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← Section II · Valvular Heart Disease
II.A

Aortic Valve, Aorta, and Subvalvular Outflow Tract

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Notes

Aortic stenosis - severity (2020 ACC/AHA)

MildModerateSevere
Peak aortic jet velocity (m/s)2.6 – 2.93.0 – 3.9≥ 4.0
Mean gradient (mmHg)< 2020 – 39≥ 40
AVA (cm²)> 1.51.1 – 1.5≤ 1.0
Indexed AVA (cm²/m²)> 0.900.61 – 0.90≤ 0.60
VTI ratio (DVI)> 0.500.26 – 0.50≤ 0.25

AV calcium score (CT): severe if ≥ 2000 AU (men) / ≥ 1200 AU (women).

Continuity equation for AVA

AVA=CSALVOT×VTILVOTVTIAV=0.785×dLVOT2×VTILVOTVTIAV\mathrm{AVA} = \frac{\mathrm{CSA_{LVOT}} \times \mathrm{VTI_{LVOT}}}{\mathrm{VTI_{AV}}} = \frac{0.785 \times d_{LVOT}^2 \times \mathrm{VTI_{LVOT}}}{\mathrm{VTI_{AV}}}

  • LVOT diameter measured in mid-systole, inner-to-inner edge, from PLAX.
  • LVOT PW sample volume placed 2–3 mm proximal to the stenotic jet (an aortic valve closing click indicates proximity to the valve).
  • Dimensionless velocity index (DVI) = VTI_LVOT / VTI_AV. Flow-independent; severe AS if ≤ 0.25.

Bernoulli & gradients

  • Peak gradient: ΔP_max = 4 · V_max² (simplified Bernoulli).
  • Use full form ΔP = 4(v₂² − v₁²) when v₁ (LVOT) > 1.5 m/s or v₂ (AV) < 3 m/s.
  • Mean gradient ≈ 0.6 × peak, or 2.4 × V_max². Compare Doppler and cath using MEAN gradients only.

Peak vs cath gradients & pressure recovery

  • Doppler measures gradient at the vena contracta (maximum).
  • Catheter measures gradient a few cm downstream, after pressure recovery.
  • Cath gradient < Doppler gradient by the amount of pressure recovery.
  • Pressure recovery clinically significant with moderate–severe AS (AVA ~0.9–1.2 cm²) and a small ascending aorta (< 30 mm).

Flow dependence

  • Gradients depend on flow rate: ↑ with anxiety, exercise, hyperdynamic state, AI (↑ SV); ↓ with sedation, hypovolemia, MR, low EF, LVH, small cavity.
  • AVA is less flow-dependent.
  • Eccentric jets read higher.
  • Use the highest velocity - obtain right-parasternal (Pedoff) window; ensure the flow duration matches the apical trace (to avoid MR/TR misidentification).

Low-flow / low-gradient AS

Classic (low EF < 50 %)

  • Use low-dose dobutamine stress echo to distinguish:
    • True-severe AS: V > 4 m/s or MG > 40 mmHg WITH AVA < 1 cm² at peak dose.
    • Pseudo-severe AS: AVA increases with augmented flow to > 1 cm².
  • Contractile (flow) reserve = ≥ 20 % increase in SV; absent flow reserve → 30-day mortality after SAVR 8–30 % (vs 5–8 % if reserve).
  • Give contrast if ≥ 2 consecutive segments cannot be seen.

Paradoxical (EF ≥ 50 %, AVA ≤ 1 cm², MG < 40)

  • Low stroke-volume index (< 35 mL/m²), often in older HTN female with small LV cavity, LVH, high SVR.
  • CT calcium scoring useful when unable to reconcile.

Discordant grading

  • Severe by V/gradient but AVA > 1.0 cm²: overestimated LVOT diameter; PW too close to valve; high transaortic flow (mod-sev AR, high-output state, large body).
  • Severe by AVA but V ≤ 4 m/s and MG < 40: underestimated LVOT diameter; PW too far from valve; low flow (low EF, small LV, mod-sev MR/MS, high SVR).

Bicuspid aortic valve (BAV)

  • Two leaflets; often with a raphe (fused commissure); best identified in systole.
  • Systolic "doming" appearance; diastolic sagging.
  • Most common phenotype: fusion of RCC + LCC (~70 %) → anterior + posterior leaflets, closure line horizontal.
  • Less common: fusion of RCC + NCC (20–30 %) → closure line runs A-P; greater aortic dilation risk.
  • Associations: coarctation and intracranial aneurysms.
  • Aortopathy: root ≥ 40 mm or ascending aorta ≥ 37 mm is abnormal; growth 0.4–0.6 mm/year.
  • ~20–30 % of first-degree relatives have BAV.
  • Complete raphe → more AR and more root dilation.

