1. Imaging Conference: Aortic REgurgitation
September 16, 2009
Ali R. Rahimi, MD MPH

2. Patient A: What is the Story?

3. Patient B: What is the Story ?

4. Patient B:

5. Patient A:

6. Patient A:

7. Patient A:

8. Patient B:

9. Patient B:

10. Patient B:

11. Patient B:

12. Patient B:

13. Diagnosis Patient A Patient B
48 yo M PMH cocaine induced aortic arch dissection s/p repair c/b recurrent VRE AV (Bicuspid) Endocarditis and 2-3+ AR
Mobile vegetation on LVOT side of Posterior Leaflet
Patient B
47 yo M PMH AV (Bicuspid) Endocarditis c/b 4+ AR
Two separate, mobile, moderate-sized vegetations (0.8cm x 0.5cm, 0.6cm x 0.6cm) located on the two leaflets of the aortic valve which prolapse across the LVOT during systole (larger vegetation on posterior leaflet)

14. Aortic Regurgitation Diastolic reflux of blood from Aorta  LV
Incidence of clinically significant AR increases with age
Typical peak in 4th to 6th decade of life
More common in men than women
Prevalence 4.9% in Framingham Heart Study
Congenital or Acquired
Caused by abnormalities of aortic root or AV

15. ≥ 2mm dilation at sinotubular junction can cause AR
Etiology
Dilation of Aortic Root and Annulus
Hypertension
Marfan Syndrome
Syphilitic Aortitis
Cystic Medial Necrosis
Aortic Dissection
Osteogenesis Imperfecta
Ankylosing Spondylitis
Ehlers-Danlos Syndrome
≥ 2mm dilation at sinotubular junction can cause AR

16. Etiology Aortic Valve Other Bicuspid Aortic Valve
Rheumatic Heart Disease
Degenerative Calcific AV Disease
Infective Endocarditis
Other
Trauma
Membranous Subaortic Stenosis
Rheumatoid Arthritis
Fenfluramine and Dexfenfluramine
Deterioration of AVR Bioprosthesis

17. Acute Aortic Regurgitation
Most commonly due to endocarditis, aortic dissection, or blunt chest trauma
Sudden large regurgitant volume imposed on LV
Abrupt increase in LVEDV  Rapid increase LVEDP & LAP
Inability of ventricle to develop compensatory chamber dilatation acutely results in a decrease in forward SV
Congestive Heart Failure, Myocardial Ischemia and/or Cardiogenic Shock

18. Chronic Aortic Regurgitation
Early Compensated
Enlarged chamber size  ↑ afterload  hypertrophy of LV which preserves compliance  normal filling pressures
LVH  ↑ LV mass  normal LV vol/mass ratio & EF
Progressive LV dilation and systolic HTN  ↑ wall stress and vol/mass ratio
↑ wall stress eventually leads to overt LV dysfunction.
Decompensated
LV systolic dysfunction accompanied by decreased LV diastolic compliance due to hypertrophy and fibrosis
Leads to high filling pressures and CHF symptoms
Exertional dyspnea common; angina can occur due to reduced coronary flow reserve with predominantly systolic coronary flow
Courtesy: Ali Mahajerin, MD

19. Stages
Bekerdjian R, et al. Circulation 2005; 112:

20. Physical Exam - Auscultation
A2 often soft/absent, P2 normal
S3 if LV function severely depressed
High frequency decrescendo diastolic murmur over the 3rd or 4th intercostal space at left sternal border
Best heard sitting up, leaning forward at end expiration
Austin Flint murmur: mid-to-late diastolic apical rumble, possibly due to vibration of anterior mitral leaflet as it is struck by a posteriorly directed AR jet.

21. Physical Exam - Peripheral Findings
Corrigan’s pulse – bounding “waterhammer” carotid pulse
deMusset’s sign – head bob with each heart beat
Mueller’s sign – systolic pulsation of uvula
Traube’s sign – pistol shot pulse over the femoral artery
Duroziez’s sign – systolic and diastolic bruits heard when femoral artery partially compressed
Becker’s sign – visible pulsations of retinal arteries and pupils
Hill’s sign – popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg
Mayne’s sign – more than 15 mmHg decrease in diastolic blood pressure with arm elevation
Rosenbach’s sign – systolic pulsations of the liver
Gerhard’s sign – systolic pulsations of the spleen

