Download - Aortic stenosis
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