Rheumatic AV disease

  • Commissural fusion, systolic doming, leaflet thickening; triangular AV opening in systole. Usually with concurrent mitral involvement.

Senile / degenerative calcific AS

  • Fibrocalcific masses on the aortic side of leaflets, increased stiffness without commissural fusion.
  • Calcific shadowing/reverberations limit imaging - avoid direct planimetry.

Aortic regurgitation - severity (severe AR criteria)

  • Vena contracta width > 0.6 cm (PLAX).
  • Color jet width > 65 % of LVOT.
  • Regurgitant volume > 60 mL.
  • Regurgitant fraction > 50 %.
  • EROA > 0.30 cm².
  • Pressure half-time < 200 ms (steep CW deceleration slope).
  • Holodiastolic flow reversal in the proximal descending or abdominal aorta.

Acute vs chronic AR - echo distinction

Acute severe AR:

  • LV often not dilated (no time to remodel).
  • Early mitral valve closure (before QRS) - rapid equalization of LV and aortic diastolic pressure.
  • Early AV opening.
  • Fluttering of AMVL on M-mode (high-frequency).
  • Soft S1, early diastolic rumble.

Chronic AR:

  • Progressive LV dilation.
  • Increased E-point septal separation on M-mode.
  • Wide pulse pressure.

Causes of AR

  • Chronic primary valve: BAV, rheumatic, calcific degenerative, systemic inflammatory (RA, SLE, ankylosing spondylitis).
  • Aortic disease: Marfan/familial aneurysm, hypertensive, inflammatory (giant cell, Takayasu).
  • Acute: endocarditis, aortic dissection, blunt chest trauma.
  • Most common cause of mild AR: hypertension.

AR - regurgitant volume calculation

  • PISA-based: Regurgitant flow = 2πr² × V_aliasing; EROA = flow / V_AR peak; RVol = EROA × VTI_AR.
  • Volumetric: RVol = SV_LVOT − SV_mitral (if MV competent); RF = RVol / SV_LVOT.
  • Do NOT use LVOT-derived SV for CO in significant AR (it's inflated); use MV inflow SV instead.

Aortic dissection (echo)

  • TEE sensitivity for dissection > 95 % (≈ CTA/MRA).
  • Blind spot on TEE: distal ascending aorta / proximal arch (air).
  • Intimal flap has independent motion oscillating with the cardiac cycle; reverberation/mirror-image artifacts move parallel to the aortic wall (no independent motion).
  • Fluid around the descending aorta on TEE = pleural effusion, not pericardial.

Subaortic membrane

  • Fibrous ring in LVOT below the aortic valve.
  • Associations: VSD, PDA, coarctation, Shone complex, BAV, persistent left SVC, PS.
  • Rule out associated anomalies (TEE).
  • Progressive AR (jet damage to aortic leaflets) → indication for surgery when at least moderate.
  • Non-calcified AV → repair favored over replacement in the young.

Supravalvular AS

  • Classic in Williams syndrome (elastin gene deletion) - often with supravalvular PS and peripheral pulmonary artery stenosis.
  • Familial hypercholesterolemia may also give supra-aortic obstruction.

Follow-up cadence

  • Severe asymptomatic AS not for AVR: repeat TTE every 6–12 months.

