AS/AR Flashcards
Bicuspid aortic valve (fused right and left coronary cusps)
Name three nonvalvular types of LVOTO
- hypertrophic obstructive cardiomyopathy (HOCM)
- membranous subaortic stenosis (subAS)
- supravalvular stenosis
***all occur less frequently than valvular AS
What percentage of the population has BAV?
What is the pathophysiology that leads to accelerated AS?
- 1% of the general population
- more common in men
- congenitally malformed leaflets –> turbulent flow –> accelerated progression of fibrosis –> stenosis
What are signs/symptoms of advanced stages of AS?
- reduced CO
- right-sided heart failure
- A-fib
- pulmonary congestion
- pulmonary hypertension
- peripheral edema
- cachexia
- hepatomegaly
- functional TR
- fatigue
What is an early finding on Echo of AS prior to calcification of the valve?
- M-mode
- eccentric line of diastolic closure
What is the current recommendation for monitoring in:
- severe, asymptomatic AS
TTE every 6-12 months
What percentage of patients with BAV will have first degree family members with BAV?
9%
What is the pathophysiology of AS?
- increased LVOTO
- LV hypertrophy
- attempts to normalize wall stress
- increasing afterload mismatch leads to:
- diastolic dysfunction
- decreased diastolic filling time
- increased LV filling pressures (leads to dyspnea)
- increasing LV hypertrophy can lead to a reduced cavity size –> reduced stroke volume
What are common associations with unicuspid aortic valve (leading to early AS)?
- ascending aortic abnormalities
- coarctation of aorta
- coronary anomalies
- PDA
What is the next best step in an asymptomatic patient with severe AS (AVA 0.47cm2, PV 4.8 m/s)?
- O2 consumption treadmill testing (Cardiopulmonary exercise testing - CPET)
- evolution of completely asymptomatic AS is not benign
- useful in clinical decision making for asymptomatic AS
- development of symptoms or decrease in BP at peak exercise would suggest a more advanced disease state
What percentage of patients > 75 years of age have AS?
Aortic sclerosis?
- 2.6%
- 33%
In Aortic Stenosis:
- What is the average reduction in aortic valve area (AVA) per year?
- What is the average increase in aortic valve gradient (AVG) per year?
- 0.1 cm2
- 7-10 mmHg
What is the mortality risk associated with severe, symptomatic AS?
50% at 2-3 years (if valve replacement not done)
What is one mutation that predisposes to rapid progression of AS in BAV’s?
mutation in the NOTCH 1 genome
What are risk factors in the rate of progression of AS?
- hyperlipidemia
- DM (possibly)
- metabolic syndrome
- smoking
- hypertension
- renal dysfunction
- increasing age
- male gender
- Pagets disease
What are the three most common causes of AS?
- Calcification of a trileaflet valve
- Secondary calcificaiton of a congenital bicuspid aortic valve
- Rheumatic valve disease
What abnormality is always associated with rheumatic AS? Why?
mitral valve abnormalities
- because mitral valve is the initial site of rheumatic involvement in nearly all patients
What are causes of supravalvular AS? (rare in adults)
- Homozygous type II hyperlipoproteinemia
- Ochronosis with alkaptonuria
- Radiation therapy
- Renal failure (accelerated leaflet calcification)
What is the most common initial symptom in adults with severe AS?
What is the best way to determine if this is present?
- decreased exercise capacity
- ask patient’s to compare his/her current exercise capacity with a specific time point (typically 1 year prior)
What is the key physical examination finding in adults with AS?
- systolic ejection-type murmur
- loudest at the cardiac base
- radiates either to the carotids or to the LV apex
- PE is critical for detection of disease but not determination of severity
What are common auscultation findings in severe AS?
- Grade 3-4 murmur (with a thrill)
- Single or paradoxically split second heart sound
-
“Pulsus parvus et tardus”
- Carotid pulse that is decreased in amplitute and delayed in occurrence
What is the anatomical valve abnormality of Congenital bicuspid aortic valves (in order)?
