eMedicine Specialties > Cardiology > Valvular Heart Disease

Aortic Regurgitation: Differential Diagnoses & Workup

Author: Stanley S Wang, MD, JD, MPH, Clinical Cardiologist, Austin Heart; Adjunct Assistant Professor of Medicine, University of North Carolina School of Medicine
Contributor Information and Disclosures

Updated: Jun 26, 2007

Differential Diagnoses

Mitral Stenosis
Pulmonic Regurgitation
Tricuspid Stenosis

Workup

Laboratory Studies

No specific laboratory blood tests are required in the workup of AR. However, serologic testing may be required when attempting to distinguish the various etiologies of AR.

Imaging Studies

  • Two-dimensional echocardiography and Doppler
    • M-mode features of AR include the following:
      • Diastolic flutter of the mitral valve (can be both anterior and posterior mitral valve leaflet)
      • Diastolic flutter of the aortic valve
      • Premature closure of the mitral valve (severe AR)
      • Premature opening of the aortic valve (severe elevated LV end-diastolic pressure)
      • Diastolic LV septal fluttering
      • LV volume overload (hyperkinesis of the LV walls with LV dilatation)
      • LVESD (>55 mm indicates poorer surgical outcome)
    • On 2-dimensional echocardiography, look for the following features:
      • Flail aortic valve
      • Dilatation of the sinuses of Valsalva (particularly in patients with Marfan syndrome or bicuspid aortic valve problems)
      • Ascending aortic aneurysm
      • Incomplete closure of the aortic valve cusps on the parasternal short-axis view of the aortic valve
      • High-frequency diastolic fluttering of the anterior leaflet of the mitral valve during diastole
      • Reverse doming of the anterior mitral valve leaflet
      • LV volume overload pattern
      • Measurements of LV end-diastolic and end-systolic dimensions and volumes, shortening fractions, and EFs - Critical in determining the optimal time for valve replacement
    • Color-flow Doppler should be used as follows:
      • Determine the regurgitant jet height and/or LV outflow tract (LVOT) height in the parasternal long-axis view (mild [1+] <25%, moderate [2+] 25-46%, moderately severe [3+] 47-64%, severe [4+] >65%).
      • Determine the regurgitant jet area and/or LVOT area in the parasternal short-axis view of the aortic valve (mild [1+] <20%, moderate [2+] 20-40%, moderately severe [3+] 40-60%, severe [4+] >60%).
      • Proximal acceleration (flow convergence) indicates aortic insufficiency is grade 3+ or 4+.
    • Continuous-wave Doppler should be used as follows:
      • Determine the spectral strength of the regurgitant jet. Grade 1+ produces spectral tracing stain sufficient for detection but is not enough for clear delineation. In grade 2+, complete spectral tracing can barely be seen. In grade 3+, distinct darkening of spectral tracing is visible, but density is less than antegrade flow. Grade 4+ produces dark-stained spectral tracing.
      • Determine the slope of the aortic insufficiency spectral display. In general, steeper slopes indicate more severe aortic insufficiency.
      • Determine the pressure half-time of the aortic insufficiency spectral display. In general, a pressure half-time less than or equal to 300 m/s indicates significant aortic insufficiency.
    • Pulsed-wave Doppler should be used as follows:
      • The pulse-wave mapping technique is used mostly prior to color Doppler.
      • Velocity of more than 1.5 m/s is consistent with marked AR.
      • Mitral inflow has a restrictive filling pattern.
      • Reversal of flow in the descending thoracic aorta and/or abdominal aorta indicates that aortic insufficiency is moderately severe (3+ or 4+). This phenomenon requires careful placement of the sample volume in the descending aorta, distal to the takeoff of the left subclavian artery. The flow in the descending aorta may also be seen with color-flow Doppler, although this method is more prone to error.
  • Radionuclide imaging should be used as follows:
    • Radionuclide angiography findings can help determine the AR regurgitant fraction and the left-to-right ventricular stroke volume ratio. An accurate noninvasive assessment of the severity of AR can be determined if concomitant mitral regurgitation, tricuspid regurgitation, or pulmonary regurgitation is not present.
    • Left-to-right ventricular stroke volume ratio of 2 or more denotes severe AR.
  • MRI or ultrafast CT scanning are as follows:
    • These techniques can provide accurate measurements of regurgitant volumes, ventricular end-systolic and diastolic volumes, ejection fraction, ventricular mass, and the regurgitant orifice.
  • Chest radiograph findings are as follows:
    • In acute AR, little cardiac enlargement may be present, but, in chronic AR, enlargement is marked.
    • Dilatation of the ascending aorta may suggest that aortic root disease is responsible for AR.
    • Pulmonary congestion can be observed in patients who have developed LV dysfunction or in those with acute AR.

