AS causes progressive obstruction to LVOT

resulting in pressure hypertrophy of LV and

S/S/O HF, angina and syncope.

obstruction most commonly occurs at

valvular level, though it may occur sub

valvular or supravalvular

Calcified Ao valve disease:

› M. C cause of AS in adults

› Related to active process of inflammation

involving RAS, lipid accumulation, resultant

calcification

› Asso. With atherosclerosis, smoking, HTN,

dyslipidemia

› Increased risk of CV death, MI.

› Other condition asso are paget’s disease and

ESRD

Bicuspid Ao Valve:

› Most common is fusion of Rt and LT cusps.

› Concurrent Coarctation, Ao root dilatation,

propensity for Ao dissection.

› Present in 1-2% of population

› Severe stenosis develops by 4th-5th decade

› Unicuspid valve are uncommon and usually

severely stenotic at early age.

Current ACC/AHA guidelines recommend

evaluation of AV valve by echo regularly

› Ao dia > 4cm and bicuspid valve shuold have

yearly follow up

› Ao dia >5 cm or increase by >0.5cm/yr surgical

intervention recommoded

› If valve requires surgery, aorta replacement is

recomomnded if >4.5cm @ time of surgery

Rheumatic AS:

› Often co exists with AR, and MV lesions

› Rare cause of isolated AS

Congenital condition, may not be apparent at

birth

Circumferential fibromuscular membrane

involving AMV leaflet (+) in LVOT below AV

Maladaptive response to abnormal flow

dynamics in LVOT. Though not clear

Difficult to diagnose when asso, HOCM and

LVH present

Shone’s syndrome:

› Supravalvular MV membrane

› Parachute MV(single PM attached to both MV leaflets)

› Sub aortic stenosis

› Coarctation of aorta

Uncommon

Caused by lipid deposition in familial hypercholesterolemia

Part of congenital Williams syndrome, caused by mutation in elastin gene

› Hypercalcemia

› Elfin facies

› Devp delay

› Small strature

› Multiple stenoses in AO and periph art

Resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta.

This outflow obstruction leads to an increase in left ventricular (LV) systolic pressure and after load

As a compensatory mechanism to normalize LV wall stress, LV wall thickness increases by parallel replication of sarcomeres, producing concentric hypertrophy.

At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance is reduced.

LV end-diastolic pressure (LVEDP) rises, which causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in cardiac output due to diastolic dysfunction.

contractility of the myocardium may also diminish, which leads to a decrease in cardiac output due to systolic dysfunction. Ultimately, heart failure develops.

Diastolic dysfunction due to:› impaired LV relaxation and/or decreased LV compliance

› increased afterload,

› LV hypertrophy, or myocardial ischemia.

Atrial contraction plays a particularly important role in diastolic filling of the left ventricle.

Development of AF in AS often leads to heart failure due to an inability to maintain cardiac output.

Myocardial perfusion compromised by:› relative decline in myocardial capillary density

› reduced diastolic transmyocardial (coronary) perfusion gradient due to elevated LV diastolic pressure.

› the subendocardium is susceptible to underperfusion, which results in MI.

myocardial oxygen requirement increased:

› Increased LV mass

› increased LV systolic pressure

› prolongation of the systolic ejection phase,

especially in the subendocardial region.

› Although coronary blood flow may be normal

when corrected for LV mass, coronary flow

reserve is often reduced.

Angina results from a

› concomitant increased oxygen requirement by

the hypertrophic myocardium

› diminished oxygen delivery secondary to

diminished coronary flow reserve

› decreased diastolic perfusion pressure

› and relative subendocardial myocardial ischemia

Risk of SCD <2%

Aymptomatic valvular AS:

Mean AVG increase by 7mm

Hg/yr

AV area decrese by 0.1cm2/yr

Severe symptomatic AS

› SCD can occur in case of hypotension, arrythmia

› Exercise stress testing is absolutely

contraindicated

Asymptomatic latent period of 10-20 years.

Exertional dyspnea is the most common initial

complaint, exertional chest pain, effort dizziness

or lightheadedness, easy fatigability, and

progressive inability to exercise.

Classic triad of

› chest pain

› heart failure

› syncope

carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus).

Narrow pulse pressure

Pulsus alternans can occur in the presence of LV systolic dysfunction.

The jugular venous pulse may show prominent a waves reflecting reduced right ventricular compliance consequent to hypertrophy of the interventricular septum.

A hyperdynamic LV is unusual and suggests concomitant aortic regurgitation or mitral regurgitation.

Palpable systolic thrill 2nd Rt IC space

S1 is usually normal or soft.