Cards

  • clozeII.A-001
    Severe aortic stenosis by 2020 ACC/AHA: peak jet velocity ≥ 4.0 m/s, mean gradient ≥ 40 mmHg, AVA ≤ 1.0 cm².
  • basicII.A-002
    State the continuity equation for aortic valve area.
    AVA = (CSA_LVOT × VTI_LVOT) / VTI_AV = (0.785 × d²_LVOT × VTI_LVOT) / VTI_AV.
  • basicII.A-003
    Where in the cardiac cycle and where anatomically is the LVOT diameter measured?
    Mid-systole, inner-edge to inner-edge, in the parasternal long-axis view, at the annulus level.
  • basicII.A-004
    Where do you place the LVOT PW sample volume for the continuity equation?
    Approximately 2–3 mm proximal to the aortic valve. Presence of an aortic valve closing click on the trace indicates the sample volume is very close to the valve.
  • clozeII.A-005
    The dimensionless velocity index (VTI_LVOT / VTI_AV) is severe AS if ≤ 0.25. Its main advantage is being flow-independent.
  • basicII.A-006
    When must you use the full form of the Bernoulli equation for AS?
    When LVOT velocity (v₁) > 1.5 m/s, or when AV velocity (v₂) < 3 m/s. Then ΔP = 4(v₂² − v₁²) rather than the simplified 4v².
  • basicII.A-007
    How do the AS mean gradient and peak gradient relate?
    Mean gradient ≈ 0.6 × peak gradient (or approximately 2.4 × V_max²).
  • basicII.A-008
    When comparing Doppler and cath gradients in AS, which values should be compared?
    Mean gradients only. Peak-to-peak cath gradient has no physiologic equivalent on Doppler. Peak instantaneous cath and Doppler gradients also do not occur at the same instant.
  • basicII.A-009
    Why is the catheter-measured gradient typically LOWER than the Doppler mean gradient in AS?
    Pressure recovery — downstream of the vena contracta some kinetic energy is reconverted to pressure. Doppler measures at the vena contracta (maximum gradient); cath measures a few cm downstream after recovery.
  • basicII.A-010
    In which patients is pressure recovery clinically significant?
    Moderate–severe AS with AVA ~0.9–1.2 cm² and a SMALL ascending aorta (diameter < 30 mm). Smaller aorta → more recovery → lower cath gradient / larger effective valve area.
  • basicII.A-011
    Give three factors that transiently INCREASE the transaortic gradient without a true change in AS severity.
    Anxiety, exercise, hyperdynamic state, concomitant AI, tachycardia — anything that raises stroke volume or transvalvular flow.
  • basicII.A-012
    Give three factors that transiently DECREASE the transaortic gradient in true severe AS.
    Sedation, hypovolemia, significant MR, low EF, LVH with small cavity — anything reducing forward stroke volume.
  • basicII.A-013
    How is 'true-severe' distinguished from 'pseudo-severe' AS in low-flow, low-gradient AS with reduced EF?
    Low-dose dobutamine stress echo. True-severe: peak velocity > 4 m/s (or MG > 40) with AVA < 1 cm² at peak dose. Pseudo-severe: AVA increases > 1 cm² with augmented flow.
  • basicII.A-014
    What defines contractile (flow) reserve on dobutamine stress echo in AS?
    ≥ 20 % increase in stroke volume. Absent flow reserve is a poor prognostic sign — 30-day SAVR mortality 8–30 % vs 5–8 % with reserve.
  • basicII.A-015
    Define paradoxical low-flow, low-gradient severe AS.
    EF ≥ 50 %, AVA ≤ 1 cm², but mean gradient < 40 mmHg, with low stroke-volume index < 35 mL/m². Typical patient: elderly, hypertensive, female, small LV cavity, LVH, high SVR.
  • basicII.A-016
    When should you use aortic valve calcium scoring (CT) to confirm severe AS?
    When there is discordance between AVA and gradient/velocity — especially in paradoxical low-flow low-gradient AS. Severe if calcium ≥ 2000 AU (men) or ≥ 1200 AU (women).
  • basicII.A-017
    How often should severe asymptomatic AS be re-imaged if not going for AVR?
    TTE every 6–12 months.
  • basicII.A-018
    What is a 'raphe' in a bicuspid aortic valve? Why is systole the key phase for identification?
    A raphe is a fibrous ridge from congenital fusion of two commissures. A BAV with a raphe can appear trileaflet in diastole; only systole (with maximal opening) reveals only two functional cusps.
  • basicII.A-019
    What is the most common bicuspid aortic valve phenotype?
    Fusion of the right coronary and left coronary cusps (RCC–LCC) — anterior + posterior leaflets, horizontal closure line. Present in ~70 %.
  • basicII.A-020
    Which BAV fusion pattern carries the highest risk of aortic dilation?
    RCC–NCC fusion (20–30 %). Associated with greater aortopathy than the more common RCC–LCC fusion.
  • basicII.A-021
