive findings
• General findings
• Abnormal aortic valve leaflets
• Fluttering of the anterior mitral valve leaflet
• Regurgitant AR jet on Doppler flow tracing
• Dilated aorta
• Findings specific to acute AR
• Reduced cardiac output
• Elevated end-diastolic left ventricular pressure
• Early mitral valve closing
• Rapid equilibration of aortic and left ventricular pressure
• Findings specific to chronic AR: increased LV size and volume
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Other
• Laboratory studies: not routinely indicated but useful for the evaluation of other causes of
symptoms
• BNP/NT-proBNP
• Blood cultures: in suspected infective endocarditis (at least three sets)
• ECG: nonspecific;
• Acute AR: possible signs of the underlying cause (e.g., signs of myocardial ischemia in aortic
dissection)
• Chronic AR
• ECG signs of LVH
• ST-segment depression and T-wave inversion in I, aVL, V5, and V6

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• Chest x-ray: used to assess
for pulmonary edema and rule out other
causes of acute dyspnea
• Acute AR
• Normal heart silhouette
• X-ray signs of pulmonary
congestion or edema
• Chronic AR
• X-ray signs of LVH
• Enlarged cardiac silhouette
• Chronic AR or acute AR caused by aortic

dissection: possible prominent aortic
root/arch
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Additional evaluation
Advanced imaging
• Cardiac MRI
• CTA chest
 Cardiac catheterization
• Coronary angiography
 Exercise stress testing

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Treatment
Approach
• Acute aortic regurgitation
• Severe acute AR requires surgical treatment as soon as possible.
• Consult cardiology and cardiothoracic surgery immediately.
• Medical management of complications (e.g., pulmonary edema) should not delay definitive
treatment.
• Identify and treat the underlying cause
• Chronic aortic regurgitation
• Surgery is the mainstay of treatment for symptomatic AR and severe asymptomatic AR.
• Optimize medical management of comorbidities (e.g., heart failure treatment), especially
if surgery is contraindicated.

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 All patients should be screened and treated for other cardiac risk factors. No medical treatments
are known to influence the progression of the disease
• Acute AR: stabilize patients and manage complications (e.g., cardiogenic shock, pulmonary
edema)
• Hypertension
• Initiate treatment if systolic blood pressure is > 140 mm Hg and follow standard hypertension guidelines.
• Vasodilators (e.g., ACE inhibitors, ARBs) may be preferable to beta blockers.
• Heart failure: Manage according to guideline recommendations
• Prophylactic antibiotics
• At-risk patients, e.g., with prosthetic valves or a history of infective endocarditis:
• Rheumatic heart disease: long-term secondary prophylaxis

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Mitral valve stenosis
 Mitral stenosis (MS) is a structural anomaly of the mitral

valve resulting in a decreased cross-sectional area of the
valve.
 The stenosis impairs blood flow from the left atrium to
the left ventricle, progressively causing left atrial
distension, pulmonary venous congestion, pulmonary
hypertension, and congestive heart failure

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Etiology
• Most commonly due to rheumatic fever

• Calcification of the mitral valve annulus
• Autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis
• Congenital
• Some conditions may mimic mitral stenosis: bacterial endocarditis of the mitral valve with
large vegetation, left atrial myxoma
• Degenerative aortic stenosis
• Radiation-associated valve disease, including MS

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Classification
American College of Cardiology/American Heart Association stages of mitral stenosis [1]

Mitral
Valve anatomy
Stage Definition Symptoms valve area Associated findings
(If + RA)
(cm2)
A •At risk for MS •Normal •None
•Rheumatic valve •Mild to moderate left atrial

B •Progressive MS changes with •> 1.5 enlargement
commissural fusion •Normal PASP
•None
and diastolic doming
of the mitral valve
leaflets •Severe left atrial
C •Asymptomatic severe MS •≤ 1.5 enlargement
•PASP > 50 mm Hg
•Severe left atrial

•Exertional dyspnea
D •Symptomatic severe MS •≤ 1.5 enlargement
•Decreased exercise tolerance
•PASP > 50 mm Hg

