Valvular

Heart Disease

Dr.Ashagre E.

Lecture for HO 12/17/24

Overview of Valves

12/17/24Lecture for HO
Normal Valve Function
 Maintain forward
flow and prevent
reversal of flow

 Valves open and

close in response to
pressure differences
(gradients) between
cardiac chambers.

12/17/24
Lecture for HO
Abnormal Valve Function
 Valve Stenosis
 Obstruction to valve flow during that phase of the
cardiac cycle when the valve is normally open.
 Hemodynamic hallmark -“pressure gradient” ~ flow// VA
 Valve Regurgitation, Insufficiency, Incompetence
 Inadequate valve closure--- back leakage
 A single valve can be both stenotic and
regurgitant; but both lesions cannot be severe!!
 Combinations of valve lesions can coexist
 Single disease process
 Different disease processes
 One valve lesion may cause another

Lecture for HO 12/17/24

Major Factors That Affect Flow
Across Any Valvular Lesion
 Valve area
 Square root of hydrostatic pressure
gradient across the valve
 Time duration of transvalvular flow (applies
to both systole and diastole)

Lecture for HO 12/17/24

Valvular Heart Disease
 Increasing any of the major factors that affect
flow across the valve increases transvalvular
flow.

 Conversely, decreasing any of these major

factors decreases transvalvular flow.

Lecture for HO 12/17/24

Adult Valvular Heart Disease
 Mitral Valve
 Aortic Valve
 Tricuspid valve
 Pulmonic valve

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12/17/24
 Major Causes of VHD
Valve Lesion Etiologies
Mitral Rheumatic fever Severe mitral annular calcification
Congenital SLE, RA
stenosis
Acute Chronic
Mitral •Endocarditis •Rheumatic fever
regurgitation •Papillary muscle rupture (post-MI) •Myxomatous (MVP)
•Trauma •Endocarditis (healed)
•Chordal rupture/leaflet flail (MVP, IE) •Mitral annular calcification
•Congenital (cleft, AV canal)
•HOCM with SAM Ischemic (LV
remodeling)
•Dilated cardiomyopathy Radiation
Rheumatic fever Degenerative calcific
Aortic Congenital (bicuspid, unicuspid) Radiation
stenosis
Valvular Root disease
Aortic •Rheumatic fever •Aortic dissection
regurgitation •Congenital (bicuspid) Endocarditis •Cystic medial degeneration
•Myxomatous (prolapse) Traumatic • Marfan's syndrome
•Syphilis • Bicuspid aortic valve
•Ankylosing spondylitis • Nonsyndromic familial
aneurysm
•Aortitis
•Hypertension

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Lecture for HO
Major Causes of VHD
Valve Lesion Etiologies
Rheumatic
Tricuspid Congenital
stenosis
Primary Secondary
Tricuspid •Rheumatic •RV and tricuspid annular dilatation
regurgitation •Endocarditis •Multiple causes of RV enlargement
•Myxomatous (TVP) (e.g., long-standing pulmonary HTN)
•Carcinoid •Chronic RV apical pacing
•Radiation
•Congenital (Ebstein's)
•Trauma
•Papillary muscle injury (post-MI)
Congenital
Pulmonic Carcinoid
stenosis
Valve disease Annular enlargement
Pulmonic •Congenital •Pulmonary hypertension
regurgitation •Postvalvotomy •Idiopathic dilation
•Endocarditis •Marfan's syndrome

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Lecture for HO
Acute Rheumatic Fever
 Multisystem disease
 Autoimmune reaction to infection with
group A streptococcus.
 Many parts of the body may be affected
 almost all manifestations resolve completely
 Exception:
cardiac valvular damage
[rheumatic heart disease (RHD)]
 May persist after other features have disappeared.