- Left-Right fusion (70-80%)
- Right-NCC fusion (20-30%)
With CAVD, this is a strong predictor of disease progression and clinical outcome?
severity of leaflet calcification
What are the key measures of AS severity?
- Peak aortic velocity
- Mean transaortic gradient
How is peak aortic velocity measured in AS?
- continuous-wave Doppler US examined from multiple acoustic windows
- to ensure stenosis severity is not underestimated
How is mean (transaortic) gradient measured in the evaluation of AS?
- Calculated by averaging instantaneous gradients over the systolic ejection period using the Bernoulli equation
- Bernoulli equation: ΔPmax = 4vmax2
What is the Bernoulli Equation?
- ΔPmax = 4vmax2
- ΔPmax = 4 (vmax2 – vproximal2)
- proximal velocity should be included in equation when > 1.0 m/s
In what AS setting is AVA useful?
How is AVA calculated?
- low-flow states
- continuity equation
Define the continuity equation.
AVA = (CSALVOT x VTILVOT) / VTIAS
AVA = (CSALVOT x VLVOT) / VMAX
- simplifed version utilizing maximum velocities instead of VTI’s
-
CSALVOT = 3.14 (D/2)2 = 0.785 x D2
- D is measured at the basal insertion of the aortic leaflets from inner edge to inner edge of the aortic annulus
What is the recommended periodic monitoring for asymptomatic AS?
- Mild –> every 3-5 years
- Moderate –> every 1-2 years
- Severe –> every 6-12 months
How are valve gradients calculated in the assessment of AS?
- continuous wave (CW) Doppler with Doppler beam aligned as parallel as possible to flow
- valve gradients are calculated using the maximum valvular velocity (Vmax)
What are ways in which stenosis is underestimated in Echo evaluation of AS?
misalignment of the US beam
How many positions should be obtained in the doppler assessment of AS?
What positions are preferred?
- at least 3 windows (to obtain highest possible velocity)
- LV apex
- subcostal
- RUSB
- suprasternal notch
What is the Doppler pattern in valvular AS?
- high-velocity flow beginning with AV opening
- convex outward rising shape, peaking in mid systole, ending at AV closure
How is subaortic velocity (LVOT) obtained?
- PW doppler from the LV apex
- recording should be traced during systole using the modal (highest amplitude) velocities on spectral display
- View should be obtained from:
- anteriorly angulated four-chamber view (five-chamber view)
- apical long-axis view
What PHT correlates with:
- mild AR
- moderate AR
- severe AR
- Mild AR –> PHT > 500 ms
- Moderate AR –> PHT 200-500 ms
- Severe AR –> PHT < 200 ms
- in some cases as the LV remodels and LV diastolic pressure decreases, a patient may have a PHT > 200 ms despite having severe chronic AR
What are common associations with subaortic stenosis?
- PDA
- Pulmonary stenosis
- VSD
- Coarctation of the aorta
- diagonsed with pulsed doppler of abdominal aorta
What is the best view for VC in the evalutation of AR?
- Parasternal long axis view
- best axial resolution
- Not Apical long axis view
- VC will be typically parallel to the US beam, reducing the spatial resolution
What is the next step in management of a 30 year old female with newly diagnosed subaortic stenosis (PG 44 mmHg) and concomitant moderate aortic regurgitation, non-calcified aortic valve, LVEF 57%, asymptomatic?
- TEE with careful inspection of pulmonary valve (pulmonary stenosis) and pulmonary artery (PDA)
Define how the continuity equation is utilized for regurgitant lesions?
What is the equation for this?
