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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).