    Two classic non-aortic-valve associations with a bicuspid aortic valve?
    Coarctation of the aorta and intracranial (berry) aneurysms. Also: ~20–30 % of first-degree relatives have BAV.
  • basicII.A-022
    What defines BAV aortopathy dimensions?
    Aortic root ≥ 40 mm or ascending aorta ≥ 37 mm are considered abnormal. Growth rate typically 0.4–0.6 mm/year.
  • basicII.A-023
    How does rheumatic AV disease look on echo?
    Commissural fusion with systolic doming and leaflet thickening; TRIANGULAR AV opening in systole. Usually with concurrent mitral involvement.
  • basicII.A-024
    How does senile calcific AS differ from rheumatic AS morphologically?
    Senile: fibrocalcific masses on the aortic side of leaflets with increased stiffness but NO commissural fusion. Rheumatic: commissural fusion. Avoid direct planimetry with heavy calcification.
  • basicII.A-025
    List the criteria for SEVERE aortic regurgitation.
    Vena contracta > 0.6 cm; color jet width > 65% of LVOT; regurgitant volume > 60 mL; regurgitant fraction > 50%; EROA > 0.30 cm²; PHT < 200 ms; holodiastolic flow reversal in the proximal abdominal/descending aorta.
  • basicII.A-026
    Why is a short pressure half-time (PHT < 200 ms) a marker of severe AR?
    Rapid decline of the CW velocity slope reflects rapid equalization of aortic and LV diastolic pressures — indicating large regurgitant volume across the valve.
  • basicII.A-027
    Give three echo findings distinguishing ACUTE from chronic severe AR.
    Acute: LV NOT dilated (no time to remodel); EARLY mitral valve closure before QRS; early AV opening; fluttering of AMVL. Chronic: LV dilation, wide pulse pressure, increased E-point septal separation.
  • basicII.A-028
    Name three causes of ACUTE severe AR.
    Endocarditis, aortic dissection, blunt chest trauma.
  • basicII.A-029
    What is the most common cause of MILD aortic regurgitation?
    Hypertension.
  • basicII.A-030
    Which volumetric measurement should NOT be used for cardiac output in significant AR, and what should be used instead?
    Do NOT use LVOT stroke volume (falsely elevated by regurgitant volume). Use mitral inflow-derived stroke volume (if the mitral valve is competent).
  • basicII.A-031
    Where is aortic flow reversal best interrogated on TTE for AR grading?
    The suprasternal notch view of the descending aorta (or the subcostal window for the proximal abdominal aorta). Holodiastolic flow reversal = severe AR (analogous to Duroziez's sign).
  • basicII.A-032
    List three causes of false-positive holodiastolic aortic flow reversal (mimics severe AR).
    Patent ductus arteriosus (PDA); left-arm arteriovenous fistula (e.g., dialysis fistula); stiff vasculature from long-standing hypertension.
  • basicII.A-033
    Estimating LV end-diastolic pressure from an AR CW jet — how?
    LVEDP = Aortic end-diastolic BP − end-diastolic pressure gradient (from CW AR jet, using Bernoulli: 4 × [end-diastolic velocity]²). Normal LVEDP ≈ 10–12 mmHg.
  • basicII.A-034
    List three conditions commonly associated with a subaortic membrane.
    VSD, PDA, coarctation, Shone complex, bicuspid AV, persistent left SVC, and pulmonic valve stenosis.
  • basicII.A-035
    When is subaortic membrane resection indicated?
    When at least moderate aortic regurgitation is present (jet damage progresses); in a young patient with a non-calcified AV, repair is favored over replacement.
  • basicII.A-036
    What congenital syndrome typically causes supravalvular aortic stenosis?
    Williams syndrome (elastin gene deletion, 7q11.23). Often with supravalvular PS and peripheral pulmonary artery stenosis.
  • basicII.A-037
    On TEE, what is the aortic 'blind spot'?
    The distal ascending aorta and proximal aortic arch — obscured by air in the trachea and mainstem bronchi lying between the esophagus and that aortic segment.
  • basicII.A-038
    How do you distinguish a real intimal flap from an artifact in a dilated ascending aorta?
    An intimal flap has independent oscillatory motion during the cardiac cycle. Reverberation/mirror-image artifacts move parallel to the aortic wall with no independent motion, and often have no rapid oscillatory motion.
  • basicII.A-039
    What is 'Duroziez's sign' and what echo finding is it equivalent to?
    Duroziez's = to-and-fro murmur over the femoral artery in severe AR. Echo analogue: holodiastolic reversal of flow in the proximal descending / abdominal aorta.
  • basicII.A-040
    Where should the CW cursor be placed to obtain the highest AS velocity, and what maneuver may help?
