f4afMitral Valve Prolapse

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    Mitral Valve Prolapse

    Dr Mohammed Haroon Rashid

    Resident, Department Cardiology

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    Mitral Valve

    Consists of 6 major anatomical

    components

    Annulus

    Leaflets

    Chordae tendinae

    Papillary muscles

    Posterior left atrial wall

    Left ventricular free wall

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    Structure of mitral valve

    Features Description

    Annulus Saddle Shaped, 4-6cm2

    Leaflets Sail shaped AML & C shaped

    PML

    Papillary Anterolateral PM at 4 O Clock,

    Posteromedial PM at 7 O

    Clock position

    Chordea Tendinae 120 in number

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    Mitral Valve Prolapse:

    Introduction

    A variable clinical syndrome that results

    from a diverse pathogenic mechanisms of

    one or more portions of mitral valve

    apparatus, valve leaflets, chordae

    tendinae, papillary muscle & valveannulus.

    Many names:

    Systolic click murmur syndrome

    Barlow syndrome

    Billowing mitral cusp syndrome

    Myxomatous mitral valve syndrome

    Floppy valve syndrome

    Redundant cusp syndrome

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    Epidemiology

    Prevalence of 2.4% of population

    Twice frequent in females than in males

    Severe MVP occurs more frequently in

    older males (>50yrs)

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    Etiology

    Primary condition

    Familial Autosomal trait

    Non familial

    Secondary conditions

    Heritable disorders of connective tissue

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    Classification

    Classification of MVP

    Mitral Valve Prolapse syndrome

    Younger age (20-50)

    Predominantly females

    Click or click murmur present

    Benign long term course

    Myxomatous Mitral Valve Disease

    Older age- 40-70yr

    Predominantly males

    Thickened & redundant valve leaflets

    Progressive disease, requires surgerySecondary Mitral Valve Prolapse

    Marfan syndrome

    Hypertrophic cardiomyopathy

    Ehlers-Danlos syndrome

    Other connective tissue disorders

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    Pathology

    Myxomatous proliferation of mitral valve

    leaflets & quantity of acid

    mucopolysaccharide is increased.

    Regions of endothelial disruption are

    common & possible site for thrombus

    formation or endocarditis.

    Degeneration of collagen & myxomatous

    changes within the central core of chordae

    tendinae causes decrease of tensilestrength & thus rupture

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    Clinical Diagnosis

    Symptoms

    Atypical chest pain

    Palpitations

    Dyspnea

    Fatigue

    Syncope

    Signs

    Asthenic, low body weight

    Normal Blood pressure

    Orthostatic hypotension

    Straight back syndrome

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    Auscultation

    Mid or late systolic click, heard over apex

    Pansystolic murmur present if associated

    with severe mitral regurgitation

    Dynamic auscultation Change in loudness as well as the time of

    occurrence of both click & murmur are

    diagnostic

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    Echocardiography

    Confirmatory

    Prolapse of mitral leaflet into left atrium

    Thickening of mitral valve (>5mm)

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    Other diagnostic tests ECG

    Negative or biphasic t waves & nonspecific ST

    changes in leads II, III, aVF & occasionallyanterolateral leads

    Arrhythmias

    Atrial or Ventricular PC

    PSVT (most common) & ventricular

    tachyarrhythmia Bradyarrhytmias due to sinus node

    dysfunction

    Varying degrees of AV blocks

    Incidence with WPW & MVP has increased

    Increased association with Long QT

    syndrome

    Mechanism of arrhythmia not clear, but diastolic

    depolarization of muscle fibers in anterior mitral

    leaflet in response to stretch has been

    demonstrated experimentally

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    Other diagnostic tests

    Stress scintigraphy

    Differentiate MVP with IHD

    Angiography

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    Disease course

    General outcome is excellent, large group

    remain asymptomatic

    Serious complications occur in 1/100

    patient years

    4% died during 8yrs

    Most of the risk factors were based on

    severity of MR , ejection fraction (40mm), age

    (>50yr)

    Risk of development of IE is greater in

    men >50yrs

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    Predictors of clinical outcomes in

    MVP

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    Sudden Cardiac Death

    Relation of SCD & MVP is not clear

    Evidence suggests that MVP increases

    the risk of SCD slightly, especially in

    patients with severe MR or severe

    valvular deformity, & those with

    complex ventricular arrhythmias, QT

    prolongation is higher.

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    Other complications

    CNS

    Acute hemiplegia

    TIAs

    Amaurosis fugax

    Cerebellar infarcts

    Unexplained stroke of young!

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    Management

    Transesophageal echo in first degree

    should be done (Circulation 2005)

    Echo should confirm the diagnosis

    Asymptomatic patients withoutarrhythmias/IE should be reassured &

    follow up examination every 3 to 5yrs to be

    done (follow up with color doppler)

    Patients with palpitations, arrhythmias

    should undergo EP study to characterize

    arrhythmias & RF if necessary for AV

    bypass tracts in prolonged SVT episodes

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    Management Beta blockers for palpitations secondary to

    PVCs & relieve chest discomfort

    Aspirin in documented cases ofneurological event or if atrial thrombus

    exists (Hayek; Mitral valve prolapse. Lancet. 2005 Feb 5-11;365(9458):507-18)

    Patients with severe MR & MVP mayrequire MV surgical repair.

    Antibiotic prophylaxis for GI & GU

    procedures (NICE Clinical Guideline (March 2008)

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    Thank You !