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    Valvular Heart Disease

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    fallenczar
    This document provides an overview of valvular heart disease, focusing on mitral valve disease and aortic valve disease. Some key points: - Mitral stenosis is usually caused by rheumatic fever and results in obstruction of blood flow from the left atrium to the left ventricle during diastole. This leads to increased left atrial pressure and pulmonary hypertension. - Chronic mitral regurgitation results in left ventricular volume overload over time, causing left ventricular dilation and eccentric hypertrophy. If left untreated, it can progress to heart failure. - Aortic stenosis is usually degenerative and causes left ventricular pressure overload, resulting in concentric left ventricular hypertrophy. It is often

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    Valvular Heart Disease

    Uploaded by

    fallenczar
    197 views32 pages
    This document provides an overview of valvular heart disease, focusing on mitral valve disease and aortic valve disease. Some key points: - Mitral stenosis is usually caused by rheumatic fever and results in obstruction of blood flow from the left atrium to the left ventricle during diastole. This leads to increased left atrial pressure and pulmonary hypertension. - Chronic mitral regurgitation results in left ventricular volume overload over time, causing left ventricular dilation and eccentric hypertrophy. If left untreated, it can progress to heart failure. - Aortic stenosis is usually degenerative and causes left ventricular pressure overload, resulting in concentric left ventricular hypertrophy. It is often

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    Valvular Heart Disease

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    This document provides an overview of valvular heart disease, focusing on mitral valve disease and aortic valve disease. Some key points: - Mitral stenosis is usually caused by rheumatic fever and results in obstruction of blood flow from the left atrium to the left ventricle during diastole. This leads to increased left atrial pressure and pulmonary hypertension. - Chronic mitral regurgitation results in left ventricular volume overload over time, causing left ventricular dilation and eccentric hypertrophy. If left untreated, it can progress to heart failure. - Aortic stenosis is usually degenerative and causes left ventricular pressure overload, resulting in concentric left ventricular hypertrophy. It is often

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    197 views32 pages

    Valvular Heart Disease

    Uploaded by

    fallenczar
    This document provides an overview of valvular heart disease, focusing on mitral valve disease and aortic valve disease. Some key points: - Mitral stenosis is usually caused by rheumatic fever and results in obstruction of blood flow from the left atrium to the left ventricle during diastole. This leads to increased left atrial pressure and pulmonary hypertension. - Chronic mitral regurgitation results in left ventricular volume overload over time, causing left ventricular dilation and eccentric hypertrophy. If left untreated, it can progress to heart failure. - Aortic stenosis is usually degenerative and causes left ventricular pressure overload, resulting in concentric left ventricular hypertrophy. It is often

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    Valvular Heart Disease

    Kenneth S. Korr M.D.


    Associate Professor of Medicine,
    Brown Medical School
    Director, Division of Cardiology
    The Miriam Hospital

    Normal Valve Function

    Maintain forward
    flow and prevent
    reversal of flow.
    Valves open and
    close in response to
    pressure differences
    (gradients) between
    cardiac chambers.

    Abnormal Valve Function

    Valve Stenosis

    Valve Regurgitation, Insufficiency, Incompetence

    Obstruction to valve flow during that phase of the cardiac


    cycle when the valve is normally open.
    Hemodynamic hallmark -pressure gradient ~ flow// VA
    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
    Certain combinations are particularly burdensome (AS & MR)

    Mitral Valve Competence:

    Integrated function
    of several anatomic
    elements

    Posterior LA wall
    Anterior & Posterior
    valve leaflets
    Chordae tendineae
    Papillary muscles
    Left ventricular wall
    where the papillary
    muscles attach

    Mitral Valve Disease:


    Etiology

    Mitral Stenosis

    Rheumatic - 99.9%!!!
    Congenital
    Prosthetic valve stenosis
    Mitral Annular
    Calcification
    Left Atrial Myxoma