22. Diagnosis and Initial Evaluation
Class 1
Echo: confirm presence and severity of acute or chronic AR. (Level of Evidence: B)
Echo: diagnosis and assessment of the cause of chronic AR (including valve morphology and aortic root size and morphology) and for assessment of LV hypertrophy, dimension (or volume), and systolic function. (Level of Evidence: B)
Echo: in patients with an enlarged aortic root to assess regurgitation and the severity of aortic dilatation. (Level of Evidence: B)
Echo: periodic re-evaluation of LV size and function in asymptomatic patients with severe AR. (Level of Evidence: B)
Echo: re-evaluate mild, moderate, or severe AR in patients with new or changing symptoms. (Level of Evidence: B)
**Radionuclide angiography or MRI: initial and serial assessment of LV volume and function at rest in patients with AR AND suboptimal echocardiograms. (Level of Evidence: B)
Bonow, R. O. et al. J Am Coll Cardiol 2008;52:e1-e142

23. M-Mode Imaging Aortic jet across anterior MV creates
High-frequency fluttering requiring rapid sampling rate
Increased duration between E and A peaks
Increased distance between the maximal anterior motion of MV in early diastole (E point) and the most posterior motion of the IVS (e.g., increased E-point septal separation)
Acute AR  premature closure of MV
Rapidly increasing LVEDP

24. M-Mode Imaging

25. 2-Dimensional Imaging Focus on AV and Root
Endocarditis
Dissection
Dilation
Perivalvular leaks around aortic prosthesis
Assessment of LV size and function
Response to volume overload

26. 2-Dimensional Imaging AVR - Dilated Aortic Root
Marfans - Dilated Aortic Root

27. 2-Dimensional and Color Flow
Aortic Regurgitation due to AV Endocarditis

28. 2-Dimensional and Color Flow
AV Prosthesis: Aortic Root Abscess and Perivalvular Regurgitation

29. 2-Dimensional and Color Flow
LV Dilated-Spherical due to Chronic Severe Aortic Regurgitation

30. Doppler Imaging: Color Flow
Critical since 2-D may at times be “unremarkable” despite severe aortic regurgitation
Most common technique to visualize AR
Sensitivity > 95%
False negatives can occur in tachycardia with mild AR
Frame rate allows only a few diastolic frames to be displayed
Can be overcome by using CW -- has a higher sampling rate
Specificity ~100%
Detects even trivial AR
Less than1% of normal subjects under age 40
10-20% of patients greater than age 60
Vast majority of individuals greater than age 80

31. Doppler Imaging: Color Flow
Composed of 3 distinct segments:
Proximal flow convergence zone = area of flow acceleration into the orifice
Vena contracta = narrowest and highest velocity region of the jet at or just downstream from the orifice
The jet itself occurs distal to the orifice in the LV cavity
Measurement of the jet area or penetration into the LV cavity is not accurate in assessing AR severity, though:
If jet width/LVOT width < 25%  specific for mild AR
If jet width/LVOT width > 65%  specific for severe AR
This works best when regurgitant orifice is relatively round in shape.

32. Doppler Imaging: Vena Contracta
The narrowest diameter of flow stream
Independent of volume flow rate and driving pressure, relatively unaffected by instrument settings
Narrow range of values though, so care needed to obtain optimal images. Ideal sample is:
Perpendicular to jet width
In zoom mode
Narrow sector
Minimum depth
For AR, vena contracta can be measured in parasternal long-axis view preferably in zoom mode

33. Doppler Imaging: Vena Contracta
Vena contracta width of ≥ 6 mm correlates with severe AR (sensitivity 95%, specificity 90%)
Vena contracta width of < 3 mm specific for mild AR
Enriquez-Sarano M, et al. NEJM 2004; 351:

34. Doppler Imaging: Color Flow
Mild Moderate Severe

35. Doppler Imaging: Color Flow
Jet Width/LVOT Width < 25%
Mild MR
Jet Width/LVOT Width > 65%
Severe AR
Bekerdjian R, et al. Circulation 2005; 112:

36. Doppler Imaging: Color Flow
Limitations as indicator for AR severity:
Eccentric jets entrained along LV wall
Jet is 3-D thus need multiple planes
Changes in instrument gain, color scale, transducer frequency and wall filters will affect AR appearance, independent of severity
ROA in chronic AR usually decreases during diastole
Thus temporal variability
Tendency to overestimate since visualized jet area would reflect peak rather than mean orifice area

