Aortic Insufficiency

  • Noble O. Fowler


The aortic valve is a tricuspid valve, consisting of two coronary cusps and one noncoronary cusp. In the adult, the aortic valve orifice area ranges from 2.6 to 3.5 cm2. Closure of the three cusps in early diastole coincides with the early aortic component (A2) of the second heart sound, S2. When there is a leakage of blood in early diastole, this begins at the time of aortic valve closure, producing an early diastolic murmur of decrescendo quality, beginning with A2 (see Fig. 5.1). The degree of leakage depends upon the magnitude of the area through which the leak occurs, the systemic arterial diastolic pressure, the level of the left ventricular diastolic pressure, and the heart rate. More rapid heart rates tend to shorten diastole more than systole, and thus reduce the amount of regurgitation for each cardiac cycle, but may not change the total amount of blood leaked per unit of time. Higher systemic vascular resistance tends to increase the leak from aorta to left ventricle; hence such vasodilator drugs as the nitrates, hydralazine, and angiotensin conversion enzyme inhibitors tend to decrease the amount of regurgitation. The lower systemic vascular resistance of pregnancy tends to make the murmur less audible. Increasing systemic vascular resistance by sustained hand grip or squatting tends to make the murmur more readily audible. Higher left ventricular end-diastolic pressures, such as may occur with severe acute aortic regurgitation, tend to lessen the duration of the regurgitant period and shorten the aortic diastolic murmur. With severe aortic regurgitation, regurgitant flow may be 50% to 90% of forward flow. A regurgitant area of 0.5 cm2 can double left ventricular output. The increased left ventricular stroke output can cause systolic blood pressure to exceed 160 mm Hg (Fowler, 1980).


Aortic Valve Infective Endocarditis Aortic Regurgitation Mitral Stenosis Aortic Insufficiency 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Assey ME, Usher BW, Hendrix GH. Valvular heart disease: use of invasive and noninvasive techniques in clinical decision-making. Part 1. Aortic valve disease. Mod. Concepts of Cardiovas. Dis.1989; 58: 55.Google Scholar
  2. Bleich A, Lewis J, Marcus FI. Aortic regurgitation in the elderly. Am Heart J. 1966; 71: 627.PubMedCrossRefGoogle Scholar
  3. Bonow RO, Rosing DR, McIntosh CL, et al. The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function. Circulation. 1983; 68: 509.PubMedCrossRefGoogle Scholar
  4. DiMarco RF, Cocco A, Pellegrini RV, et al. Traumatic aortic insufficiency after blunt chest trauma. Tex Heart Inst J. 1986; 13: 309.PubMedGoogle Scholar
  5. Fowler NO . Cardiac Diagnosis and Treatment. 3rd ed. Hagerstown, MD: Harper & Row; 1980; Chapter 26.Google Scholar
  6. Goldschlager N, Pfeifer J, Cohn K, et al. The natural history of aortic regurgitation: a clinical and hemodynamic study. Am J Med. 1973; 54: 577.PubMedCrossRefGoogle Scholar
  7. Grayburn PA, Smith MD, Handshoe R, et al. Quantitative assessment of the hemodynamic consequences of aortic regurgitation by means of continuous wave Doppler recordings. J Am Coll Cardiol. 1987; 10: 135.PubMedCrossRefGoogle Scholar
  8. Grayburn PA, Smith MD, Handshoe R, et al. Detection of aortic insufficiency by standard echocardiography, pulsed Doppler echocardiography, and auscultation. Ann Intern Med. 1986; 104: 599.PubMedGoogle Scholar
  9. Guiney TE, Davies MJ, Parker DJ, et al. The aetiology and course of isolated severe aortic regurgitation: a clinical, pathological, and echocardiographic study. Br Heart J. 1987; 58: 358.PubMedCrossRefGoogle Scholar
  10. Harvey WP, Corrado MA, Perloff JK. “Right-sided” murmurs of aortic insufficiency (diastolic murmurs better heard to the right of the sternum rather than to the left). Am J Med Sci. 1963; 245: 533.PubMedCrossRefGoogle Scholar
  11. Morganroth J, Perloff JK, Zeldis SM. Acute severe aortic regurgitation. Pathophysiology, clinical recognition, and management. Ann Intern Med. 1977; 87: 223.PubMedGoogle Scholar
  12. Rahko PS. Abstract. Evaluation of mechanisms producing the Austin Flint murmur. Circulation. 1987; 76 (IV): 316.Google Scholar
  13. Roberts WC. Anatomically isolated aortic valvular disease. The case against its being of rheumatic etiology. Am J Med. 1970; 49: 151.PubMedCrossRefGoogle Scholar
  14. Roman MJ, Devereux RB, Niles NW, et al. Aortic root dilatation as a cause of isolated, severe aortic regurgitation. Ann Intern Med. 1987; 106: 800.PubMedGoogle Scholar
  15. Segal J, Harvey WP, Hufnagel C. A clinical study of one hundred cases of severe aortic insufficiency. Am J Med. 1956; 21: 200.PubMedCrossRefGoogle Scholar
  16. Waller BF, Roberts WC. Severe aortic regurgitation secondary to systemic hypertension (without aortic dissection). Cardiovasc Reviews Reports. 1982; 3: 1504.Google Scholar

Copyright information

© Springer-Verlag New York Inc. 1991

Authors and Affiliations

  • Noble O. Fowler
    • 1
  1. 1.Division of CardiologyUniversity of Cincinnati Medical CenterCincinnatiUSA

Personalised recommendations