    Chronic Mitral
    Regurgitation

    Acute Mitral Regurgitation

    Infective endocarditis
    Ischemic Heart disease

    Mitral valve prolapse

    Papillary ms rupture
    Chordal rupture

    Chest trauma

    Ischemic Heart disease

    Papillary ms dysfunction
    Inferior & posterior MI

    Mitral Valve prolapse


    Infective endocarditis
    Rheumatic
    Prosthetic
    Mitral annular calcification
    Cardiomyopathy

    LV dilatation
    IHSS

    Mitral RegurgitationPathophysiology

    MR: Leakage of blood


    into LA during systole
    10 Abnormality -Loss
    of forward SV into LA
    Compensatory
    Mechanisms

    Increase in SV (& EF)


    Forward SV +
    regurgitant volume
    LV (LA) dilatation
    Left Ventricular Volume
    Overload (LVVO)

    Chronic Mitral Regurgitation LVVO

    LVVO

    LV dilatation
    Eccentric hypertrophy

    Increased LA
    pressure
    Pulmonary HTN
    Dyspnea
    Atrial arrhythmias
    Low output state

    Pathophysiology Acute vs
    Chronic Mitral Regurgitation

    Acute MR

    Chronic MR

    Normal (noncompliant) LA
    Increase LA pressure
    large V waves
    Acute Pulmonary Edema
    Dilated, compliant LA
    LA pressure normal or
    slightly increased
    Fatigue, low output state
    Atrial arrhythmias- a. fib.

    Most patients fall between


    these two extremes!!

    Mitral Regurgitation:
    Physical Findings

    Auscultatory Findings

    S1 soft or normal
    P2 increased
    Holosystolic blowing murmur @ apex

    MVP mid-systolic click


    IHSS murmur increases with Valsalva
    Acute MR descrescendo systolic murmur

    S3 gallop & diastolic flow rumble

    Hyperdynamic Left Ventricle

    Brisk carotid upstrokes


    Hyperdynamic LV apical impulse
    LA lift; RV tap

    Mitral Stenosis
    -Pathophysiology

    Restriction of blood flow


    from LA LV during
    diastole.
    Normal MVA 4-6cm2.

    MV Pressure gradient
    MV grad ~ MV flow//MVA.

    Mild MS 2-4cm2.
    Severe MS < 1.0cm2.

    Flow = CO/DFP (diastolic


    filling period).

    As HR increases, diastole
    shortens disproportionately
    and MV gradient increases.

    Relationship between MV
    gradient and Flow for different
    Valve Areas

    Cross hatched area indicates


    range of normal resting flow.
    The vertical line represents
    the threshold for developing
    pulmonary edema.
    Pressure gradient increases
    as flow increases:

    to a small degree with


    normal valve area(4-6cm 2).
    to greater degrees with
    smaller valve areas.
    in severe stenosis, a
    significant gradient is
    present at rest.

    Mitral StenosisPathophysiology

    MV gradient Incr LA pr
    Pulmonary HTN

    RV Pressure Overload

    Passive
    Reactive- 2nd stenosis
    RVH
    RV failure
    Tricuspid regurgitation
    Systemic Congestion

    Paradoxes of MS

    Disease of Pulm Arts & RV


    LV unaffected (protected)
    As RV fails, pulmonary
    symptoms diminish

    Mitral Stenosis- Clinical Symptoms

    Symptoms related to
    severity of MVA reductionSymptoms unrelated to
    severity of MS Atrial fibrillation
    Systemic
    thromboembolism
    Symptoms due to Pulmonary
    HTN and RV failure Fatigue, low output state
    Peripheral edema and
    hepato-splenomegaly
    Hoarseness recurrent
    laryngeal nerve palsy

    Mitral Stenosis: Physical


    Findings

    Auscultatory findings

    S1 variable intensity; increased early, progressively


    decreases
    OS opening snap, variable intensity
    A2-OS interval varies inversely with severity of MS;
    shortens as MVA diminishes
    Low-pitched diastolic rumble @ apex

