Path o Physiology Edited

7/27/2019 Path o Physiology Edited

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PATHOPHYSIOLOGYOF

AORTIC VALVE DISEASEWALID ALAYADHI

PGY-III


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EMBRYOLOGIC

DEVELOPMENT

During the early stages the main arterialsegment (truncus arteriosus) of the primaryheart tube is connected to the primitiveright ventricle

With subsequent cardiac loop formation(the truncus arteriosus) together with distalsegments of the ventricular outletcomponent is divided by endocardiaccushion tissue into subaortic andpulmonary outflow tracts

The truncus arteriosus eventuallydevelops into the pulmonary arteries andaorta


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EMBRYOLOGIC

DEVELOPMENT

septum develops within thetruncus arteriosus andsubsequently fuses with the

underlying ventricular septum At the point of fusion between

these two septal componentsseparation of the ventricularchamber is accomplished bydevelopment of the aortic valve


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EMBRYOLOGIC

DEVELOPMENT

The right and left cusps of the aortic

valve develop from the aortic side of

the truncal septum

Opposing this septum theembryonic posterior aortic valve

develops from the truncoconal lining

As development continues the aortic

valve leaflets grow to become nearly

uniform in size


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EMBRYOLOGIC

DEVELOPMENT
http://cardiacsurgery.ctsnetbooks.org/content/vol3/issue2008/images/large/825fig1.jpeg


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ANATOMY

Separates the terminal portion of theLVOT from the aorta

Tricuspid valve consisting of threesemilunar cusps (left, right, and noncoronary) and the aortic valveannulus

The sinus of Valsalva is defined asthe space between the edge of theleaflets and the aorta


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ANATOMY


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ANATOMY

The physiologic ventriculoarterial (VA) junction ismarked by attachments of the semilunar valves thatdefine the separation between the ventricularoutflow chamber and proximal aorta

There is a discrepancy between this physiologicjunction and the anatomic (VA) junction owing to inpart muscular tissue of the ventricle and in partfibrous tissue of the septum and mitral valve


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ANATOMY


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ANATOMY

The extracellular matrix is composed ofcollagen, elastin, and glycosaminoglycans

layers : Fibrosa or Arteriosa, Spongiosaand Ventricularis

The outer layers of the leaflet form a

continuum with the aortic or ventricularendothelium


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ANATOMY


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ANATOMY

In an artery endothelial cells are aligned inthe direction of blood flow because flowstress is the major stress

Endothelial cells on the aortic valve leafletare arranged in a circumferential pattern

( perpendicular to blood flow )

The major stress across the aortic valve isin the circumferential direction and isperpendicular to blood flow


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Opening

During diastole the pressure differencebetween the aorta and the ventricle createsstress on the valve leaflets

This stress toward the central portion of

the aortic opening constricts the base ofthe aortic root

During late diastole as blood fills theventricle a 12% expansion of the aortic rootoccurs approximately 20 to 40 ms prior to

aortic valve opening Dilatation of the root alone helps in

opening the leaflet to about 20%


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Opening

As pressure rises in the ventricular outflowtract tension across the leaflets lessens

As pressure continues to rise, the pressuredifference across the valve leaflets is

minimal, and no tension is present withinthe leaflet

At this point without constriction of theaortic root at the leaflet attachments owingto redistributed stress during diastole the

aortic root expands to allow the valve toopen rapidly at the beginning of ejection


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Closure

A principal theory involved in closure is thevortex theory

recognizes the importance of the sinus ofValsalva in providing a reservoir of blood

for small developing vortices These small vortices allow full expansion

of the opened valve leaflets

by maintaining the space between theedge of the leaflet and the aortic wallreversal of flow at the end of systoleprovides rapid closure


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Closure

As ejection occurs deceleration of blood atthe stream edge creates small eddycurrents of vortices

These small vortices along the aortic wallmove gradually toward the base of theventricular arterial junction at the edge ofthe leaflet and the top of the sinus ofValsalva

As flow declines at the end systole, thepressure difference across the opened

aortic valve leaflets decreases At the end of ejection and prior to valve

closure the vortices within the sinus ofValsalva balloon the valve leaflets towardthe center of the aorta


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Closure This small flow reversal causes the leaflets

to close rapidly Apposition of the valve leaflets occurs

briskly

The second heart sound occurs aftercomplete closure of the aortic valve

The valve leaflets act as an elasticmembrane, with stretch and recoilproducing the sound the sound is notproduced by physical apposition of thevalve leaflets

The second heart sounds depends on theelasticity of the valve leaflets and diastolicblood pressure to cause reverberation ofthe leaflets


