Aortic stenosis and mitral valve prolapse
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AORTIC STENOSIS AND MITRAL VALVE PROLAPSE. PRESENTED BY: FADAIRO OLUMAYOWA BEATRICE 692. AORTIC STENOSIS.

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Aortic stenosis and mitral valve prolapse

AORTIC STENOSIS ANDMITRAL VALVE PROLAPSE

PRESENTED BY:

FADAIRO OLUMAYOWA BEATRICE

692


Aortic stenosis

AORTIC STENOSIS


Aortic stenosis and mitral valve prolapse

Aortic valve is the valve located between the left ventricle of the heart and the aorta, the largest artery in the body which carries the entire output to the systemic circulation.


Aortic stenosis and mitral valve prolapse

Aortic valve have 3 cusp – one located on the anterior wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)


Aortic stenosis and mitral valve prolapse

The normal aortic valve area is approximately 3.5–4.0 cm2.

Critical aortic stenosis is usually present when the area is less than 0.8 cm2.


Incidence

Incidence

¼ of all with patient chronic VHD

Male> female

(80% of adult pt with symptomatic valvular AS are male )

It is the most common form of VHD in US


Etiology

Etiology

Congenital- Stenotic since birth (< 30 yr)

Bicuspid – 1-2 % of population (40-60 yr )

- Male > female (3 : 1 )

- 6% have coartation of aorta

- Mechanical shear stress

produce injury & stenosis


Aortic stenosis and mitral valve prolapse

Cont.


Aortic stenosis and mitral valve prolapse

Cont.

Secondary to inflammation (40-60 yr ):-

-Mainly rheumatic

-MC cause of AS in India and world

-Isolate rheumatic AS- rare

(Rheumatic AS always associated with mitral valve

involvement and AR )

-Post inflammation -> commissural

fusion


Aortic stenosis and mitral valve prolapse

Cont.

Degenerative:-

-MC cause of AS in US and EUROPE

->30% people of >65yr –have AV

sclerosis

-Stenosis is due to sclerosis and

calcification

-Progress from the base of the cusp

to the leaf-lets


Rheumatic and calcified valves

Rheumatic and Calcified Valves

Calcific Bicuspid

Valve

Rheumatic

Valve

Calcific Tricuspid

Valve


Mixed valves

Mixed Valves

Congenital Bicuspid

Valve affected by Rheumatic

Disease and Calcification

Tricuspid Valve with

Rheumatic Disease

creating a functional bicuspid

valve, and calcification


Aortic stenosis clues to diagnosis

Aortic StenosisClues to diagnosis

Aortic Stenosis

Aortic RegurgitationIsolated AS

or MV involvement with calcification

Rheumaticunder 70 yrs. Oldover 70 yrs. Old

bicuspid valvesenile degeneration


Risk factors of as

Risk factors of AS

Bicuspid aortic valve

Risk factors for atherosclerosis

- age

- male sex

- smoking

- DM, HTN

- ↑ LDL , ↓ HDL , ↑ CRP

Rheumatic fever

Conditions with ↑SV and altered calcium metabolism


Pathophysiology

Pathophysiology

Aortic stenosis

Obstruction to LV ejection

Pressure overload

↑LV mass (↑wall thickness)

← ← ← → → →

↓ ↓

Compensated Decompensated

↓LV compliance Fibrosis:↓ contractility

Normal contractility

↓ ↓

LV filling ; ↓early LV dilatation

↑late

↓ ↓

SV: normal SV: decreased


Aortic stenosis and mitral valve prolapse

Cont.

The LVH is due to increase wall tension,in accordance with Laplace”s law:

Wall tension = P*R/2H

p - intraventricular pressure

r – inner radius

h – wall thickness


Aortic stenosis and mitral valve prolapse

Cont.

Pressure overload

↑Peak systolic pressure

↑Wall tension

Parallel replication of sacromeres (-)

Increase wall thickness

Concentric hypertrophy

Concentric hypertrophy normalizes wall stress and thus preserve myocardial contractility


Aortic stenosis and mitral valve prolapse

Cont.