    Duration of murmur correlates with severity of MS


    Pre-systolic accentuation

    Increased P2

    Body habitus thin, asthenic, female


    Low BP
    LA lift & RV tap

    Mitral Valve Disease Echo


    findings

    Mitral Stenosis

    Thickened, deformed MV
    leaflets
    2D MVA
    Doppler Gradient
    Associated LAE, RVH,
    PHTN, TR,MR, LV function

    Mitral Regurgitation

    Determine etiology
    leaflets, chordae, MVP, MI
    Doppler severity of MR jet
    LV function

    Mitral Valve Disease :


    Treatment

    Mitral Stenosis

    Medical Rx for Class I & II

    HR control Dig & BB


    Anticoagulation

    Afib, >40yrs, LAE, MR,


    prior embolic event

    Surgical Rx -Class III &IV


    Balloon Mitral
    Valvuloplasty
    Commissural fusion
    pliable, noncalcified
    leaflets
    No MR of LA thrombus
    Mitral Valve Surgery
    Open commissurotomy
    MV replacement

    Chronic Mitral
    Regurgitation

    Medical Rx for mild to mod


    MR with vasodilators,
    diuretics, anticoagulation
    Surgical Rx ideally before
    LV systolic function
    declines.

    MV replacement
    MV ring & CABG
    MR repair associated
    with improved long-term
    LV funvtion

    MVP, ruptured chords,


    infective endocadritis,
    pap ms rupture.

    Balloon Mitral
    Commissurotomy

    Aortic Valve Disease: Etiology

    Aortic Stenosis

    Degenerative calcific
    (senile)
    Congenital Uni or
    bicuspid
    Rheumatic
    Prosthetic

    Chronic Aortic Insufficiency


    Aortic leaflet disease

    Aortic root disease

    Acute Aortic Insufficiency

    Infective endocarditis
    Acute Aortic Dissection

    Marfans Syndrome
    Chest trauma

    Infective endocarditis
    Rheumatic
    Bicuspid Aortic valve
    Prolapse & congenital VSD
    Prosthetic

    Aortic aneurysm/dissection
    Marfans syndrome
    Connective tissue disorders
    Syphilis
    HTN
    Annulo-aortic ectasia

    Aortic Stenosis Pathophysiology

    Normal AVA 2.5-3.0cm2

    Severe AS <1.0cm2
    Critical AS <0.7cm2;
    <0.5cm2/m2

    Hemodynamic Hallmark

    Systolic pressure gradient


    AV grad ~ AV flow//AVA

    AV flow = CO/SEP (systolic


    ejection period)

    50-100mmHg gradients
    are common in severe AS

    Relationship between AV
    gradient and Flow for different
    Aortic valve areas.

    Like Mitral Stenosis


    as flow increases so
    does the gradient.
    Unlike Mitral Stenosis

    Resting flows are higher

    smaller AV area
    shorter SEP

    Larger gradients
    Significant (>50mmHg)
    gradient can be present
    at rest in asymptomatic
    individuals.

    Pathophysiology of Aortic
    Stenosis- LVPO

    Chronic LV Pressure
    Overload Concentric LVH
    Stiff noncompliant LV

    LVEDP
    LV mass
    MVO2

    Well tolerated for decades

    Increased
    Increased
    Increased

    LV fails CHF

    Atrial fibrillation

    Poorly tolerated

    Loss of atrial kick


    Rapid HR
    Acute pulmonary edema
    and hypotension.

    Aortic Stenosis: Natural


    History & Clinical Symptoms

    Asymptomatic for many


    years
    Symptoms develop when
    valve is critically narrowed
    and LV function
    deteriorates

    Bicuspid AV 5th - 6th decade


    Senile AS 7th-8th decades

    Natural History Studies

    Classic Symptom Triad

    Angina pectoris 5 years


    CHF 1-2 years
    Syncope 2-3 years
    Sudden Death

    Pts grad 25mmHg 20%


    chance of intervention in
    15 years
    Pts with asymptomatic
    severe AS require close
    f/u
    Gradient progression