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Pathophysiology
• Mitral valve stenosis → obstruction of blood flow into the left

ventricle (LV) → limited diastolic filling of the LV (↓ end-
diastolic LV volume) → decreased stroke volume
→ decreased cardiac output (forward heart failure)
• Mitral valve stenosis → increase in left atrial pressure
→ backup of blood into lungs → increased
pulmonary capillary pressure → cardiogenic
pulmonary edema → pulmonary hypertension → backward h
eart failure and right ventricular hypertrophy

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Clinical features
Symptoms
 Patients with MS typically progress over many years from being asymptomatic to having symptoms of
profound heart failure.
 Acute symptoms may occur in patients with tachyarrhythmias or an increased cardiac output secondary
to pregnancy, sepsis, or exercise.
• Dyspnea
• Fatigue
• Hoarseness
• Dysphagia
• Palpitations

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• Symptoms of embolic disease (e.g., stroke, mesenteric ischemia)
• Later stages
• Symptoms of right heart failure
• Paroxysmal nocturnal dyspnea
• Orthopnea
• Hemoptysis
• Hoarseness
 Hemoptysis — The increased pulmonary pressures and vascular congestion can lead to hemoptysis,
which may have a variety of clinical manifestations:
 Sudden hemorrhage (pulmonary apoplexy)
 Blood-tinged sputum
 Pink frothy sputum

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Examination findings
• ↓ pulse volume
• Mitral facies or Malar flash
• Sequelae of embolic disease (e.g., focal neurologic deficits, cool and cyanotic extremity)
• Irregular heart rhythm secondary to atrial fibrillation
• Tapping apex beat – palpable S1
• Diastolic thrill at apex
• Left parasternal heave due to RVH
• Clinical features of right heart failure, e.g., ↑JVP, lower limb pitting edema , bibasilar rales

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• Auscultation
• Diastolic murmur heard best at the 5th left intercostal space at the midclavicular line (the
apex)
• Loud first heart sound (S1)
• Opening snap
• A high frequency, early to middiastolic sound, heard after S2
• Occurs when mitral leaflet motion suddenly stops during diastole because the stenosed valve has reached
• A shorter interval its maximum
between opening snap indicates
S and opening
2
more severe disease; occurs because left atrial pressure is
greater than left ventricular end-diastolic pressure (LVEDP).
• Early diastolic murmur due pulm regur from pulm HTN
(Graham steell murmur) may be rarely heard

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Diagnostics
 Approach
• All patients with suspected mitral stenosis should undergo transthoracic
echocardiography (TTE).
• TTE is the best initial test to evaluate the mitral valve and quantify the anatomical extent of the
stenosis.
• Discordance between the patient's symptoms and the echocardiographic classification of the
disease should prompt further testing.
• Chest x-ray and ECG may show characteristic changes depending on the stage and extent
of disease.
• Laboratory studies are typically nonspecific, although they may support a diagnosis of
associated heart failure.

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ECG
• Often normal
• Characteristic findings include:
• Left atrial enlargement/P mitrale
• Right ventricular hypertrophy (e.g., right axis deviation,
dominant R wave in lead V1)

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Chest x-ray (PA and lateral views)
• Left atrial enlargement
• The main bronchi appear elevated and have >
90% angulation (splayed).
• Straightening or convexity of the left cardiac border
• Double density sign -large LA
• X-ray features of pulmonary congestion
• X-ray features of right ventricular enlargement

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Laboratory tests
• BNP or NT-proBNP: Levels increase in proportion to disease severity.
• CBC: Leukocytosis may indicate an underlying infectious (e.g., infective endocarditis) or
inflammatory process.
• BMP: may demonstrate evidence of renal impairment
• Liver chemistries: may show elevations secondary to congestive hepatopathy
• CRP: suggests ongoing inflammation in rheumatic heart disease

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Treatment
Approach
 The following recommendations are for rheumatic MS. For all other causes of MS, early
consultation with cardiology is recommended as treatment can vary significantly.
• Initial management
• General cardiac care and serial TTEs until signs or symptoms of disease progression occur
• In case of acute heart failure: immediate medical stabilizations and treatment of the precipitating
cause

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Optimizing medical therapy .
• Screen for and treat all cardiac risk factors, e.g., diabetes, hyperlipidemia,
and hypertension.
• Consider heart rate control (e.g., beta blockers) in younger patients in sinus rhythm with
high resting or exercise-induced heart rates.
• Decreasing the heart rate in patients with symptoms of mild to moderate CHF may improve
cardiac symptoms.
• Beta blockers, e.g., metoprolol
• Ivabradine
• Treat atrial fibrillation with rate control.