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12/17/24
Lecture for HO 12/17/24
Lecture for HO 12/17/24
 Acute Rheumatic Fever
 Treatment: heart failure and other symptoms
 Prevention:
 Primary:
 elimination of major risk factors for streptococcal infection,
particularly overcrowded housing.
 difficult to achieve in most places where ARF is common
 1ry prophylaxis (i.e., timely & complete treatment of group
A strept sore throat with antibiotics)
 mainstay of 1ry prevention for ARF
 Secondary:
 Mainstay of controlling ARF and RHD
 long-term penicillin prophylaxis to prevent recurrences

Lecture for HO 12/17/24

Mitral Valve

Lecture for HO
12/17/24
 Mitral Valve Competence:
 Integrated function of
several anatomic
elements
 Posterior LA wall
 Anterior & Posterior
valve leaflets
 Chordae tendineae
 Papillary muscles
 LV wall where the
papillary muscles attach

Lecture for HO 12/17/24

Normal MVA = 4 – 6 cm2

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Mitral Stenosis

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Mitral Stenosis
Etiology

• Rheumatic (nearly all adult MS- 99.9%!!! )

Women >> Men

• Degenerative (calcification)

• Congenital (parachute MV)

• Others: post-inflammatory, metabolic syndromes etc.,,

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Pathophysiology of Mitral
Stenosis
Obstruction to LA emptying

Decreased LV filling Increased Increased

LA pressure LA size

Pulmonary Increased pulmonary Atrial fibrillation

edema venous pressure

Increased pulmonary
artery pressure

RV overload

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 Mitral Stenosis
linical Presentations

• Asymptomatic

• Dyspnea, PND, Orthopnea

• Hemoptysis

• Atrial fibrillation

• Systemic embolization

12/17/24 Lecture for HO

 Mitral Stenosis
Diagnosis

• Clinical
- Loud S1 and P2 (pulmonary hypertension)
- mid diastolic rumble
- OS indicating pliable leaflets
- short OS-S2 interval indicates severe MS
- other auscultatory signs as per co-existing disease

• ECG
- P mitrale: broad, notched P wave in II and biphasic in V1
- RVH and rightward axis if significant PHT
12/17/24 Lecture for HO
 Mitral Stenosis
Diagnosis
•CXR
- LAA and LA enlargement
- increased upper lobe vascularity
- Kerley B and A lines
- dilated PA
- MV calcification

•Echocardiogram
•Cardiac catheterization
12/17/24 Lecture for HO
COMPLICATIONS OF MS
 Atrial fibrillation
 Systemic embolization
 Pulmonary hypertension
 Tricuspid regurgitation
 Pulmonary infarction
 Chest infections
 Infective endocarditis (rare)

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12/17/24
 Mitral Stenosis
Management Principles
• Asymptomatic
- no specific therapy
- endocarditis prophylaxis
- if appropriate, rheumatic fever prophylaxis

• Mild and Mod MS ( MVA > 1.5 sq cm and 1.0 to 1.4 sq cm)
- Normal physical activity
- No specific therapy, restoration of NSR in case of AFib
- restoration of NSR and anticoagulation in case of Afib

12/17/24 Lecture for HO

Mitral Regurgitation
(Insufficiency)

Lecture for HO 12/17/24

Mitral Regurgitation
(Insufficiency)
 Valve leaflets

 Chordae tendineae

 Papillary muscles

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 Mitral Regurgitation:
Etiology
 Chronic Mitral
 Acute Mitral
Regurgitation
Regurgitation
 Rheumatic (50%)
 Infective
 Ischemic Heart disease
endocarditis
 Ischemic Heart  Papillary ms dysfunction
disease  Inferior & posterior MI
 Papillary ms  Mitral Valve prolapse
rupture  Infective endocarditis
 Mitral valve prolapse
 Prosthetic
 Chordal rupture
 Mitral annular calcification
 Chest trauma
 Cardiomyopathy
 LV dilatation
 IHSS
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Pathophysiology of Mitral
Regurgitation
Backward flow of blood from LV to LA (Systolic)

Left atrial enlargement

Increased
LA volume and
pressure
Increased
pulmonary
Increased LV filling venous pressures
(Increased LVEDV)

Pulmonary
edema
Increased SV

Blood ejected into aorta

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Pathophysiology –Acute vs
Chronic Mitral Regurgitation
 Acute MR Chronic MR
 Normal • Dilated, compliant LA
(noncompliant) LA • LA pressure normal or
 Increase LA pressure slightly increased
 Acute Pulmonary • Fatigue, low output state
Edema • Atrial arrhythmias- a. fib.

Most patients fall between

these two extremes!!