- According to the continuity equation, the flow converging to the valve must be equal to the flow through the valve
- As blood acclerates toward a narrowing orifice (in this case the regurgitant orifice), the spatial distribution of points in which the fluid has the same velocity (Isovelocity surface) is approximated by a hemisphere = Proximal isovelocity surface area (PISA)
- Isovelocity flow = regurgitant flow
- Isovelocity area x aliasing velocity = EROA x Regurgitant velocity
- EROA = PISA area x aliasing velocity / regurgitant velocity
What is the value of the suprasternal notch window in the evaluation of AR?
- Doppler evaluation of flow reversals in the descending thoracic aorta
- holodiastolic flow reversal is suggestive of severe AR
What is the Bernoulli (simplified) equation?
When should it be used?
- AV pressure gradient (in mmHg) = 4Vmax2 (m/sec)
- Equation should only be used when the maximum valve velocity is much greater than ( > 2.5 or more times) the peak subaortic velocity
Why may maximum instantaneous AVG (which comes from Vmax) be higher than the peak-to-peak AVG?
- Because the peak of aortic pressure often occurs later than the peak of LV pressure
- “tardus and parvus”
- Holodiastolic flow reversal in the descending aorta suggestive of severe AR
- PW doppler from the suprasternal notch window
- can also be taken from the subcostal view of the abdominal aorta
When may you see the use of velocity to calculate gradients in patients with AS lead to overestimation of AS severity?
- small aortic root size –> overestimation of AS severity
- Pressure-Recovery Phenomenon
Why are nonimaging probes used in the evaluation of AS?
- smaller footprint
- allows US interrogation from a deeper position (better penetrance)
- better alignment of Doppler signal with direction of blood flow
What may result in elevated aortic valve velocities in the absence of significant valvular stenosis?
How can this be clarified?
- High cardiac output
- anemia, fever, subvalvular AS, significant vavlular regurgitation
- Dimensionless Index “DI”
How is LVOT measured?
- PLAX on 2D Echocardiogram
- LVOT diameter measured in mid-systole
- perpendicular to flow
- 3-5 mm below the hinge points of the valve
What are causes of reduced flow states in severe AS?
- LV dysfunction
- RV dysfunction
- Small LV cavity size (from increased LV hypertrophy)
- MR
- TR
What does a dobutamine echo help to distinguish in AS patients?
- Pseudo-severe AS
- Truly severe AS
Define “low-flow, low-gradient severe AS” effects with Dobutamine Echo?
- Increase in flow –> gradients rise
- AVA index remains low because the LVOT and valve velocities increase proportionally.
Describe “pseudo-severe” AS and the changes that take place during Dobutamine Echo.
- Pseudo-severe stenosis
- if the gradient is moderate and during infusion
- and it does not increase substantially while the valve area increases
- LV dysfunction may not be a result of the AS, and the AS may be less than severe
What is the grading scale for AS: Indexed AVA (cm2/m2)
- Mild > 0.85 cm2/m2
- Moderate 0.60-0.85 cm2/m2
- Severe < 0.60 cm2/m2
What is the largest potential error in derivation of orifice size?
- errors in measuring LVOT diameter
- because it is squared in the calculation
What test is not indicated in paradoxical LF-LG severe AS?
What is the pathophysiology in these patients?
- Dobutamine Echo
- Normal LVEF but small cavity size –> low stroke volume
What can be done to avoid the error created with the assumption that the LVOT is circular (and not elliptical)?
- Direct planimetry of the LVOT
- 3D TEE
- MSCT
What is one major limitation of the standard continuity equation in the evaluation of AS?
- Assumption of a circular outflow tract shape
- Because LVOT is more/less elliptical, area may be underestimated and as a consequence flow and AVA will be understeimated as well
What is the preferred site for LVOT measurement?
What may occur, preventing this measurement or location?
How can you fix this problem?
- Aortic valve annulus
- only when a smooth velocity curve can be obtained
- Flow acceleration may occur at the annulus
- Move the sample volume apically by 0.5-1.0 cm
- to obtain a laminar flow curve without spectral dispersion
What etiologies lead to LF-LG severe AS?