    6-10mmHg/yr

    Risk Factors

    Age > 70
    CAD, hyperlipidemia
    Chronic renal failure

    Aortic Stenosis: Physical


    Findings
    Severity of
    AS

    Moderate

    Severe

    Carotid pulse normal

    Slow rising

    Parvus et
    Tardus

    LV apical
    impulse

    heaving

    Heaving &
    sustained

    +/-

    ++

    Auscultatio
    n
    S4 gallop

    Mild

    normal

    Systolic
    ejection
    Click

    +/-

    SEM,
    peaking
    S2

    Early
    systole
    normal

    midsystole

    mid-to-late
    systole
    Single or

    Normal or

    Aortic InsufficiencyPathophysiology

    10 abnormality LVVO
    Severity of LVVO

    Size of regurgitant orifice


    Diastolic pressure gradient
    between Ao & LV
    HR or duration of diastole

    Compensatory Mechanisms

    LV dilatation & eccentric


    LVH
    Increased LV diastolic
    compliance
    Peripheral vasodilation

    LV Volume vs Pressure
    Overload
    Feature
    LV Volume
    Wall
    thickness

    LVPO (AS)

    LVVO (MR,AI)

    normal

    Dilated**

    Conc. LVH

    LV
    compliance
    LV diastolic
    Pr

    stiff
    noncompliant

    Normal to
    slightly
    increased
    Increased
    compliance

    increased

    LV systolic Pr Increased**
    LVEF

    normal

    Normal to
    slightly
    increased
    Normal to
    slightly
    increased
    increased

    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 PVCs

    Chronic Aortic Regurgitation:


    Physical Findings

    Widened Pulse Pressure > 70mmHg (170/60)


    Low diastolic pressure <60mmHg
    Hyperdynamic LV
    DeMussets signs
    Corrigans pulse
    Quinckes pulsations,
    Duroziers murmur
    Auscultation:
    Diminished A
    2
    Descrescendo diastolic blowing murmur @ LSB
    Austin-Flint murmur diastolic flow rumble @ apex

    Due to interference with trans-mitral filling by impignement from


    aortic regurgitant jet.
    DDx - mitral stenosis(increases intensity with amyl nitrite)

    Aortic Valve Disease:


    Diagnostic Testing

    Aortic Stenosis

    Aortic regurgitaiton

    EKG- NSR, LVH with strain,


    LAE,LAD
    CXRay frequently normal
    2D-ECHO

    EKG- LVH without strain


    CXRay-

    Aortic cusps thickened,


    calcified, decreased
    mobility
    Assessment of LVH & LV
    systolic function
    Concomitant MR, AR
    Doppler assesment of AoV
    gradient
    Planimetry of AV area

    Chronic AI cor bovinum


    Acute AI pulmonary
    edema with nl heart size

    2D ECHO

    Assess Ao valve and root


    Assess LV
    function/dilatation

    LVES dimension>55mm

    Doppler severity of
    regurgitant jet

    Relationship between AV
    gradient and Flow for different
    Aortic valve areas.

    Like Mitral Stenosis


    as flow increases so
    does the gradient.
    Unlike Mitral Stenosis

    Resting flows are higher

    smaller AV area
    shorter SEP

    Larger gradients
    Significant (>50mmHg)
    gradient can be present
    at rest in asymptomatic
    individuals.

    Balloon Aortic Valvuloplasty

    Indications for BAV in critical Aortic Stenosis

    Younger patients with congenital AS and


    predominant commissural fusion
    Bridge to eventual AVR
    Moderate to severe heart failure/cardiogenic shock
    Extremely high risk for AVR
    Urgent/emergent need for noncardiac surgery
    Patient with limited lifespan cardiac or noncardiac
    Patient refuses surgery

    Aortic Valve Surgery: Ross


    Procedure

    Autotransplant of
    pulmonic valve to the
    aortic position
    Reimplantation of the
    coronary arteries
    Homograft valve in the
    pulmonic position
    Indications

    Younger patients
    No anticoagulation
    Requires similar sized
    aortic and pulmonic
    roots

    Valvular Heart Disease

    The End

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