Other Tests

  • Electrocardiography findings can reveal the following, although they are not an accurate predictor of the severity of AR:
    • LV hypertrophy
    • Left axis deviation
    • Left atrial enlargement
    • LV volume overload pattern (prominent Q waves in leads I, aVL, and V3 to V6 and relatively small r waves in V1)
    • LV conduction defect (late in disease process)
  • Exercise treadmill testing
    • Assessment of functional capacity and symptomatic responses in patients with a history of equivocal symptoms
    • Evaluation of symptoms and functional capacity before participation in athletic activities

Procedures

  • Cardiac catheterization
    • Indications
      • This should be performed for coronary angiography studies before aortic valve surgery in patients at risk for CAD, including men older than 35 years, premenopausal women older than 35 years with coronary risk factors, and postmenopausal women.
      • It can be used to assess the severity of regurgitation when noninvasive test results are inconclusive or discordant with clinical findings regarding the severity of regurgitation or the need for surgery.
      • Use cardiac catheterization to assess LV function when noninvasive test results are inconclusive or discordant with clinical findings regarding LV dysfunction and the need for surgery in patients suspected of having severe AR.
    • Qualitative assessment (aortic angiogram)
      • In mild AR (1+), a small amount of contrast enters the left ventricle during diastole and clears with each systole.
      • In moderate AR (2+), contrast enters the LV with each diastole, but the LV chamber is less dense than the aorta.
      • In moderately severe AR (3+), the LV chamber is equal in density with the ascending aorta.
      • In severe AR (4+), complete dense opacification of the LV chamber occurs on the first beat and the left ventricle is more densely opacified than the ascending aorta.
    • Simultaneous aortic and LV pressure tracing (signs of severe AR)
      • Wide pulse pressure may be present.
      • Brisk aortic pressure upstroke can be observed.
      • LV diastolic pressure increases rapidly.
      • Near equilibration of aortic and LV pressure occurs at diastole.

Histologic Findings

Histological changes in the left ventricle include fiber hypertrophy and increased interstitial fibrous tissue. In decompensated LV, disruption of the collagen support system and subsequent fiber layer slippage occur. In the subendocardium, evidence of necrosis, replacement fibrosis, and apoptosis is abundant.

Recent data suggest that patients with a wide variety of congenital heart lesions (including bicuspid aortic valves) have underlying distortion of the aortic root. These patients have abnormalities of smooth muscle, elastin, collagen, and ground substance in the ascending aorta. Programmed cell death (apoptosis) of neural crest derivative cells within the proximal aorta has also been demonstrated in patients with bicuspid aortic valve problems.

These aortic abnormalities predispose to progressive proximal aortic dilatation, aneurysm formation, or aortic rupture. These proximal aortic changes occur regardless of the underlying severity of aortic valvular disease and can be observed in patients with nonregurgitant bicuspid valves.

More on Aortic Regurgitation

Overview: Aortic Regurgitation
Differential Diagnoses & Workup: Aortic Regurgitation
Treatment & Medication: Aortic Regurgitation
Follow-up: Aortic Regurgitation
Multimedia: Aortic Regurgitation
References
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References

  1. ACC/AHA guidelines for the management of patients with valvular heart disease. A report of the American College of Cardiology/American Heart Association. Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease). J Am Coll Cardiol. Nov 1998;32(5):1486-588. [Medline].

  2. Bekeredjian R, Grayburn PA. Valvular heart disease: aortic regurgitation. Circulation. Jul 5 2005;112(1):125-34. [Medline].

  3. Bonow RO, Dodd JT, Maron BJ, et al. Long-term serial changes in left ventricular function and reversal of ventricular dilatation after valve replacement for chronic aortic regurgitation. Circulation. Nov 1988;78(5 Pt 1):1108-20. [Medline].