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Interventional management
 Patients with severe or symptomatic MS should be considered for intervention.
 Indications
• Asymptomatic patients with MVA ≤ 1.5 cm2 and either of the following:
• Pulmonary artery systolic pressure > 50 mm Hg
• New-onset atrial fibrillation
• Symptomatic patients with:
• MVA ≤ 1.5 cm2
• MVA > 1.5 cm2 and hemodynamically significant MS on stress test

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Procedures
• Percutaneous mitral valve balloon commissurotomy (PMBC)
• Surgery
• Surgical interventions include open commissurotomy and mitral valve (mechanical or
bioprosthetic) replacement.
• Indications
• Unfavorable anatomy for PMBC + NYHA class III/IV
• In NYHA I/II pts for MVA ≤1.5 cm2 AND pulm HTN
• Presence of thrombus in the left atrium
• Mixed valvular disease (e.g., severe MR, tricuspid disease)
• Contraindicated if there is a prohibitively high surgical risk

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Summary of RF
Pathology
 Typically occurs several weeks after a streptococcal pharyngitis. Usually group A beta haemolytic
streptococci: Streptococcus pyogenes serotype M. Antigenic mimicry is implicated—antibodies to
carbohydrate in cell wall (anti-M antibodies) of group A Streptococcus cross-react with
protein in cardiac valves
 Delay from acute infection to onset of rheumatic fever (RF) is usually 3–4 weeks
 Commonly causes a pancarditis. Pericarditis can cause haemodynamic instability or constriction.
Myocarditis may cause acute heart failure and arrhythmias. Endocarditis affects the mitral valve
(65–70%), aortic valve (25%), and tricuspid valve (10%, never in isolation) causing acute
regurgitation and heart failure, and eventually chronic stenosis.

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•Prophylactic antibiotics
• Rheumatic heart disease: should receive secondary
prophylaxis, e.g., penicillin
G benzathine or sulfadiazine
• Dental procedures: consider prophylaxis for infective
endocarditis for at-risk patients (e.g., after aortic valve
replacement)

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Mitral regurgitation
(Mitral valve regurgitation)
 Mitral regurgitation (MR) is the leakage of blood from the left ventricle into the left
atrium due to incomplete closure of the mitral valve during systole.
 It is a common form of valvular disease and categorized according to onset (into acute and
chronic forms) and etiology.
 Primary MR involves the structure of the mitral valve whereas secondary MR is a result of
different pathologies that lead to valvular incompetence (e.g., cardiomyopathy).
 Ischemic MR can be acute (e.g., papillary muscle rupture in myocardial infarction) or
chronic (in coronary artery disease).

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Etiology
• Primary MR (organic): mitral regurgitation caused by direct involvement of the valve leaflets or chordae
tendinae
• Degenerative mitral valve disease (mitral valve prolapse, mitral annular calcification, ruptured chordae tendinae)
• Rheumatic fever
• Infective endocarditis
• Ischemic MR (e.g., papillary muscle rupture following acute MI)
• Trauma → ruptured chordae and acute MR
• Secondary MR (functional): caused by changes of the left ventricle that lead to valvular incompetence
• Coronary artery disease or prior myocardial infarction causing papillary muscle involvement
• Dilated cardiomyopathy (e.g., peripartum cardiomyopathy) and left-sided heart failure
• Hypertrophic cardiomyopathy
• Atrial functional MR