Consequence of LVH –

- Alternation in diastolic compliance

- Imbalance in myocardial

supply/demand relationship

- Possible deterioration of intrinsic

contractile performance of

myocardium


Aortic stenosis and mitral valve prolapse

Cont.

  • Pressure –volume loop in AS


Aortic stenosis and mitral valve prolapse

Cont.

Increased chamber stiffness impedes early left ventricular filling

Hence atrial systole is critical in maintaining ventricular filling and SV

In AS atrial systole accounts for 40% of LVEDV. (Normally it contribute 15-20% of LVEDV )


Aortic stenosis and mitral valve prolapse

Cont.

  • Although contractility is preserved, hypertrophied ventricle is sensitive to ischemia and LVF


Natural history

Natural history

Prolonged latent period

Once moderate stenosis present rate of progression is –

-0.3m/s jet velocity/yr

-Mean pressure gradient=

7 mm-hg/yr

-↓in valve area= 0.1cm2 /yr


Aortic stenosis clinical manifestations

Aortic StenosisClinical Manifestations

  • History

    • Angina

      • Occurs in 2/3 of patients with critical AS

      • Half of the patients have normal coronaries

      • Results from increased oxygen demand by a hypertrophied myocardium and decreased oxygen delivery secondary to compression of the vessels

      • Average survival is 5 years


Aortic stenosis clinical manifestations1

Aortic StenosisClinical Manifestations

  • History

    • Syncope

      • Due to reduced cerebral perfusion

      • May be orthostatic, exertional, medication related (nitrates, diuretics, etc.), or due to arrhythmias

      • Average survival is 3 years


Aortic stenosis clinical manifestations2

Aortic StenosisClinical Manifestations

  • History

    • Heart Failure

      • Manifest as orthopnea, dyspnea, PND, pulmonary edema

      • Average survival is 1 – 2 years

      • Microangiopathic hemolytic anemia

      • Sudden death


Aortic stenosis clinical manifestations3

Aortic StenosisClinical Manifestations

  • Physical Examination

    • Carotid Arterial Pulse

      • The classic arterial pulse is called pulsusparvus et tardus(slow and late)

    • Precordium

      • The apical impulse has a sustained lift

      • There is little or no displacement of the Point of maximal impulse


Aortic stenosis clinical manifestations4

Aortic StenosisClinical Manifestations

  • Physical Examination

    • Auscultation

      • S1 – usually normal, may be soft if CHF present

      • S2 – the intensity of A2 decreases as the valve stiffens

      • S2 splitting – with prolongation of LV ejection time A2 will occur later than P2 and cause paradoxical splitting of S2


Aortic stenosis clinical manifestations5

Aortic StenosisClinical Manifestations

  • Physical Examination

    • S3 – usually not a normal finding in aortic stenosis, it’s presence suggests LV dysfunction

    • S4 – is usually present and suggests LV hypertrophy and decreased LV compliance

    • Ejection click occurs when the leaflets abruptly halt after maximal upward excursion and imply a mobile valve. It disappears as the valve becomes severely calcified.


Murmur of aortic stenosis

Murmur of Aortic Stenosis

Heard best at the 2nd

RICS radiating to the

carotids, sometimes

throughout the

precordium.

S 2

S4 S 1


Aortic stenosis severity

Aortic Stenosis Severity

Mild

Moderate

Severe


Aortic stenosis and mitral valve prolapse

ekg


Physical findings

Physical findings

Delayed sustain peak of arterial pulse

(pulsusparvus et tardus )

Bifid apical LV impulse

Systolic thrill

Late peaking Systolic ejection murmur

(2nd right intercostsl space )

Paradoxical S2

S4 (with LVH ) & S3 (with LVF )

(Thrill and intensity of murmur does not correlate with severity )


Investigation

Investigation

CXR and ECG

- LVH

- Dilatation of ascending aorta

- Aortic calcification


Echocardiography

Echocardiography

2D/Doppler TTE- test of choice

Provide information about-

- Etiology, location

- Valve gradient and area

- Systolic/diastolic LV function

- Coartation associated with

bicuspid valve


Cardiac catheterization

Cardiac Catheterization

Provide information about

- Pressure gradient

- Aortic valve area

- Cardiac output


Severity of as

Severity of AS


Aortic stenosis and mitral valve prolapse

Cont.