  4. Bonow RO, Nikas D, Elefteriades JA. Valve replacement for regurgitant lesions of the aortic or mitral valve in advanced left ventricular dysfunction. Cardiol Clin. Feb 1995;13(1):73-83, 85. [Medline].

  5. Bonow RO, Picone AL, McIntosh CL, et al. Survival and functional results after valve replacement for aortic regurgitation from 1976 to 1983: impact of preoperative left ventricular function. Circulation. Dec 1985;72(6):1244-56. [Medline].

  6. Bonow RO, Rosing DR, McIntosh CL, et al. The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function. Circulation. Sep 1983;68(3):509-17. [Medline].

  7. Borer JS, Bonow RO. Contemporary approach to aortic and mitral regurgitation. Circulation. Nov 18 2003;108(20):2432-8. [Medline].

  8. Borer JS, Hochreiter C, Herrold EM, et al. Prediction of indications for valve replacement among asymptomatic or minimally symptomatic patients with chronic aortic regurgitation and normal left ventricular performance. Circulation. Feb 17 1998;97(6):525-34. [Medline].

  9. Clark DG, McAnulty JH, Rahimtoola SH. Valve replacement in aortic insufficiency with left ventricular dysfunction. Circulation. Feb 1980;61(2):411-21. [Medline].

  10. Daniel WG, Hood WP, Siart A, et al. Chronic aortic regurgitation: reassessment of the prognostic value of preoperative left ventricular end-systolic dimension and fractional shortening. Circulation. Apr 1985;71(4):669-80. [Medline].

  11. [Best Evidence] Evangelista A, Tornos P, Sambola A, Permanyer-Miralda G, Soler-Soler J. Long-term vasodilator therapy in patients with severe aortic regurgitation. N Engl J Med. Sep 29 2005;353(13):1342-9. [Medline].

  12. Fioretti P, Roelandt J, Sclavo M, et al. Postoperative regression of left ventricular dimensions in aortic insufficiency: a long-term echocardiographic study. J Am Coll Cardiol. Apr 1985;5(4):856-61. [Medline].

  13. Forman R, Firth BG, Barnard MS. Prognostic significance of preoperative left ventricular ejection fraction and valve lesion in patients with aortic valve replacement. Am J Cardiol. Jun 1980;45(6):1120-5. [Medline].

  14. Gaasch WH, Andrias CW, Levine HJ. Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function. Circulation. Nov 1978;58(5):825-36. [Medline].

  15. Gaasch WH, Carroll JD, Levine HJ, Criscitiello MG. Chronic aortic regurgitation: prognostic value of left ventricular end- systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol. Mar 1983;1(3):775-82. [Medline].

  16. Goldschlager N, Pfeifer J, Cohn K, et al. The natural history of aortic regurgitation. A clinical and hemodynamic study. Am J Med. May 1973;54(5):577-88. [Medline].

  17. Greenberg B, Massie B, Bristow JD, et al. Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial. Circulation. Jul 1988;78(1):92-103. [Medline].

  18. Greves J, Rahimtoola SH, McAnulty JH, et al. Preoperative criteria predictive of late survival following valve replacement for severe aortic regurgitation. Am Heart J. Mar 1981;101(3):300-8. [Medline].

  19. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. Jul 1975;56(1):56-64. [Medline].

  20. Hwang MH, Hammermeister KE, Oprian C, et al. Preoperative identification of patients likely to have left ventricular dysfunction after aortic valve replacement. Participants in the Veterans Administration Cooperative Study on Valvular Heart Disease. Circulation. Sep 1989;80(3 Pt 1):I65-76. [Medline].

  21. Kawanishi DT, McKay CR, Chandraratna PA, et al. Cardiovascular response to dynamic exercise in patients with chronic symptomatic mild-to-moderate and severe aortic regurgitation. Circulation. Jan 1986;73(1):62-72. [Medline].

  22. Klodas E, Enriquez-Sarano M, Tajik AJ, et al. Aortic regurgitation complicated by extreme left ventricular dilation: long-term outcome after surgical correction. J Am Coll Cardiol. Mar 1 1996;27(3):670-7. [Medline].

