Evaluation of severity of as

EVALUATION OF SEVERITY OF AORTIC STENOSIS

DR. RAJESH DAS

Aortic stenosis- brief Introduction..

Aortic stenosis: Classification based on location

Valvular- most common type.

Subvalvular.Supravalvular.

Valvular Aortic Stenosis: Etiology

Most common :-Calcific Aortic Valve Disease

Congenital Bicuspid aortic valve with superimposed calcification.Age related calcific AS of normal trileaflet valve.

Rheumatic AS

Less common:-CongenitalType 2 HyperlipoproteinemiaOchronosis

Aortic Sclerosis

Irregular thickening of the valve leaflets seen on echo but without significant obstruction.

preserved mobility of the cusps.

Typically associated with peak doppler velocity of less than 2.6 m/sec.

29% of persons > 65 yrs of age exhibited age-related aortic valve sclerosis without stenosis.

Bicuspid Aortic Valve

The most common congenital cardiac abnormality is bicuspid aortic valve affecting 1-2% of the U.S. population.

Over time, 1/3rd to 1/2 of such valves become stenotic.

significant narrowing of the aortic orifice typically develops in the 5th and 6th decades of life.

Bicuspid Aortic Valve

Fusion of the right and left coronary cusps (70-80%).

Fusion of the right and non-coronary cusps(20 -30%)

In adults, stenosis in BAV is d/t calcific changes, which often obscures the number of cusps.

Calcific Aortic Stenosis of trileaflet valve

Nodular calcific masses on aortic side of cusps, most prominent in central part.

No commissural fusion.

Free edges of cusps are not involved.

stellate-shaped systolic orifice.

Valve calcification - predictor of clinical outcome.

Rheumatic aortic stenosis

Characterized by Commissural fusionTriangular systolic orificethickening & calcification

Accompanied by rheumatic mitral valve changes.

Subvalvular aortic stenosis

Thin discrete membrane consisting of endocardial fold and fibrous tissue.

A fibromuscular ridge.

Diffuse tunnel-like narrowing of the LVOT.

Accessory or anomalous mitral valve tissue.

Supravalvular aortic stenosis

Type I – Thick, fibrous ring above the aortic valve with less

mobility and has the easily identifiable 'hourglass' appearance of the aorta.

Type II – Thin, discrete fibrous membrane located above the aortic

valve .The membrane usually mobile and may demonstrate

doming during systole

Type III- Diffuse narrowing.

Evaluation of severity

• Clinical

• Echocardiographic

• Cardiac Catherization

• Others- CT, MRI etc.

Clinical evaluation of severity

Symptoms of severe AS

Cardinal symptoms of AS:Exertional dyspnea and other symptoms of HF.AnginaSyncope

Other complaints: effort intolerance, fatigue. GI or mucosal bleeding.

there is wide individual variability in the severity of outflow obstruction that produces symptoms.

Signs of severity

Pulsus parvus et tardus (low amplitude, delayed upstroke).Sustained LV impulse.2nd heart sound-

Diminished A2 component.Single d/t absent A2.Paradoxically split S2- in severe AS with LV dysfunction (or in LBBB

d/t LVH)

Prominent S4.Late peaking systolic murmur (though murmur can be absent)

Echocardiographic assessment of severity

Doppler assessment of AS

The primary haemodynamic parameters recommended (EAE/ASE Recommendations for Clinical Practice 2009).

Peak transvalvular velocity.

Mean transvalvular gradient.

Valve area by continuity equation.

Classification of AS severity(based on 2014 AHA/ACC Valvular heart disease guideline)

Peak transvalvular velocity measurement

CW Doppler ultrasound

Defined as the highest velocity signal obtained from any window after a careful examination.

Multiple acoustic windows Apical, suprasternal or right parasternal most frequently yield the highest velocity.

≥3 are averaged in sinus rhythm, with irregular rhythms at least 5 consecutive beats.

Peak transvalvular velocity

Deviation from a parallel intercept angle →velocity underestimation

Degree of underestimation is ˂ 5% if the intercept angle is within 15 of parallel.⁰

‘Angle correction’ should not be used.


to optimize identification of the velocity curve.Wall filters → set at a high levelgain → decreased

A smooth velocity curve with a dense outer edge and clear maximum velocity should be recorded


The shape of the CW Doppler velocity curve helps distinguishing the level and severity of stenosis.

With severe stenosis, max. velocity occurs later in syst. and the curve is more rounded in shape.

With mild stenosis, the peak is in early syst. with a triangular shape.