  • Gradient across valve normal until orifice area reaches less than half of normal

  • Onset of symptoms

    • 0.9 cm2 with CAD

    • 0.7 cm2 without CAD


Aortic stenosis medical management

Aortic StenosisMedical Management

All patients should follow SBE prophylaxis guidelines

Avoid vigorous exercise

Use nitrates and diuretics with caution

Asymptomatic patients should report the onset of any symptoms promptly


Aortic stenosis and mitral valve prolapse

Bio prosthetic valves- patient do not need an anticoagulant but it does not last long

Mechanical prosthetic valve- patient will need to be using anticoagulant (warfarin) with INR of 2.0-3.0


Prosthetic valves

Prosthetic Valves


Prosthetic valves1

Prosthetic Valves


Aortic stenosis surgical management

Aortic StenosisSurgical Management


Aortic stenosis valvuloplasty

Aortic StenosisValvuloplasty


Mitral valve prolapse

Mitral Valve Prolapse


Mitral valve

Mitral Valve

  • Consists of 6 major anatomical components

    • Annulus

    • Leaflets

    • Chordae tendinae

    • Papillary muscles

    • Posterior left atrial wall

    • Left ventricular free wall


Structure of mitral valve

Structure of mitral valve


Mitral valve prolapse introduction

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 & valve annulus.

  • Many names:

    • Systolic click murmur syndrome

    • Barlow syndrome

    • Billowing mitral cusp syndrome

    • Myxomatous mitral valve syndrome

    • Floppy valve syndrome

    • Redundant cusp syndrome


Epidemiology

Epidemiology

Prevalence of 2.4% of population

Twice frequent in females than in males

Severe MVP occurs more frequently in older males (>50yrs)


Etiology1

Etiology

  • Primary condition

    • Familial – Autosomal trait

  • Secondary conditions

    • Heritable disorders of connective tissue


Classification

Classification


Pathology

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 tensile strength & thus rupture


Clinical diagnosis

Clinical Diagnosis

  • Symptoms

    • Atypical chest pain

    • Palpitations

    • Dyspnea

    • Fatigue

    • Syncope

  • Signs

    • Asthenic, low body weight

    • Normal Blood pressure

    • Orthostatic hypotension


Auscultation

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


Echocardiography1

Echocardiography

Confirmatory

Prolapse of mitral leaflet into left atrium

Thickening of mitral valve (>5mm)


Other diagnostic tests

Other diagnostic tests

  • ECG

    • Negative or biphasic t waves & nonspecific ST changes in leads II, III, aVF & occasionally anterolateral leads

    • Arrhythmias

      • Atrial or Ventricular PC

      • Paroxysmal supraventriculartachycardial (most common) & ventricular tachyarrhythmia

      • Bradyarrhytmias due to sinus node dysfunction

      • Varying degrees of AV blocks

      • 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


Other diagnostic tests1

Other diagnostic tests

  • Stress scintigraphy

    • Differentiate MVP with IHD

  • Angiography


Disease course

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 (<50%), left atrial dimensions (>40mm), age (>50yr)

Risk of development of IE is greater in men >50yrs


Sudden cardiac death

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.


Management

Management

Transesophageal echo in first degree should be done (Circulation 2005)

Echo should confirm the diagnosis

Asymptomatic patients without arrhythmias/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 Electrophysiogicstudy to characterize arrhythmias & RF if necessary for AV bypass tracts in prolonged SVT episodes


Management1

Management

Beta blockers for palpitations secondary to Premature ventricular contractions& relieve chest discomfort

Aspirin in documented cases of neurological event or if atrial thrombus exists

Patients with severe MR & MVP may require MV surgical repair.

Antibiotic prophylaxis for GI & GU procedures (NICE Clinical Guideline (March 2008)


Aortic stenosis and mitral valve prolapse

Thank You !


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