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• Acute MR: Acute dysfunction of the mitral valve leads to volume overload and symptoms
of acute heart failure.
• There is no compensatory LV enlargement, forward EF is reduced, leading to low CO
• Chronic MR
• To preserve cardiac output, valve dysfunction is initially compensated for by cardiac remodeling,
meaning the LV dilates, and large stroke volume compensates for regurgitation, maintaining the
forward EF.
• Over time, remodeling affects LVEF, leading to heart failure

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Pathophysiology
• Acute MR: ↑ LV end-diastolic volume → rapid ↑ LA and pulmonary pressure →

pulmonary venous congestion → pulmonary edema
• Chronic (compensated) MR: progressive dilation of the LV (via eccentric
hypertrophy) → ↑ volume capacity of the LV (preload and afterload return to normal
values) → ↑ end-diastolic volume → maintains ↑ stroke volume (normal EF)
• Chronic (decompensated) MR: progressive LV
enlargement and myocardial dysfunction → ↓ stroke volume → ↑ end-systolic and end-
diastolic volume → ↑ LV and LA pressure → pulmonary congestion, possible
acute pulmonary edema, pulmonary hypertension, and right heart strain

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Clinical features
Acute mitral regurgitation

• Dyspnea
• Symptoms of left-sided heart failure
• Signs and symptoms of pulmonary edema (e.g., bibasilar, fine, late inspiratory crackles)
• Cardiogenic shock: poor peripheral perfusion, tachycardia, tachypnea, and hypotension
• Palpitations
• Auscultation
• Soft, decrescendo murmur
• No murmur in severe regurgitation with LV systolic dysfunction or hypotension
• Potentially: S3 heart sound

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Chronic mitral regurgitation
• Dyspnea (including exertional dyspnea), dry cough
• Fatigue (due to ↓ forward CO)
• Palpitations
• Symptoms of left-sided heart failure (potentially also symptoms of right-sided heart failure)

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Auscultation
• Lateral displacement of the apical impulse
• Quiet S1 heart sound
• S3 heart sound in advanced stages of disease (a mid diastolic murmur may follow S3 even
in the absence of MS)
• Holosystolic murmur (high-pitched, blowing)
• Radiates to the left axilla and heard best over the apex (5th intercostal space at the
left midclavicular line)
• Intensity can be increased by increasing preload (e.g., leg raise) or afterload (e.g., handgrip) due
to increased regurgitation.

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AHA staging for mitral valve regurgitation
Stage Extent of mitral regurgitation
A •At risk of MR (minimal regurgitation)
B •Progressive MR (moderate regurgitation)
C1 •Asymptomatic severe MR (LVEF > 60%)
C2 •Asymptomatic severe MR (LVEF ≤ 60%)
D •Severe symptomatic MR
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 Carpentier classification: according to mechanism
 Type I—normal leaflet motion, e.g. dilated annulus from dilated
cardiomyopathy, leaflet perforation due to endocarditis
 Type II—leaflet prolapse, e.g. myxomatous degeneration
 Type IIIa—restricted leaflet opening, e.g. rheumatic disease
 Type IIIb—restricted leaflet closing, e.g. ischaemic dilated cardiomyopathy
(functional).
• Uses echocardiography findings to classify leaflet motion (Carpentier types I–III).
• Used in the planning of surgical repair

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Diagnostics
Echocardiography
 Indications: to assess the valve apparatus, size and function of left ventricle and atrium, and grade the severity of MR
ECG
• Acute MR: Findings are often nonspecific.
• Normal sinus rhythm
• Sinus tachycardia with nonspecific ST and T-wave abnormalities
• Signs of acute ischemia in ischemic MR
• Chronic MR: ECG changes usually reflect cardiac remodeling.
• Left ventricular hypertrophy (50% of patients) [6]
• P mitrale
• Signs of right heart strain with P pulmonale in later stages

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Chest x-ray
 Indications: assess for pulmonary edema, rule out other causes of acute dyspnea
• Supportive findings: Decompensated MR and acute MR: signs of pulmonary congestion
• Acute MR: normal-sized cardiac silhouette
• Chronic MR: Changes related to cardiac remodeling and associated heart failure may be
visible.
• LV enlargement: laterally displaced left cardiac border
• LA enlargement: straightening of the left cardiac border and double density sign
• Annular calcification may be visible as a C-shaped densit