The shape of the CWD velocity curve also helps in determining whether the obstruction is fixed or dynamic.

Dynamic sub aortic obstruction:late- peaking velocity curve, often with a

concave upward curve in early systole

Mean transvalvular gradient

Gradients are calculated from velocity information

simplified Bernoulli equations: ΔP =4v²

The mean gradient is calculated by averaging the instantaneous gradients over the ejection period.

Mean transvalvular gradient

The simplified Bernoulli equation assumes that the proximal velocity can be ignored.

When the proximal velocity is over 1.5 m/s or the aortic velocity is <3.0 m/s, the proximal velocity should be included in the Bernoulli equation ΔP max =4 (v² max- v2

proximal)

Sources of error for pressure gradient calculations

Malalignment of jet and ultrasound beam.Recording of MR jet.

How to differentiate? MR jet is wider (isovolumic periods +E.T.)MR is more symmetrical.In any given pt., MR is faster than AS.MR jet is not recorded in the suprasternal

notch.CW Doppler of AS is superimposed on the

lower velocity of the LVOT.


Neglect of an ↑ proximal velocity.

Any underestimation of aortic velocity results in an even greater underestimation in gradients.

Aortic valve area Continuity equation


Calculation of continuity-equation valve area requires three measurements:

AS jet velocity by CWDLVOT diameter for calculation of a circular CSALVOT velocity recorded with pulsed Doppler.


LVOT diameter and PW of the LVOT needs to taken from the same location in the LVOT.

LVOT diameter → PLAX view

LVOT velocity (or VTI) → apical view – beware of distance error.

The PW sample volume is positioned just prox. to the AV.


LVOT Diameter• LVOT diameter is measured in

the PLAX view in mid-systole from the white–black interface of the septal endocardium to the anterior mitral leaflet, parallel to the aortic valve plane and within 0.5–1.0 cm of the valve orifice.


Velocity or VTI measurement• LVOT velocity is measured from the apical

approach either in an apical long-axis view or an anteriorly angulated four-chamber view

• An optimal signal shows a smooth velocity curve with a narrow velocity range at each time point.

• The VTI is measured by tracing the modal velocity (middle of the dense signal)

Advantage of the Continuity Equation over Peak velocity Pressure gradient

More reliable in coexisting AR which results in increased stroke volume.

Pitfalls of the Continuity Equation

Depends on the variability in each of the three measurements (variability in acquiring the data / measuring the recorded data).

When subaortic flow velocities are abnormal e.g. dynamic subaortic obstruction or a subaortic membrane, SV calculations at this site are not accurate.

Pitfalls of the Continuity Equation

observed changes in valve area with changes in flow rate.

When LV function is normal , the effects of flow rate are minimal and valve area calculations are accurate.

This effect may be significant in concurrent LV dysfunction d/t decreased cusp opening and a small effective orifice area even though severe stenosis is not present.

Low-flow low-gradient AS

• Effective orifice area ˂1.0 cm2.

• Mean pressure gradient ˂ 30–40 mmHg

Clinical situation where we get Low-flow low-gradient AS are:• AS with LV systolic dysfunction with low LVEF (˂50%):

• Severe AS causing LV syst. dysfunction. • Moderate AS with another cause of LV syst. dysfunction (e.g. MI or a primary

cardiomyopathy).

• AS with small hypertrophied left ventricle with a low stroke volume.• These patients have normal LVEF ( ≥50% ).

Low Dose Dobutamine Stress Echo

• Measures

• contractile response• changes in aortic velocity, MG, and valve area as flow rate

increases.

• Helps to find out • Severe AS causing LV syst. dysfunction• Moderate AS with another cause of LV dysfunction

Low Dose Dobutamine Stress Echo- Protocol

• Low dose - 2.5 or 5 µg/kg/min with an incremental increase of 5µg/kg in the infusion every 3–5 min to a maximum dose of 10–20 mg/kg/min.

• The infusion is stopped-• As soon as a positive result is obtained • Heart rate begins to rise more than 10–20 bpm over baseline or

exceeds 100 bpm.• Symptoms, blood pressure fall, or significant arrhythmias.


RESULTS• AS velocity, MG, valve area, and EF preferably at each stage (to

judge reliability of measurements)

• Severe AS → AS jet ≥ 4.0 m/s or a MG ≥ 40 mmHg provided that valve area does not exceed 1.0 cm2 at any flow rate.

• An increase in valve area to a final valve area of >1.0 cm2 → AS not severe.


• Absence of contractile reserve (failure to increase SV or EF by 20%)

• predictor of a high surgical mortality• poor long-term outcome.

• If no contractile reserve (no change in SV) and no change in AVA and mean AVG, then we can’t comment on severity of AS

• If doubt remains then TEE may be necessary to assess AV anatomy (3D may be very useful)

Effects of concurrent conditions on assessment of severity

Effect of LVH

• LVH commonly accompanies AS• either as a consequence of valve obstruction• or due to chronic hypertension.

• Ventricular hypertrophy typically results in a small ventricular cavity with thick walls and diastolic dysfunction.

• particularly in elderly women with AS.

Effect of LVH

• The small LV ejects a small SV→• even when severe stenosis is present, the AS velocity and mean gradient may be

lower.

• Continuity-equation valve area is accurate in this situation.

• Many women with small LV size also have a small body size (and LVOT diameter), so indexing valve area to body size may be helpful.

Effect of Hypertension

• HTN accompanies AS in 35–45% of patients.

• The presence of HTN primarily affect flow and gradients but less AVA measurements.

• Thus, control of BP is recommended before echo evaluation, whenever possible.

Effect of Aortic Regurgitation

• About 80% of adults with AS also have AR.

• When mild or moderate in severity• measures of AS severity are not significantly affected.

• When severe AR accompanies AS →• transaortic volume flow rate, Vmax, and MG will be higher than expected for a given valve area.

• The combination of moderate AS and moderate AR is consistent with severe combined valve disease.

Effect of Mitral valve disease

• With severe MR, transaortic flow rate may be low resulting in a low gradient even when severe AS is present.

• Second, a high-velocity MR jet may be mistaken for the AS.

• Mitral stenosis (MS) may result in low cardiac output and, therefore, low-flow low-gradient AS.

M Mode- Aortic Stenosis

Maximal aortic cusp separation (MACS)Vertical distance between right CC and non CC during systole

DeMaria A N et al. Circulation.Suppl II. 58:232,1978

Cardiac Catheterization to assess severity

When to do Cath Study in AS

When noninvasive tests are inconclusive; or

When clinical and echo findings are discrepant.

Comparing pressure gradients calculated fromdoppler velocities to pressures measured at cardiac catheterization

Transvalvular gradient Measurement - techniques

AO & peripheral artery (femoral sheath) showing peripheral amplification of 20 mmHg

Left ventricular (LV) and right femoral artery (RFA) pressure tracings in a patient who presented with exertional syncope owing to aortic stenosis

demonstrating the significant time delay for the pressure waveform to reach the RFA.

Carabello Sign…


Pressure recovery

Across a narrowed valve there conversion of potential energy to kinetic energy → high velocity and a drop in pressure.

Distal to the orifice, flow decelerates again. Kinetic energy will be reconverted into potential energy with a corresponding increase in pressure, the so-called Pressure Recovery.


Pressure recovery

• Doppler derived gradients- using CW doppler @ vena contracta

• Catheter derived gradients- downstream vena contracta- pressure recovery.

Gradient derived by cath is lower than doppler derived gradient


Pressure recovery• Stenosis severity

underestimated- “recovered” pressure, rather than vena contracta pressure, is rec


Pressure recoveryExaggerated in….

Smaller aortaStiffer aortaHypertension

Aortic stenosis with its abrupt widening from the small orifice to the larger aorta has an unfavorable geometry for PR.

Aortic Valve area Calculation by cath

Gorlin equation can be used to calculate AVA from pressure gradients, independent of CO.

Hakki formula:

Low Gradient low flow AS- Cath Study

Dobutamine Stress Test

Role of CT……..

Role of CT……..

• The degree of valve calcification measured by MDCT is directly related to valve area.

• Calcium score >1,650 AU indicates of severe AS (sensitivity and specificity ≥ 80%).

• Advantage: • not influenced by hemodynamic conditions, may thus be particularly

useful in the presence of low LV outflow states.• Helpful before TAVR

• Disadvantage: • exposure to ionizing radiation, which limits serial short-time interval

follow-up.• Cost – effectiveness.

Role of MRI……..

Role of MRI……..

• Allows direct planimetry of aortic valve orifice at spatial resolution.

• Additionally , can quantify myocardial fibrosis and thus help in prognostication.

But unrealistic due high cost.

Take Home Message……..

• Transthoracic Echocardiographic evaluation is the mainstay in evaluation of the severity of AS.

• When using Cath study, we should be highly cautious about the technical errors.

THANK YOU..

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Evaluation of severity of as