Aortic Valve Disease



Aortic Valve Disease


Brian R. Lindman

Suzanne V. Arnold






Severity of Aortic Stenosis









Table 9-1 Severity of Aortic Stenosis








































  Aortic sclerosis Mild Moderate Severe
Aortic jet velocity (m/s) ≤2.5 2.6–2.9 3.0–4.0 >4.0
Mean gradient (mmHg) <20 (<30a) 20–40b (30–50a) >40b (>50a)
AVA (cm2) >1.5 1.0–1.5 <1.0
Indexed AVA (cm2/m2) >0.85 0.60–0.85 <0.6
Velocity ratio >0.50 0.25–0.50 <0.25
aESC guidelines.
bAHA/ACC guidelines.
AVA, aortic valve area.
Adapted from Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22(1):1–23, with permission from Elsevier.



Severity of Aortic Regurgitation









Table 9-2 Severity of Aortic Regurgitation
















































































  Mild Moderate Severe
Structural parameters
LA size Normala Normal or dilated Usually dilatedb
Aortic leaflets Normal or abnormal Normal or abnormal Abnormal/flail, or wide coaptation defect
Doppler parameters
Jet width in LVOT—color flowc Small in central jets Intermediate Large in central jets; variable in eccentric jets
Jet density—CW Incomplete or faint Dense Dense
Jet deceleration rate—CW (PHT, ms)d Slow >500 Medium 500–200 Steep <200
Diastolic flow reversal in descending aorta—PW Brief, early diastolic reversal Intermediate Prominent holodiastolic reversal
Quantitative parameterse
VC width, cmc <0.3 0.3–0.60 >0.6
Jet width/LVOT width, %c <25 25–45 46–64 ≥65
Jet CSA/LVOT CSA,%c <5 5–20 21–59 ≥60
R Vol, mL/beat <30 30–44 45–59 ≥60
RF, % <30 30–39 40–49 ≥50
EROA, cm2 <0.10 0.10–0.19 0.20–0.29 ≥0.30
aUnless there are other reasons for LV dilation. Normal 2D measurements: LV minor axis ≤2.8 cm/m2, LV end-diastolic volumes ≤82 mL/m2.
bException: Would be acute AR, in which chambers have not had time to dilate.
cAt a Nyquist limit of 50 to 60 cm/s.
dPHT is shortened with increasing LV diastolic pressure and vasodilator therapy, and may be lengthened in chronic adaptation to severe AR.
eQuantitative parameters can subclassify the moderate regurgitation group into mild-to-moderate and moderate-to-severe regurgitation as shown.
LA, left atrium; LVOT, left ventricular outflow tract; CW, continuous wave; PHT, pressure half-time; PW, pulsed wave; VC, vena contracta; CSA, cross-sectional area; R Vol, regurgitant volume; RF, regurgitant fraction; EROA, effective regurgitant orifice area.
Adapted from Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22(1):1–23, with permission from Elsevier.



Anatomy



  • Leaflets



    • The normal aortic valve (AoV) is trileaflet.


    • A bicuspid valve occurs in 1% to 2% of the population, unicuspid and quadricuspid valves are rare. The abnormal leaflet number may cause inherent valvular stenosis and regurgitation.


  • Annulus



    • The leaflets form semi-lunar attachments at the annulus forming a “crown”-like interlocking of ventricular and arterial tissue.


    • They also attach at the sinotubular junction.


  • Sinuses of Valsalva



    • As the proximal aortic root meets the left ventricular outlet there are three sinuses that bulge out and form the supporting structure for the corresponding aortic valve leaflets.


    • The sinuses and corresponding valve leaflet (or cusp) are named according to the origin of the coronary arteries.


    • Two sinuses give rise to coronary arteries (right and left) while the third, lying immediately adjacent to the mitral valve, does not (non).


  • Sinotubular junction



    • The place where the superior portion of the sinuses narrows and joins the proximal tubular portion of the ascending aorta.


Aortic Stenosis



  • Pathophysiology

    The pathophysiology for aortic stenosis (AS) involves both the valve and the ventricular adaptation to the stenosis. Within the valve, there is growing evidence for an active biologic process that begins much like the formation of an atherosclerotic plaque and eventually leads to calcified bone formation.




    image



  • Etiology and morphology









    Table 9-3 Etiology and Morphology of Aortic Valve Disease



















    Etiology Prevalence, presentation, and associated features
    Normal

    • Asymptomatic
    Calcific/Degenerative

    • Most common cause in the United States
    • Presents in seventh to ninth decades (mean age mid-70s)
    • Risk factors similar to CAD
    • Calcification leading to stenosis affects both trileaflet and bicuspid valves
    Bicuspid

    • 1–2% of population (the most common congenital lesion)
    • Presents in sixth to eighth decades (mean age mid-late 60s)
    • More prone to endocarditis than trileaflet valves
    • Associated with aortopathies (i.e., dissection, aneurysm, coarctation)
    Rheumatic

    • Most common cause worldwide, much less common in the United States
    • Presents in third to fifth decades
    • Almost always accompanied by mitral valve involvement
    Adapted from Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16(7):777–802, with permission from Elsevier.






    Figure 9-1. Typical appearance of aortic valve in diastole (row A) and systole (row B) suggestive of underlying etiology. (Adapted from C. Otto, Principles of Echocardiography, 2007.)



  • Echocardiographic assessment of AS



    • 2D assessment



      • Leaflets



        • Motion of the valve



          • Aortic valve area (AVA) can be planimetered in the parasternal short-axis view—this is most often only possible in TEE studies using a side-by-side zoomed short-axis 2D image with corresponding color Doppler image to ensure that correct margins are drawn.


          • Ensure that your visual estimate of valve orifice area corresponds with other measurements; if, for example, the valve appears to open fairly well but measured gradients are considerably higher than you would expect, there may be a supra/subvalvular obstruction. Conversely if the valve appears calcified and stenotic; however, the recorded gradients are lower than expected consider: (1) Doppler acquisition not parallel to flow, (2) low flow, low gradient, reduced LVEF AS, (3) low flow, low gradient, normal LVEF AS (discussed later).


          • Eccentric closure, doming, and prolapse of the valve in the parasternal long-axis view suggest the presence of a bicuspid valve.


        • Bicuspid aortic valves (BAVs)—most commonly due to fusion of the right and left coronary cusps (∼80%) or fusion of the right and non-coronary cusps (∼20%); bicuspid valves have an elliptical orifice during systole; they can easily be mistaken for trileaflet valves during diastole, particularly when a raphe is present. Leaflet doming is present because of restricted leaflet motion. Valvular regurgitation is usually highly eccentric and posteriorly directed (Fig. 9-2E). There may be associated aortic abnormalities (dilation of aortic root, coarctation).

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Oct 20, 2016 | Posted by in CARDIOLOGY | Comments Off on Aortic Valve Disease

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