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Treatment
Acute mitral regurgitation

 General principles.
• All patients with acute primary MR should undergo urgent surgical repair or valve replacement.
• While awaiting surgery, any symptoms of heart failure should be managed with medical therapy
(e.g., diuretics, nitrates, antihypertensive drugs).
• If secondary MR is suspected, identify and treat the underlying cause (e.g., revascularization
therapy for ischemic MR)

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Chronic mitral regurgitation
 Medical management
• Identify and treat any underlying cause (particularly in secondary MR).
• Heart failure management:
• Diuretics (e.g., furosemide )
• ACE inhibitors (e.g., lisinopril )
• Beta blockers (e.g., metoprolol tartrate )

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 Surgical management and transcatheter mitral repair
• Chronic primary MR
• Indications
• Asymptomatic patients with LV dysfunction (LVEF 30–60% or LV end-systolic diameter ≥ 40 mm) (stage C2)
• Symptomatic patients with LVEF 30–60 % (stage D)
• Contraindications: Once LVEF is < 30%, surgery is generally not recommended because of the
high mortality rate and low likelihood of symptom improvement.
• Procedure
• Valve repair is preferred to replacement because it is associated with reduced mortality and fewer
complications.
• Transcatheter mitral valve procedures, such as a clip device, can be considered in patients who are considered
to be unsuitable for surgical repair and severely symptomatic.

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• Chronic secondary MR
• Indications: consider for patients with severe MR and persistent symptomatic heart
failure (NYHA classes III–IV) despite optimal medical management [9]
• Procedure:
• Transcatheter mitral valve procedures: consider on an individual basis in specialized centers
• LVAD and cardiac transplant: consider for patients whose heart failure is driven by severe LV remodeling

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Mitral valve prolapse
 Mitral valve prolapse (MVP) is caused by a structural defect of the mitral valve that results
in mitral leaflets bulging into the left atrium during systole. In developed countries,
 MVP is the most common heart valve abnormality and the most common cause of mitral
regurgitation (MR)

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Etiology
• Mostly idiopathic
• Connective tissue disorders: Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis
imperfecta
• Fragile X syndrome
• Myocardial infarction: infarction of papillary muscles → rupture of chordae
tendineae → mitral valve prolapse
• Acute rheumatic heart disease
• Infective endocarditis
• Autosomal dominant polycystic kidney disease

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Pathophysiology
• The most common underlying pathology in the case of mitral valve prolapse
is myxomatous degeneration (deposition of glycosaminoglycan such as dermatan
sulfate) of the mitral valve due to a primary disease or connective tissue disorder
• Long, floppy mitral valve leaflets with excessive valvular tissue → the mitral annulus becomes
dilated and the chordae tendineae become elongated (and may rupture) → prolapse of one or
both mitral valve leaflets into the left atrium during systole
• The leaflets may also exhibit fibrous thickening at regions where they rub against each other.
• Mitral valve prolapse sets into motion a vicious cycle of events.
• If prolapse happens without the rupture of chordae tendineae → mitral valve leaflets billow into
the left atrium → mild to moderate mitral regurgitation
• If the papillary muscles become severely ischemic and the chordae tendineae rupture → mitral
valve leaflets flail about in the left atrium → severe mitral regurgitation

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Clinical features
• Most patients are asymptomatic.

• Rarely: atypical chest pain and anxiety
• In case of complications: fatigue, dyspnea, cough, syncope, and palpitations (see
“Complications” below)
• Auscultatory findings
• Mitral valve prolapse click: high-frequency, midsystolic click that is best heard at the mitral
region
• High-frequency, mid-to-late systolic murmur that is best heard at the mitral region and may
radiate to the axilla (squatting diminishes the murmur)
• Patients with severe MR: S3 may be heard as a result of left ventricular overload (especially in the
left decubitus position)

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Diagnostics
• ECG: mostly normal

• Transthoracic echocardiography (test of choice) to confirm diagnosis
• Echocardiographic definition of MVP: displacement of the mitral valve during systole by more
than 2 mm above the mitral valve annulus in the parasternal long-axis view
• Classical MVP (∼ 60%): leaflet thickness ≥ 5 mm
• Non-classical MVP (∼ 40%): leaflet thickness < 5 mm
• Transesophageal echocardiography (TEE) is used as an adjunct to TTE and

intraoperatively to guide mitral valve repair procedures.