- Low LVEF
- Normal LVEF (paradoxical LF-LG severe AS)
What are some limitations to indexing AVA in LF-LG AS evaluations?
- Obesity
- current algorithms for defining body size (BSA) don’t reflect normal AVA in obese patients
- AVA does not increase with excess body weight
What are positive results of Dobutamine Echo in LF-LG AS evaluation?
- Increase in effective AVA > 1.0 cm2 –> AS not severe
- Severe stenosis suggested by:
- AS velocity > 4 m/s or MG > 30-40 mmHg
- provided AVA does not exceed 1.0 cm2
- AS velocity > 4 m/s or MG > 30-40 mmHg
- Absence of contractile reserve (failure to increase SV by > 20%)
- predictor of high surgical mortality and poor long-term outcome
- although valve replacement may improve LV function and outcome even in this subgroup
What percentage of patients with BAV will have an abnormally dilated aortic root?
50%
What is one subgroup of patients with LF-LG AS who carries a very high mortality risk?
- Absence of contractile reserve (failure to increase SV by > 20%) with Dobutamine Echo
- predictor of high surgical mortality and poor long-term outcome although valve replacement may improve LV function and outcome even in this subgroup
- “Projected AVA” can be calculated
- calculated AVA if SV would have increased and been in normal range
This can influence peak velocity/mean gradients in AS evaluation and should be measured/recorded in every examination?
BP / Hypertension
What is valvuloarterial impedance (Zva)?
- Ratio of the estimated LV systolic pressure (sum of arterial pressure and AVGm) to the SVI
- Parameter reflects the total LV afterload
- results from peripheral arterial resistance in addition to the valve stenosis
- Zva is elevated in patients with uncontrolled HTN
- Elevated Zva –> adverse outcomes
What are factors that may influence SV during DSE evaluation of AS?
- severity of AS
- afterload mismatch
- concomitant change in MR
What is useful in patients with low LVEF, low-flow, low-gradient AS?
- Low-dose (up to 20 microgram/kg/min) DSE
- class II recommendation
- to assess AS severity and evaluate contractile reserve
When should contrast be utilized in evaluation of Low LVEF, LF-LG, severe AS patients?
two consecutive segments
or
< 80% myocardium is visible
What is a major factor that may result in decreased gradients in AS evaluation?
- Hypertension
- increase in LV afterload –> decrease in LV outflow and transvalvular gradients
What is the formula for projected AVA?
Q = SV/LV ejection time
Describe the algorithm for Classical LF-LG AS
Describe the algorithm for Paradoxical LFLG AS
Define Paradoxical LFLG AS
- LVEF > 50%
- AVA < 1.0 cm2
- AVAI < 0.6 cm2/m2
- MG < 40 mmHg
- SVI < 35 ml/m2
Define Clasical LFLG AS
- LVEF < 50%
- AVA < 1.0 cm2
- AVAI < 0.6 cm2/m2
- MG < 40 mmHg
- SVI < 35 ml/m2
What differentiates Classical and Pardoxical LFLG AS?
- LVEF
- Clasical LVEF < 50%
- Paradoxical LVEF > 50%
What is the first step in the evaluation of Classical LFLG AS?
What is considered a positive test/result?
- DSE
- Increased SV (flow reserve) > 20%
- True Severe (AVA < 1, MG > 40)
- Pseudo-severe (AVA +/- 1, MG < 40)
In the evaluation of Classical LFLG AS, with DSE resulting in increased SV (flow reserve) ≥ 20% leading to indeterminant results, what is the next step?
HF therapy
In the evaluation of Classical LFLG AS, with DSE resulting in increased SV (flow reserve) < 20%, what is the next step?
- MDCT Calcium score
- True Severe AS if Ca score:
- male > 2000 (or Ca load > 500)
- femal > 1200 (or Ca load > 300)
- True Severe AS if Ca score: