Fuad Farooq

Aortic valve is composed of three cusps of equal size, each of which is surrounded by a sinus

Cusps are separated by three commissures and supported by a fibrous anulus

Each cusp is crescent shaped and capable of opening fully to allow unimpeded forward flow, then closing tightly to prevent regurgitation

Free edge of each cusp curves upward from the commissure and forms a slight thickening at the tip or midpoint, called the Arantius nodule When the valve closes, the three nodes meet in the

center, allowing coaptation to occur along three lines that radiate out from this center point

Overlap of valve tissue along the lines of closure produces a tight seal and prevents backflow during diastole

When viewed from a 2D echo parasternal short-axis projection, these three lines of closure are seen as an “inverted Mercedes Benz sign”

Normal leaflets are so delicate that they are hard to visualize, generally an indication that they are morphologically normal

Behind each cusp is its associated Valsalva sinus

Sinuses represent outpunching in the aortic root directly behind each cusp

Function to support the cusps during systole and provide a reservoir of blood to augment coronary artery flow during diastole

Left and right coronary arteries arise from the left and right sinuses, respectively, and are associated with the left and right aortic cusps

Third, or noncoronary sinus, is posterior and rightward, just above the base of the interatrial septum, and is associated with the noncoronary aortic cusp

RCC

LCC

NCC

LA

LAA

RA

RVOT

RV

The area of a normal aortic valve is 3 to 4 cm2

Normal opening generally produces 2 cm of leaflet separation Maintained throughout the cardiac cycle

until low cardiac output or LVOT obstruction

The most common form of aortic stenosis is caused by degenerative valvular calcification Leaflets are thickened and calcified Decreasing systolic opening

Other causes include bicuspid aortic valve and rheumatic heart disease

Establishing the diagnosisQuantifying severityAssessing left ventricular function Identify concomitant valvular

abnormalities

Visualizes the entire aortic valve structure

Helpful in identifying noncalcific as well as calcific aortic stenosis

Degree of valvular calcification, the size of the aortic anulus and the supravalvular ascending aorta, and the presence of secondary subvalvular obstruction are easily evaluated

Useful for determining the degree of LV hypertrophy (wall thickness and mass), LA enlargement, ventricular function, and the integrity of the other valves

Cusps are thickened and showed restricted mobility

Their position during systole is no longer parallel to the aortic walls, and the edges are often seen to point toward the center of the aorta

In severe cases, a nearly total lack of mobility may be present and the anatomy may become so distorted that identification of the individual cusps is impossible

Unfortunately only give qualitative assessment and attempts to quantify the degree of stenosis based on two-dimensional echocardiographic findings have been unsuccessful

Rheumatic Heart disease

Unicuspid Aortic Valve

Bicuspid Aortic Valve

Bicuspid Aortic Valve

Bicuspid Aortic Valve

Bicuspid Aortic Valve

Quardicuspid Aortic Valve

Subaortic Membrane

Subaortic Membrane

Hemodynamic assessment of severity of aortic stenosis determined with Doppler echo is based on

Peak aortic flow velocity Mean pressure gradient Aortic valve area LVOT and aortic valve (AoV) velocity time

integral (VTI) ratio (LVOTVTI : AoV VTI)

Meticulous search for the maximal aortic velocity is essential because all the variables are derived from the peak aortic flow velocity

All available transducer windows should be used to obtain the Doppler signal most parallel with the direction of the jet flow, which provides the highest velocity recording

Failure to achieve parallel alignment will result in underestimation of true velocity

Nonimaging continuous wave Doppler transducer is smaller and thus easier to manipulate between the ribs and suprasternal notch

Peak velocity usually occurs in mid systole

As aortic stenosis worsens, velocity tends to peak later in systole Offering a clue to severity

Blood flow velocity and pressure gradient increase as the valve becomes smaller as long as stroke volume remains constant

Blood flow velocity (v) measured with Doppler echocardiography reliably reflects the pressure gradient according to the modified Bernoulli equation (give peak instantaneous gradients because Doppler measure velocity over time)

Pressure gradient = 4v2

Often obtained by planimetry of the Doppler envelope

Mean gradients can also be calculated as:

Mean gradients = Peak gradient/1.45 + 2

A technically poor recording may fail to display the highest velocity signals Resulting in underestimation of the true

gradient

An inability to align the interrogation angle parallel to flow also results in underestimation

Overestimation of the true pressure gradient is less common but can occur

Result of mistaken identity of the recorded signal e.g., MR jet has a contour similar to that of a jet of severe AS

Avoid by sweeping the transducer back and forth to clearly indicate to the interpreter which jet is which

Another helpful clue involves the timing of the two jets MR is longer in duration, beginning during isovolumic contraction and extending into isovolumic relaxation

Valve gradients are dynamic measurements that vary with

Heart rate Loading conditions Blood pressure Inotropic state

For a given valve area, flow velocity and pressure gradient vary with the change in stroke volume and cardiac output

Cardiac output or stroke volume should be taken into account when the severity of valvular stenosis is determined

Hydraulic formula Flow = Area x Flow

velocity

The continuity equation use law of conservation of mass, states that, “what goes in must come out”

Reliably estimate valve area

For calculating aortic valve area following measurements must be performed

Cross-sectional area of the LVOT Time velocity integral of the LVOT Time velocity integral of the aortic stenosis jet

Continuity equation has advantages over Bernoulli equation for the assessment of aortic stenosis

Not affected by the presence of aortic regurgitation

Continuity equation is relatively unaffected and will allow an accurate estimation of valve area whether the stroke volume is normal or reduced

Potential factors that may contribute to errors include

Image quality Annular calcification (which obscures the true

dimension) Noncircular anulus (which invalidates the

formula) Failure to measure the true diameter

Always preferable

Because VTI or peak velocity ratio is inversely proportional to the area ratio of the LVOT and aortic valve

Also useful in determining the severity of aortic stenosis

Velocity or TVI ratio is independent of any change in stroke volume because the LVOT and aortic valve velocities change proportionally

Also helpful in the presence of aortic regurgitation

Normal Ratio > 0.75

In patients with normal LV systolic function and cardiac output, aortic stenosis is usually severe when

Peak aortic valve velocity is 4 m/s Mean pressure gradient is 40 mm Hg Aortic valve area is less then 1 cm2

LVOTVTI: AoVVTI is 0.25

LV dysfuction with severe AS than two diagnostic possibilities: True anatomically severe aortic stenosis Functionally severe aortic stenosis

(pseudosevere)

Because an aortic valve with mild or moderately severe stenosis may not open fully if the stroke volume is low

Gradual infusion of dobutamine (up to 20 µg/kg/minute) to increase stroke volume may be helpful in differentiating morphologically severe aortic stenosis from a decreased effective stenotic orifice area caused by low cardiac output (pseudosevere aortic stenosis)

Dobutamine infused gradually from 5 µg/kg/minute in 5µg increments every 3 minutes until the LVOT velocity or VTI reaches a normal value i.e., 0.8 to 1.2 m/s or 20 to 25 cm, respectively

Maximal velocity or stroke volume is usually obtained with 15 to 20 µg/kg/minute of dobutamine

In true severe AS, the infusion of dobutamine increases the peak velocity and VTI of both the LVOT and aortic valve proportionally (hence, the LVOTVTI: AoV VTI remains constant)

In pseudosevere AS increase in velocity and VTI of the LVOT is far greater than that of the aortic valve hence, LVOTVTI : AoVVTI increases

LVOT VTI : Aortic valve VTI = 0.22 LVOT VTI : Aortic valve VTI = 0.22

True aortic stenosis

When LV systolic function is abnormal and cardiac output is reduced, aortic stenosis is probably severe if

Aortic valve area by the continuity equation is 1.0 cm2 or less

LVOTVTI :AoVVTI is 0.25 or less

Another most important role of dobutamine infusion in patients who have severe aortic stenosis and a low gradient is to assess inotropic reserve Defined as an increase in stroke volume of more

than 20% with dobutamine

Lack of inotropic reserve with dobutamine portends poor perioperative mortality (50% vs. 7%) if aortic valve replacement is attempted

If Dobutamine infusion is able to increase stroke volume (or LVOT VTI) by 20% or more and the aortic valve area remains 1.0 cm2 or less, aortic valve replacement should be recommended

If no inotropic reserve is demonstrated with dobutamine, aortic valve replacement is still better than no treatment, but the mortality rate is very high

If transthoracic is difficult to perform TEE can be used to measure aortic valve area

by planimetry The number of aortic cusps can be determined

Not routine practice to use TEE to evaluate aortic stenosis

Intraoperatively in AVR for assessment of severity of MR and need for mitral valve replacement

Diastolic function varies in patients with aortic stenosis

Usually have at least a mild degree (grade 1) of diastolic dysfunction

As aortic stenosis progresses to a symptomatic stage, diastolic function also deteriorates to grades 2 and 3