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Treatment
• No treatment is required in most cases.

• Patients with severe mitral regurgitation : mitral valve repair or replacement
• Additional treatment is required when complications arise (see “Complications” below)

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Auscultation in valvular defects
Maximum point Murmur Characteristics
•Aortic •Radiation to the carotids
valve (parasternal 2nd right intercostal •Harsh crescendo-decrescendo systolic
Aortic stenosis •Soft S2
space) ejection murmur
•Erb point •Possibly ejection click
•Immediately following the 2ndheart sound

•Aortic valve (parasternal 2nd right ICS) •Diastolic murmur with a decrescendo
Aortic regurgitation (“immediate diastolic murmur”)
•Erb point •Possible additional quiet systolic murmur
•Austin Flint Murmur
•Delayed diastolic murmur with •“Tympanic” 1stheart sound

Mitral stenosis •Heart apex (midclavicular 5th left ICS)
a decrescendo •Mitral opening murmur/opening snap (OS)
•Midsystolic high-frequency click (due to

Mitral valve prolapse •Heart apex (midclavicular 5th left ICS) •Late-systolic crescendo the tensing of the chordae tendinae)
•Loudest before S2
•Holosystolic murmur
•Heart apex (midclavicular 5th left ICS) •Blowing
Mitral regurgitation •3rdheart sound audible
•Left axilla •Radiation into the axilla
•Quiet 1stheart sound
•Possible radiation into the back

•Crescendo-
Pulmonary stenosis •Pulmonary valve (parasternal 2 left ICS)
nd
•Possible early systolic pulmonary ejection
decrescendo ejection systolic murmur
click and/or widely split 2ndheart sound
•Graham Steell murmur: high-

Pulmonary regurgitation •Pulmonary valve (parasternal 2nd left ICS) •Diastolic murmur with a decrescendo
frequency decrescendo diastolic murmur
•Delayed diastolic murmur with a
Tricuspid stenosis (extremely rare) •Tricuspid valve (parasternal 4 left ICS)
th
decrescendo
•Possible pre-systolic crescendo
•Augmentation of the murmur's intensity
Tricuspid regurgitation •Tricuspid valve (parasternal 4th left ICS) •Holosystolic murmur
with inspiration (Carvallo sign)
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Valvular heart diseases
REFERENCES
 UPTODATE 2023
 AHA/ACA 2023
 OXFORD HAND BOOK OF CARDIOLOGY 2nd EDITION
 Harrison’s principle of internal medicine 21 st edition

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Valvular Heart Diseases

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Valvular Heart Diseases

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Valvular heart diseases

(Valvular heart defects)

DR DAVID ELIA SARIA

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 Aortic valve stenosis (AS) is a valvular heart disease characterized by narrowing of

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• Aortic valve sclerosis: calcification and fibrosis of aortic valve leaflets

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Stage A aortic valve

Mild: 1.5–2.9 cm2 2.0– 2.9 m/second 10–19 mm Hg None

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 Low-dose dobutamine stress testing

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• On-demand imaging is indicated for patients with:

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• Vascular complications, thromboembolism/stroke

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Antithrombotic therapy for patients with prosthetic aortic valves [8][14]

Choice of agent Target INR Duration of therapy

Mechanical valve and no risk

•Antiplatelet agents: lifelong

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 Aortic regurgitation can be acute (primarily caused by bacterial endocarditis or aortic

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Acute aortic regurgitation

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• Chronic AR or acute AR caused by aortic

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 Mitral stenosis (MS) is a structural anomaly of the mitral

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• Most commonly due to rheumatic fever

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American College of Cardiology/American Heart Association stages of mitral stenosis [1]

•Rheumatic valve •Mild to moderate left atrial

•Severe left atrial

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• Mitral valve stenosis → obstruction of blood flow into the left

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