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


The normal aortic valve area is approximately 3.5–4.0 cm wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)2.

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


Incidence
Incidence wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

Calcific Bicuspid

Valve

Rheumatic

Valve

Calcific Tricuspid

Valve


Mixed valves
Mixed Valves wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clues to diagnosis

Aortic Stenosis

Aortic Regurgitation Isolated AS

or MV involvement with calcification

Rheumatic under 70 yrs. Old over 70 yrs. Old

bicuspid valve senile degeneration


Risk factors of as
Risk factors of AS wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

Consequence of LVH –

- Alternation in diastolic compliance

- Imbalance in myocardial

supply/demand relationship

- Possible deterioration of intrinsic

contractile performance of

myocardium


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

  • Pressure –volume loop in AS


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 )


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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


Natural history
Natural history wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clinical 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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clinical 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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clinical 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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clinical 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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clinical 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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Clinical 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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

Mild

Moderate

Severe


ekg wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)


Physical findings
Physical findings wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

CXR and ECG

- LVH

- Dilatation of ascending aorta

- Aortic calcification


Echocardiography
Echocardiography wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

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 wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

Provide information about

- Pressure gradient

- Aortic valve area

- Cardiac output


Severity of as
Severity of AS wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)


Cont. wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)

  • 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 Stenosis wall(right coronary cusp)& two located in the posterior wall(left and posterior cusp)Medical 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


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 but it does not last long


Prosthetic valves1
Prosthetic Valves but it does not last long


Aortic stenosis surgical management
Aortic Stenosis but it does not last longSurgical Management


Aortic stenosis valvuloplasty
Aortic Stenosis but it does not last longValvuloplasty


Mitral valve prolapse

Mitral Valve Prolapse but it does not last long


Mitral valve
Mitral Valve but it does not last long

  • 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 but it does not last long


Mitral valve prolapse introduction
Mitral Valve Prolapse: Introduction but it does not last long

  • 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 but it does not last long

Prevalence of 2.4% of population

Twice frequent in females than in males

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


Etiology1
Etiology but it does not last long

  • Primary condition

    • Familial – Autosomal trait

  • Secondary conditions

    • Heritable disorders of connective tissue


Classification
Classification but it does not last long


Pathology
Pathology but it does not last long

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 but it does not last long

  • Symptoms

    • Atypical chest pain

    • Palpitations

    • Dyspnea

    • Fatigue

    • Syncope

  • Signs

    • Asthenic, low body weight

    • Normal Blood pressure

    • Orthostatic hypotension


Auscultation
Auscultation but it does not last long

  • 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 but it does not last long

Confirmatory

Prolapse of mitral leaflet into left atrium

Thickening of mitral valve (>5mm)


Other diagnostic tests
Other diagnostic tests but it does not last long

  • 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 but it does not last long

  • Stress scintigraphy

    • Differentiate MVP with IHD

  • Angiography


Disease course
Disease course but it does not last long

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 but it does not last long

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 but it does not last long

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 but it does not last long

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)


Thank You ! but it does not last long


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