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AORTIC STENOSIS

Valvular aortic stenosis (AS) without accompanyingmitral valve disease is more common in men

Age-related degenerative calcific AS is the most

common cause of AS in adults and the mostfrequent reason for aortic valve replacement (AVR)in patients with AS

2% of people 65 years of age or older having

isolated calcific AS whereas 29% exhibit age-related aortic valve sclerosis without stenosis


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AORTIC STENOSIS

Proliferative and inflammatory changes:

- lipid accumulation

- upregulation of (ACE) activity

- cellular infiltration ( macrophages andT lymphocytes )

- Calcification

Progressive calcification starts along theflexion lines at the leaflet bases leads toimmobilization of the cusps


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AORTIC STENOSIS

Calcified bicuspid aortic valverepresents the most common form ofcongenital AS (2% of the generalpopulation)

The abnormal architecture bicuspid

aortic valve induces turbulent.( accelerated degeneration)


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AORTIC STENOSIS

Recent work suggests that a DNA

transcriptional error, possibly for the

gene encoding endothelial nitric

oxide synthetase may be implicated

in the genetic abnormality that leads

to bicuspid aortic valve

Levinson GE, Alpert JS Valvular Heart

Disease, 3rd ed


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AORTIC STENOSIS

Rheumatic AS represents the leastcommon form of AS in the adult population

Characterized by diffuse fibrous leafletthickening with fusion of one or twocommissures


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Myocardial response

AS causes gradual obstruction to leftventricular outflow leading to LVH.

Progressive pressure gradient across thestenotic valve may occur without anydecrease in cardiac output, dilatation of theleft ventricle, or symptoms for years

As the left ventricle becomes less

compliant atrial systole becomes moreimportant for maintaining cardiac outputand onset of atrial fibrillation may result inclinical worsening and ventricular decompensation


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Myocardial response

LVH with AS is characterized by increasedgene expression for collagen I and II andfibronectin that is associated with activation

of the reninangiotensin system

In late stages of severe AS the left ventricledecompensates with resulting dilatedcardiomyopathy


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Myocardial response


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Coronary circulation

Left ventricular outflow obstruction resultsin elevation of left ventricular systolic anddiastolic pressures and increased leftventricular ejection time

Decrease in diastolic time leads todecreased myocardial perfusion time

LVH and prolongation of ejection result inincreased myocardial oxygen consumption


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Myocardial ischemia in patients with AScan be induced by an increase inmyocardial oxygen demand as a result ofexercise even in the absence of CAD

Myocardial oxygen supply-demanddisparity is the main mechanism for anginain patients with AS


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Syncope

Syncope most commonly is due to thereduced cerebral perfusion that occursduring exertion secondary to the decreasein arterial pressure consequent toperipheral vasodilation in the presence of a

fixed cardiac output Syncope also may be the result of

dysfunction of baroreceptor mechanismsand a vasodepressor response to theincreased left ventricular systolic pressure

during exercise Approximately 15% of patients present with

syncope only 50% survive 3 years


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Hemodynamics

The severity of AS is assessed by

estimating the mean systolic gradient and

aortic valve area (AVA)

The Gorlin formula is used to determine the

stenotic orifice area derived from thepressure gradient and cardiac output from

the fundamental relationships linking the

area of an orifice to the flow and pressure

drop across the orifice


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Hemodynamics

Transvalvular pressure gradient isbest measured with a catheter in theleft ventricle and another in theproximal aorta

The peak-to-peak gradient measuredas the difference between peak left

ventricular pressure and peak aorticpressure is used commonly toquantify the valve gradient


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Hemodynamics

Using Doppler methods, velocity isconverted to gradient using the Bernoullliequation: Gradient = 4 x V2

Echocardiographic measurements of AVA

represent the current clinical standard forassessment of the severity of AS

Transesophageal echocardiography (TEE)offers an alternative method forassessment of AVA using planimetry of the

multiplane systolic TEE short-axis views ofthe aortic valve

J Am Coll Cardiol, 1990; 15:1012-1017


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Clinical Presentation

The cardinal manifestations ofacquired AS are angina pectorissyncope and ultimately heart failure

Other late manifestations of severeAS include atrial fibrillation andpulmonary hypertension

Infective endocarditis can occur in

younger patients with AS it is lesscommon in elderly patients with aseverely calcified valve


