1. What causes AI?
    • -Congenital valve abnormality (bicuspid)
    • -Calcification/sclerosis with age
    • -Inflammatory disease: Rheumatic, lupus, ankylosing spondylitis
    • -Myxomatous degeneration
    • -Endocarditis
    • -Idiopathic Aortic Root/annulus dilation
    • -Aortic Root abnormalities eg: aortic aneurysm, dissection, coarctation
    • -Other: syphyllis, Phen-fen, infiltrative disease (amyloid or glycogen storage), sarcoidosis, hemodosis
  2. What is Myxomatous valve disease?
    • Connective tissue disorder >
    • -cusps become thickened, elongated, and redundant
    • -sagging cusp in short axis can appear as a cylindrical mass
    • -flail cusp may flutter in LVOT during diastole or appear as flutter on m-mode closure line
    • -primarily associated with MVP
  3. What is the most common cause of acute AI?
  4. What is Endocarditis?
    • Infection of endocardium leading to vegetation on leaflets or perforation of valvular tissue
    • most commonly occurs with staff infections, IV drug users, prosthetic valves
  5. What is the most common cause of chronic AI?
    Idiopathic AoR dilation and annulus dilation
  6. What is coarctation?
    congenital stenosis of aorta >> narrows near insertion of ductus arteriosus (pre or post ductal)
  7. What other conditions can cause AoR abnormalities?
    • -Chronic hypertension
    • -Marfans
    • =inherited connective tissue disorder, affects eyes, skeleton, CV system >> valve dilation, dissection
    • -Cystic medial necrosis
    • =disorder of large arteries >> focal degeneration of elastic tissue and muscle in the media, associated with aneurysm, dissection, and Marfans
    • -syphyllis >> uncommon extensive calcification of dilated root
    • -Phen-phen >> thickened MV/AV and insufficiency
    • -Infiltrative diseases >> amyloid or glycogen storage, sarcoidosis, hemodosis
  8. What are the common Echo findings of AI?
    • -Diastolic jet in LVOT
    • -incomplete closure of cusps
    • -anatomic abnormality of valve or root
    • -initial hyperkinesis of LV walls due to volume overload (may see early diastolic dip of IVS)
    • -progressive dilation of LV due to volume overload >> increased LVEDP
    • -eventual decrease in LV systolic function
    • -fine fluttering and damping of AMVL
    • -premature closure of MV and opening of AV on m-mode seen in acute/severe AI
    • -raised fibrotic lesion on septum or AMVL may be seen with chronic AI
  9. What are the signs/sx of AI?
    • -DOE
    • -fatigue
    • -palpitations (LV dilation, irritible wall > arrythmias)
    • -angina
    • -dizziness
    • -syncope (uncommon)
    • -signs of CHF = syncope, cough, SOB, crackles, paroxysmal nocturnal dyspnea
    • -signs of RHF = JVD, ascites, hepatomegaly, peripheral edema
    • -wide pulse pressure (decreased DBP < 50% SBP)
  10. How is AI treated?
    • -CHF treatment = afterload reduction therapy
    • -valve replacement when indicated
    • >>LVID > 5.5cm and FS < 25%, or significant change in LV size/function
  11. What kind of murmur/s may be heard with AI?
    • -Diastolic high pitched blowing decrescendo murmur at LSB
    • -severe AI >> Austin Flint murmur = low pitch diastolic rumble at apex
  12. What are possible EKG finding with AI?
    • -LVH due to increased mass (dilation)
    • -LAE
  13. What does the cath pressure tracing show in AI?
    significantly decreased aortic pressure with increased LV pressure in diastole, loss of dicrotic notch
  14. What kind of pulse might be felt in cases of significant/severe AI?
    pulsus bisferiens/biphasic = two strong systolic peaks, caused by midsystolic pressure dip (decrease in the lateral wall pressure of the ascending aorta)
  15. How can AI severity be measured/calculated using 2D color flow, and what are the criteria?
    • 1. Jet area/LVOT area * 100
    • > 25-64% = moderate AI (ASE)

    • trace LVOT and ROA (regurgitant orifice area) in PSSAX
    • OR trace ROA and calculate LVOT (.785 * LVOTd2 )

    • 2. Jet (vena contracta) diameter/LVOT diameter
    • > 25-64% = moderate AI

    • 3. Vena Contracta (neck of jet) width
    • > .3-.6 cm = moderate AI (OTTO)

    4. Presence of a PISA = moderate to severe AI

    *Color flow often eyeballed, not specifically measured (jet <1/4 LVOT = mild)
  16. How is AI evaluated in CW Doppler?
    -Intensity of signal

    -slope of signal or PHT* (.29*decel time)

    • >500msec = mild
    • 200-500 = moderate
    • <200 = severe

    *correlates poorly to jet area (poor R-value)
  17. How is AI evaluated in PW Doppler?
    1. Calculate regurgitant fraction:

    • RV= Aortic SV - Mitral SV (total SV - forward SV)
    • > 30-59cc/ml = moderate AI

    • RF = Aortic SV - Mitral SV/Aortic SV *100
    • > 30-49% = moderate AI

    • EROAcm2 = RV/VTIRJ
    • > .10-.29 = moderate AI

    * remember SV = CSA * VTI

    2. PW of MV inflow shows reduced decel time or steep slope in significant AI due to increased LVEDP
  18. How can AI be distinguished from MS when using a Pedoff probe?
    AI starts with AV closure, MS starts with MV opening
  19. Color and PW Doppler may reveal flow reversal where/when?
    with severe AI:

    1. Holodiastolic flow reversal in descending aorta (2D SSN)

    2. flow reversal in abdominal aorta
  20. Evaluation of valvular regurgitation involve assessment of what specific factors?
    • -valve anatomy
    • -severity of the regurgitation
    • -chamber enlargement due to volume overload
    • -ventricular function
    • -degree of pulmonary hypertension
Card Set
Aortic Insufficiency