    Multiple windows: apical five-chamber, right parasternal (Pedoff nonimaging probe), and suprasternal. Use the highest velocity. Match systolic duration to the apical trace to avoid confusing MR/TR jets with AS.
  • basicII.A-041
    What is valvulo-arterial impedance (Zva) and what does an elevated value indicate?
    Zva = (mean gradient + systolic BP) / stroke volume index. It combines valvular and vascular load; a low value (< 3.5 mmHg·m²·mL⁻¹) is normal, high values suggest increased global LV afterload and worse prognosis in AS.
  • basicII.A-042
    State the 2020 ACC/AHA valve staging system for aortic stenosis (Stages A–D).
    Stage A: at risk (BAV or aortic sclerosis). Stage B: progressive (mild-moderate). Stage C1: asymptomatic severe with preserved LVEF. Stage C2: asymptomatic severe with LVEF < 50%. Stage D1: symptomatic high-gradient severe. Stage D2: symptomatic low-flow/low-gradient severe with reduced EF. Stage D3: symptomatic paradoxical low-flow/low-gradient severe with preserved EF.
  • basicII.A-043
    State the 2020 ACC/AHA Class I indications for AVR in severe aortic stenosis.
    1) Symptomatic severe high-gradient AS (D1). 2) Asymptomatic severe AS with LVEF < 50% (C2). 3) Severe AS undergoing other cardiac surgery.
  • basicII.A-044
    What thresholds define 'very severe' aortic stenosis?
    Peak aortic velocity ≥ 5 m/s (or mean gradient ≥ 60 mmHg). Class IIa indication for AVR even if asymptomatic.
  • basicII.A-045
    Give three imaging findings that trigger consideration of AVR in asymptomatic severe AS despite preserved EF.
    1) Abnormal exercise test (BP drop or symptoms). 2) Rapid progression (velocity increase ≥ 0.3 m/s per year). 3) Very severe AS (velocity ≥ 5 m/s). 4) Elevated BNP.
  • basicII.A-046
    Which 2020 ACC/AHA aortic root threshold triggers surgery in BAV patients?
    Aortic root or ascending aorta > 5.5 cm (any patient). > 5.0 cm if additional risk factors (family history of aortic dissection, growth > 5 mm/year, or coarctation). > 4.5 cm if undergoing AVR for AS/AR.
  • basicII.A-047
    Estimating LV end-diastolic pressure from an AR jet — write the formula.
    LVEDP = Diastolic BP − 4 × (end-diastolic AR jet velocity)². Normal LVEDP ~ 10–12 mmHg.
  • basicII.A-048
    Describe the CW jet contour of chronic vs acute severe AR.
    Chronic severe AR: relatively slow deceleration (PHT > 200 ms early on, shortens as chronicity progresses). Acute severe AR: steep deceleration slope (PHT < 200 ms) with rapid diastolic equalization of aortic and LV pressures.
  • basicII.A-049
    Indications for AVR in chronic severe aortic regurgitation?
    Class I: 1) Symptomatic severe AR. 2) Asymptomatic severe AR with LVEF ≤ 55%. 3) Severe AR undergoing other cardiac surgery. Class IIa: LVESD > 50 mm (or LVESDi > 25 mm/m²).
  • basicII.A-050
    How does isometric handgrip affect an AR murmur?
    Handgrip increases afterload (SVR) → increases regurgitant gradient → INTENSIFIES the AR murmur. Also intensifies MR. Reduces HCM and MVP murmurs.
  • basicII.A-051
    How does amyl nitrite inhalation affect an AR vs an AS murmur?
    Amyl nitrite reduces preload and afterload. AR murmur DECREASES (less regurgitant gradient). AS murmur INCREASES (higher gradient across the valve from tachycardia). HCM murmur INCREASES (unmasks obstruction).
  • basicII.A-052
    State the ACC/AHA aortic root replacement thresholds for Marfan syndrome.
    Aortic root or ascending aorta > 5.0 cm in Marfan. > 4.5 cm if additional risk factors (family history of dissection, growth > 3 mm/year). Loeys-Dietz uses even earlier thresholds.
  • basicII.A-053
    How do you differentiate a suprasternal Doppler descending aortic flow pattern of severe AR from coarctation?
    Severe AR: holodiastolic reversal in the descending aorta, but normal systolic ejection contour proximally. Coarctation: sustained antegrade DIASTOLIC flow (saw-tooth pattern) distal to the narrowing with elevated peak systolic velocity, and diastolic run-off is preserved (not reversed).
  • basicII.A-054
    Which finding differentiates severe from moderate AR by CW deceleration slope?
    Pressure half-time (PHT). PHT < 200 ms → severe AR. PHT > 500 ms → mild AR. Reflects rate of LV/aortic diastolic pressure equalization.
  • basicII.A-055
    When is the aortic root measured for growth surveillance?
    At the sinus of Valsalva in end-diastole (leading-edge to leading-edge, PLAX). Serial studies to detect growth > 3 mm/year (Marfan/genetic aortopathy) or > 5 mm/year (BAV).