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Echocardiography


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Echocardiography

Define the severity and etiology of

the primary valvular lesion

Define the hemodynamics

Define coexisting abnormalities

Detect secondary lesions

Evaluate cardiac chamber size and

function Re-evaluate the patient after

intervention


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Echocardiography

The normal area of the adult

aortic valve measures on

average 3.0 to 4.0 cm2

accepted criteria for the

gradation of AS define Mild AS as area >1.5 cm2

Moderate AS as area of 1 to 1.5 cm2 Severe AS as area


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INVESTIGATION

Exercise testing

Cardiac catheterization

Cardiac computed tomography

Magnetic resonance imaging


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Indications for Surgery

Class I

Symptomatic patients with severe AS

Severe AS in patients undergoing coronary

artery bypass graft surgery (CABG)

Severe AS in patients undergoing surgery onthe aorta or other heart valves

Asymptomatic patients with severe AS and LV

systolic dysfunction(ejection fraction less than 50%)


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Class IIa

Moderate AS in patientsundergoing CABG or surgeryon the aorta or other heartvalves


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Class IIb Asymptomatic patients with severe AS and

abnormal response to exercise

Severe asymptomatic AS if there is a highlikelihood of rapid progression (age,calcification, and CAD) or if surgery might bedelayed at the time of symptom onset

Mild AS in patients undergoing CABG whenprogression may be rapid

( moderate to severe valve calcification)

Asymptomatic patients with extremely severeAS if expected operative mortality is 1.0% orless

SUMMERY


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SUMMERY


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AORTIC REGURGITATION

Aortic regurgitation (AR) is a diastolicreflux of blood from the aorta into theleft ventricle owing to failure ofcoaptation of the valve leaflets

during diastole The presentation varies depending

on the acuity of onset severity ofregurgitation compliance of the

ventricle and aorta andhemodynamic conditions prevalentat the time


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Prevalence and Etiology

There are a number of common causes ofAR

Idiopathic dilatation of the aorta

congenital abnormalities of the aortic valve(most notably bicuspid valves)

Calcific degeneration

Rheumatic disease

Infective endocarditis

Systemic hypertension

Myxomatous degeneration Dissection of the ascending aorta

Marfan syndrome


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Pathophysiology

Acute aortic regurgitation By definition acute AR is a

hemodynamically significant aorticincompetence of sudden onset

across a previously competent aorticvalve into a left ventricle notpreviously subjected to volumeoverload

The inability to adapt is worse forconcentrically thickened hypertrophicmyocardium typically seen in thosewith chronic hypertension


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Pathophysiology

Chronic aortic regurgitation The left ventricle responds to

the volume load of chronic AR

with a series of compensatorymechanisms increase in end-diastolic volume

increase in chamber compliance

without an increase in fillingpressures

combination of eccentric and

concentric hypertrophy


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NATURAL HISTORY


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Echocardiography

Presence and degree of aorticinsufficiency

Its etiology

Valve morphology and presenceof vegetations and calcification

Quantification of pulmonary

hypertension Determination of ventricular

function


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Echocardiography


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Echocardiography

Doppler color-flow mapping, has

been used routinely to diagnose

and assess the severity of AR

The color-flow jets typically are

composed of three segments proximal flow convergence zone

vena contracta the jet itself distal to the orifice in the

left ventricular cavity


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Echocardiography

The severity of AR can be

defined by the ratio of the

proximal jet width to LVOT width

with a ratio of less than 25%consistent with mild AR

A ratio of greater than 65%

diagnostic of severe AR


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Diagnostic Evaluation

Catheterization

MRI


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Class I

AVR is indicated for symptomaticpatients with severe AR irrespective ofLV systolic function

AVR is indicated for asymptomaticpatients with chronic severe AR and LVsystolic dysfunction (ejection fraction0.50 or less) at rest

AVR is indicated for patients with

chronic severe AR while undergoingCABG or surgery on the aorta or otherheart valves


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Class IIa

AVR is reasonable for

asymptomatic patients with

severe AR with normal LV systolicfunction (ejection fraction greater

than 0.50) but with severe LV

dilatation (enddiastolic dimension

greater than 75 mm or end-systolic dimension greater than 55

mm)


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Class IIb AVR may be considered in patients with

moderate AR while undergoing surgery on theascending aorta

AVR may be considered in patients withmoderate AR while undergoing CABG

AVR may be considered for asymptomaticpatients with severe AR and normal LV systolicfunction at rest (ejection fraction greater than0.50) when the degree of LV dilatation exceedsan end-diastolic dimension of 70 mm or end-systolic dimension of 50 mm, when there is

evidence of progressive LV dilatation decliningexercise tolerance or abnormal hemodynamicresponses to exercise


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summery


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THANK YOU

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