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SYMPTOMS
 Asxic for many years
 Palpitation: increased stroke volume
 LV failure: dyspnoea and orthopnoea
 Reduced COP: fatigue and lethargy
 Late stages: symptoms of right heart failure and
eventually CHF
 Cardiac cachexia may develop.
 Thromboembolism: less common than in mitral
stenosis
 Subacute infective endocarditis is much
more common than in MS

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INVESTIGATIONS

 Chest X-ray: LA and LV enlargement, increase in

CTR

 ECG: bifid P waves, and LVH +/- atrial fibrillation

 Echocardiogram: dilated left atrium and left

ventricle.

 Cardiac catheterization

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Mitral Regurgitation:
Treatment
 Medical Rx (vasodilators, diuretics,
anticoagulation)
 Mild to mod MR
 Prophylaxis against endocarditis
 Surgical Rx –ideally before LV systolic function
declines.
 MV replacement
 MV ring & CABG
 MR repair
 MVP, ruptured chords, infective endocarditis,
papillary muscle rupture.

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 Aortic Valve

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Aortic Stenosis

Etiology
1. Tricuspid Aortic Valve
Degeneration
2. Bicuspid Aortic Valve
3. Congenital Aortic Stenosis
4. Rheumatic Fever
 Almost always in
combination with mitral
valve abnormality
5. Other Causes

12/17/24
Lecture for HO
 Aortic Stenosis

 A – Normal Valve
 B – Congenital AS
 C – Rheumatic AS
 D – Bicuspid AS
 E – Senile AS

12/17/24 Lecture for HO

Degree of Aortic Stenosis
 Normal AVA = 2.6 – 3.5 cm2
 Mild AS
 1.5 – 2.0 cm2
 Moderate AS
 1.0 – 1.4 cm2
 Critical AS
 Peak systolic pressure gradient > 50 mmHg
 AVA < 0.9 cm2

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Pathophysiology of Aortic
Stenosis
Aortic Stenosis

Obstruction to LV Ejection

Pressure Gradient Created Across the Valve

Chronic LV Pressure Overload

LV Hypertrophy
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Natural History of AS
 May be a long asymptomatic period
 Symptomatic
 Usually have severe AS with AVA of 0.9 cm2 or
less
 Presenting symptoms:
 Angina
 Syncope
 CHF
 Average life span of sxic patients without surgery:
 Angina = 5 years
 Syncope = 3 years
 CHF = 2 years

Lecture for HO 12/17/24

Physical Exam
 Carotid upstroke evaluation
 “Pulsus parvus et tardus” (small volume & slow-rising or
plateau in nature: delay in reaching its peak)
 Apical impulse evaluation
 usually not displaced, laterally displaced in AS with severe CHF,
 abnormally forceful & sustained in nature
 A double impulse sometimes felt because S4 or atrial contraction ('kick')
may be palpable.
 A systolic thrill may be felt in the aortic area .
 Auscultation of murmurs/heart sounds
 Systolic Ejection Murmur: RUSB radiating to carotids
 Paradoxic Splitting of S2, Absent/Soft A2, S4, S3, ejection click with bicuspid
valve
 Heart failure signs

Lecture for HO 12/17/24

Diagnostics
 EKG: LV 'strain' pattern due to 'pressure overload' (depressed
ST segments and T wave inversion in leads I, AVL, V5, V6).
 CXR: a relatively small heart with a prominent, dilated,
ascending aorta ('post-stenotic dilatation‘), +/- calcified aortic
valve, increased CTR in heart failure
 ECHO
 Cardiac Catheterization

Lecture for HO 12/17/24

Treatment
 The only effective treatment is relief of the mechanical
obstruction via…
 Surgical AVR
 Aortic Valve Debridement (AI)
 Pharmacologic Therapy
 Aortic Balloon Valvuloplasty

 Symptoms are a good index of severity

 All sxic patients should have AV replacement
 Asymptomatic: regular review for assessment of sxs and echo.
 Antibiotic prophylaxis against infective endocarditis is essential.