37. Doppler Imaging: Pulsed Wave
Relies on demonstration of turbulent flow in LVOT on ventricular side of AV
Due to high AR velocity, aliasing occurs, with prescence of turbulence establishing the diagnosis
Highly sensitive but requires methodical search for AR
False-Positive in setting of Mitral Stenosis or Prosthetic MV with turbulent diastolic flow
Assumption the AR is centrally located and can be tracked toward apex
Holodiastolic flow reversal in descending aorta correlated with severe AR

38. 2-Dimensional and Doppler Imaging
Eccentric AR Jet
Displacement of Anterior MV

39. Doppler Imaging: Continuous Wave
Due to high velocity AR jet, CW necessary for contour of the envelope to be recorded
Density of jet ≈ volume of regurgitation
Approximation of number of RBCs being sampled
Velocity of AR jet and Rate of Deceleration of retrograde flow can be measured
AR results in increased antegrade volume flow rate across AV, which is reflected in an increase in the antegrade velocity across the valve
The greater the severity of AR, the higher the antegrade velocity across the AV
Must also consider possibility of coexisting AS
Helpful to distinguish AR from Mitral Stenosis Jet
Based on velocity and contour of jet

40. Doppler Imaging: Continuous Wave
Compare AR signal to Antegrade Flow
Weak  mild
Equal  severe AR
Antegrade

41. Doppler Imaging: CW and PHT
AR velocity reflects pressure gradient between aorta and LV throughout diastole
Early diastole – gradient is the highest with velocity 4-6 m/sec, depending on BP
Diastole progresses – gradient diminishes as aortic pressure decreases and LV pressure increases
Mild AR – compliant LV allows a slow and modest increase in LVEDP and Ao EDP is maintained throughout
AR velocity remains high and CW envelope appears flat
Severe AR – increasing LVEDP and more rapid decrease Ao pressure leads to a more rapid decel of AR velocity

42. Doppler Imaging: CW and PHT
Flat slope (P1/2 > 500 msec)  mild AR
Steep slope (P1/2 < 200 msec)  severe AR
Limitations of pressure half-time assessment:
Aortic compliance, BP, and LV size/compliance will affect measures
Pressure half-time sensitive to chronicity of AR
Acute AR leads to much shorter values than chronic AR when LV is dilated with increased compliance
Thus, a rapid P1/2 is more indicative of acuity than severity
Pressure half-time varies with SVR
Vasodilators may shorten the pressure half-time even as the aortic regurgitant fraction improves.

43. Doppler Imaging: CW and PHT
Acute AR due to Aortic Dissection
Chronic AR due to Ca AV disease

44. Doppler Imaging: Regurgitant Volume and Fraction
Can compare flow through AV versus MV or PV
Stroke volume at any valve annulus is derived as the product of CSA and TVI of flow at the annulus
In the absence of regurgitation, SV determinations at different sites should be equal
In the presence of regurgitation of one valve, without any intracardiac shunt the flow through the affected valve is larger than the other valves
RV is the difference between the two flows
RF = RV/ Forward SV through the regurgitant valve

45. Doppler Imaging: Regurgitant Volume and Fraction
Regurgitant Volume (fraction):
Mild: < 30cc (< 30%)
Mild-Moderate: 30-44cc (30-39%)
Mod-Severe: 45-59cc (40-49%)
Severe: ≥60cc (≥50%)
Limitations:
Assumes normal flow through comparison valve
Cannot be used in presence of shunts
Sensitive to small measurement errors (measurement errors of the radius and tracing the VTI)

46. Summary:
Zoghbi WA, et al. JASE 2003; 16:

47. Serial Testing by Echocardiography
If chronic nature of lesion uncertain and no initial surgical indication, should repeat exam and echo within 2-3 months after initial evaluation
Asx, mild AR, little/no LV dilation, normal LV systolic function: see yearly, echo q2-3 years
Asx, severe AR, significant LV dilation (LVEDD > 60 mm), normal LV fx: echo q6-12 months
Asx, severe AR, severe LV dilation (LVEDD > 70 mm), normal LV fx: echo q4-6 months.
Repeat echo for onset of symptoms, equivocal history of changing symptoms or exercise tolerance, or clinical findings to suggest worsening regurgitation or progressive LV dilatation.
Bonow RO, et al. J Am Coll Cardiol, 2008; 52:1-142

48. Bonow, R. O. et al. J Am Coll Cardiol 2008;52:e1-e142
Management Strategy for Patients With Chronic Severe Aortic Regurgitation
Bonow, R. O. et al. J Am Coll Cardiol 2008;52:e1-e142
Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply.

49. Thank You