A2, is usually diminished or absent

Paradoxical splitting of the S2 also occurs,

resulting from late closure of A2 in case of

severe AS

S3- poor LV systolic function

S4- reduced LV compliance

The classic crescendo-decrescendo systolic murmur of aortic stenosis› begins shortly after the first heart sound

› intensity increases toward midsystole, then decreases, and the murmur ends just before the second heart sound.

› rough, low-pitched sound that is best heard at the second intercostal space in the right upper sternalborder in sitting position at the end of full expiration

› radiates to 1 or both carotid arteries.

In elderly persons with calcific aortic stenosis, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardinphenomenon). Mistaken as a MR.

ECG:

› LVH with strain pattern

› LA enlargement

› AF

› IV conduction defect

CXR:

› Mostly normal

› Concentric LVH cardiac silhoutee boot shaped

› Cardiomegaly if concomitant AR +

Two-dimensional and Doppler echocardiography is the imaging modality of choice to diagnose and determine the severity of aortic stenosis

Regular follow with echo

› Asymptomatic severe: yearly

› As pt became symptomatic or develop new symptoms

› moderate AS: 1-2 years follow up

› Mild AS: 3-5 yrs

PLAX:

› Mechanism and severity of AS

› Degree of LVH

› LA/LV enlargement

› LVOT dia.

› Systolic leaflet doming can be seen in congenital

or rhematic AS

PSAX:

› Most useful for cause of congenital AS

A5C:

› CWD in LVOT recorded for conitnuity equation

› From suprasternal view As Ao and Ds Ao

diameter can be measured

TEE:

› Morphology of valve

› Diagnosis of sub aortic membrane to differentiate

b/w HOCM or valvular AS

Doppler echocardiography:

› Standard for TVPG and AVA

› Simplified bernoullis equation

› Continuity principle(physiologic area)

Cardiac catheterization:

› Pt >50yrs of age, angina, significant CAD risk factors

› Severe AS low osmolar non ionic contrast

› Gorlin fromula to calculate AVA(true anatomic area)

› Hakki equation: simplified gorlin firmula

Asymptomatic:› Primary CAD prevention, BP control, maintain sinus

rhythm

Symptomatic:› Rx for HF: diuretics and NTG: used cautiously

› LVD /AF: digitalis/ACEI, avoid Beta blocker

› Severe AS + CAD: surgical Mx optimal

Vasodialtors relatively C/I:› Aggravates syncope ; decrease SVR

Statins:

Antibiotic prophylaxis:› Prior to dental surgery only in H/O IE and prosthetic

valves

Percutaneous Aortic Balloon Valvuloplasty:

› Pediatric, congenital, non-calcified AS

› AR can occur as a complication

› AVR necessray after 10 years of PABV

› Not useful for adults

› In all symptomatic pt and asymptomatic pt with

TVG >60mmHg or ST-T changes on ecg

Symptomatic pt with severe AS

Severe AS + LVEF <50%

Severe AS or moderate AS undergoing CABG or other valvular surgeries

Ross procedure: (homografts)› In pediatrics or adolescent

› IE of naive or prosthetic valve with pyogeniccomplication

› When LVOT is very small

Mechanical valves

› St. Jude, medrotonic hall and carbomedics

› Requires anti coagulant life long

Bioprosthetic valves

› Porcine heterografts or bovine pericardial

prostheis

› Age >60 yrs

› Low thromboembolism

› No long term anticoagulant

CABG in Mod MS:

› Benefit + if AVA <1.5 cm2

High risk pt AVR recommended:

› Highly calcified AV valve & rapid rise in pressure gradient

› Trans aortic flow velocity >4m/s

› LVD d/t AS

› Exercise induced hypotension

› PAH >60mmHg

› Before pregnancy

LVD d/t afterload mismatch Sx corretion

leads to improvement/ normalization of LVEF

Primary contractile dysfunction: overall poor

prognosis/ unlikely to get benefit from AVR

High TVG:

› Measure of high afterload mismatch

› TVG >40 mmHg= AVR recommended

Low TVG:

› Severe AS <1.0cm2 and low TVG < 30 mmHg

poor prognosis with out surgical correction

› Improved after surgical treatment if they

demonstrate contractile reserve

Contractile reserve:

› Ability to increase TV flow >20% from baseline

when challenged with dobutamine

True AS: (dobutamine)

› Increase CO, TVG

› AVA same

Vasodilator:

› TVG increase

› CO not

› AVA same/ decrease

Aorti

pseudostenosis:

(dobutamine)

› Increase CO

› TVG not increase

› AVA incr. >0.3 cm2

Vasodiator:

› Increase CO

› Dec. TVG

› AVA increase

Severe AS; low gradient; preserved LVEF

early surgical intervention recommended

Subaortic stenosis: surgical removal of

membrane

› Symptomatic

› Asymptomatic: PG >50mmHg or assoicated

more than mod AR.