  23. Klodas E, Enriquez-Sarano M, Tajik AJ, et al. Optimizing timing of surgical correction in patients with severe aortic regurgitation: role of symptoms. J Am Coll Cardiol. Sep 1997;30(3):746-52. [Medline].

  24. Krayenbuehl HP, Hess OM, Monrad ES, et al. Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement. Circulation. Apr 1989;79(4):744-55. [Medline].

  25. Kumpuris AG, Quinones MA, Waggoner AD, et al. Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic predictors of normalization of left ventricular dilatation after valve replacement in chronic aortic insufficiency. Am J Cardiol. Apr 1 1982;49(5):1091-100. [Medline].

  26. Lin M, Chiang HT, Lin SL, et al. Vasodilator therapy in chronic asymptomatic aortic regurgitation: enalapril versus hydralazine therapy. J Am Coll Cardiol. Oct 1994;24(4):1046-53. [Medline].

  27. Niwa K, Perloff JK, Bhuta SM, et al. Structural abnormalities of great arterial walls in congenital heart disease: light and electron microscopic analyses. Circulation. Jan 23 2001;103(3):393-400. [Medline]. [Full Text].

  28. Scognamiglio R, Negut C, Palisi M, Fasoli G, Dalla-Volta S. Long-term survival and functional results after aortic valve replacement in asymptomatic patients with chronic severe aortic regurgitation and left ventricular dysfunction. J Am Coll Cardiol. Apr 5 2005;45(7):1025-30. [Medline].

  29. Scognamiglio R, Rahimtoola SH, Fasoli G, et al. Nifedipine in asymptomatic patients with severe aortic regurgitation and normal left ventricular function. N Engl J Med. Sep 15 1994;331(11):689-94. [Medline].

  30. Siemienczuk D, Greenberg B, Morris C, et al. Chronic aortic insufficiency: factors associated with progression to aortic valve replacement. Ann Intern Med. Apr 15 1989;110(8):587-92. [Medline].

  31. Singh JP, Evans JC, Levy D, et al. Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study). Am J Cardiol. Mar 15 1999;83(6):897-902. [Medline].

  32. Stone PH, Clark RD, Goldschlager N, et al. Determinants of prognosis of patients with aortic regurgitation who undergo aortic valve replacement. J Am Coll Cardiol. May 1984;3(5):1118-26. [Medline].

  33. Tornos MP, Olona M, Permanyer-Miralda G, et al. Clinical outcome of severe asymptomatic chronic aortic regurgitation: a long-term prospective follow-up study. Am Heart J. Aug 1995;130(2):333-9. [Medline].

  34. Turina J, Turina M, Rothlin M, Krayenbuehl HP. Improved late survival in patients with chronic aortic regurgitation by earlier operation. Circulation. Sep 1984;70(3 Pt 2):I147-52. [Medline].

  35. Verheul HA, van den Brink RB, Bouma BJ, et al. Analysis of risk factors for excess mortality after aortic valve replacement. J Am Coll Cardiol. Nov 1 1995;26(5):1280-6. [Medline].

  36. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin- angiotensin-aldosterone system. Circulation. Jun 1991;83(6):1849-65. [Medline].

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Further Reading

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Keywords

aortic regurgitation, AR, aortic insufficiency, aortic disease, syphilitic aortitis, rheumatic valvulitis, aortic root disorders, Marfan disease, Marfan syndrome, degeneration of bicuspid aortic valves, bicuspid aortic valve degeneration, regurgitant aortic flow

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Contributor Information and Disclosures

Author

Stanley S Wang, MD, JD, MPH, Clinical Cardiologist, Austin Heart; Adjunct Assistant Professor of Medicine, University of North Carolina School of Medicine
Stanley S Wang, MD, JD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, American Stroke Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Martin Keane, MD, FACC, FAHA, Associate Professor, Cardiovascular Medicine Division, Department of Medicine, University of Pennsylvania School of Medicine
Martin Keane, MD, FACC, FAHA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Echocardiography, Pennsylvania Medical Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, Professor and Executive Vice Chairman, Department of Medicine, University of Texas Health Science Center at San Antonio
Richard A Lange, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, and Association of Subspecialty Professors
Disclosure: Nothing to disclose.

 
 
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