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Aortic Regurgitation

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 Aortic Insufficiency: Etiology
 Chronic Aortic Insufficiency
 Acute Aortic  Aortic leaflet disease
Insufficiency  Infective endocarditis
 Infective  Rheumatic
endocarditis  Bicuspid Aortic valve
 Prolapse & congenital VSD
 Acute Aortic  Prosthetic
Dissection  Aortic root disease
 Marfan’s  Aortic aneurysm/dissection
 Marfan’s syndrome
Syndrome  Connective tissue disorders
 Chest  Syphilis
trauma  HTN
 Annulo-aortic ectasia

Lecture for HO 12/17/24

 Pathophysiology of Aortic
Regurgitation
Backward flow of blood from aorta into LV (Diastolic)

Rapid fall of aortic Increased

pressure during diastole LV volume
and pressure
Increased
LA pressure
Increased SV
(Frank-Starling Mechanism)
Increased
pulmonary
Peak systolic pressure venous pressure
increased because of
increased SV ejected into aorta
Pulmonary
edema

Increased diastolic
Increased pulse pressure wall-tension produces
eccentric hypertrophy
12/17/24 Lecture for HO
Pathophysiology
 10 abnormality – LV overloading
 Severity of LVVO
 Size of regurgitant orifice
 Diastolic pressure gradient between Ao & LV
 HR or duration of diastole
 Compensatory Mechanisms
 Increased diastolic wall-tension produces eccentric
hypertrophy (increase both in chamber size and wall
thickness)
 Increased LV diastolic compliance
 Peripheral vasodilation
 Reduced diastolic compliance (Acute AI)
 Very high diastolic compliance (Chronic AI)
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Pathophysiology
 Baseline myocardial oxygen demand higher than
normal because of increased LV mass
 Reduced coronary perfusion pressure
 Lower diastolic pressure
 Increased LVEDP
 Myocardial contractility is usually preserved until
late in course of the disease
 Late in disease there is progression to irreversible
contractile impairment

Lecture for HO 12/17/24

Acute vs Chronic AR
Pathophysiology and Clinical
Presentation
 Acute Aortic
Regurgitation
 Sudden AoV
incompetence
 Noncompliant LV
 Acute Pulmonary Edema
 Emergency AVR
 Chronic Aortic
Regurgitation
 Long asymptomatic phase
 Progressive LV dilatation
 DOE, orthopnea, PND
 Frequent PVC’s
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Natural History
 Long asymptomatic period during which the LV
undergoes progressive eccentric hypertrophy
 significant symptoms occur late and do not
develop until left ventricular failure occurs.
 Common symptom: 'pounding of the heart‘
[~MR]
 b/c of increased LV size and its vigorous pulsation.
 Angina pectoris is a frequent complaint.
 CHF: varying grades of dyspnoea depending on
extent of left ventricular dilatation and
dysfunction.
 Arrhythmias: relatively uncommon
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Chronic Aortic Regurgitation:
Physical Findings
 Pulse: bounding or collapsing.
 Widened Pulse Pressure > 70mmHg (170/60)
 Low diastolic pressure <60mmHg
 Hyperdynamic LV –
 DeMusset’s signs(head nodding with each
heartbeat)
 Corrigan’s pulse
 Quincke's sign (capillary pulsation in the nail
beds)
 Durozier’s murmur (a to-and-fro murmur heard
when the femoral artery is auscultated with
pressure applied distally-it is a sign of severe
aortic regurgitation)
 pistol shot femorals.

Lecture for HO 12/17/24

Chronic Aortic Regurgitation:
Physical Findings
 Apex beat: displaced laterally & downwards
and is forceful in quality.
 Auscultation:
 Diminished A
2
 Descrescendo early diastolic blowing
murmur @ LSB
 Austin-Flint murmur – mid-diastolic flow
rumble @ apex
 Due to interference with trans-mitral filling by
impignement from aortic regurgitant jet on the
ant MV cusp.
 DDx – mitral stenosis

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INVESTIGATIONS

 Chest X-ray: LV enlargement and possibly

dilatation of the ascending aorta.
 ECG: LVH
 Echocardiogram: vigorous cardiac contraction and
a dilated left ventricle. The aortic root may also be
enlarged.
 Cardiac catheterization

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TREATMENT

 Underlying cause
 Aortic valve replacement: before significant
symptoms
 Antibiotic prophylaxis against infective
endocarditis

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Thank you!

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