Etiology and pathology

  • Valvular disease
    • Common causes-
      • Rheumatic
      • Bicuspid aortic valve
      • Calcific aortic valve disease (usually AR is mild)
      • Infective endocarditis (cusp damage, vegetation interfering with coaptation)
      • Trauma (ascending aortic tear causes cusp prolapse)
      • Large VSD
      • Membranous subaortic stenosis
    • Less common causes-
      • After percutaneous balloon valvulotomy
      • Myxomatous degeneration of aortic valve
      • Congenital AR- unicommissural, quadricuspid
      • Rupture of congenitally fenestrated valve (usually due to hypertension)
      • Connective tissue disease- SLE, RA, AS, Takayasu, Whipple, Crohn, Jaccoud arthropathy
      • Anorectic drugs
  • Aortic root disease-
    • Root dilation-
      • Marfan syndrome
      • Cystic medial necrosis other than Marfan
      • Bicuspid aortic valve
      • Syphilis
      • Hypertension
      • Age related
      • Connective tissue disease- ankylosing spondylitis, osteogenesis imperfecta, Behcet syndrome, psoriatic arthritis, ulcerative colitis with arthritis, relapsing polychondritis, reactive arthritis, GCA
      • Appetite suppressants
      • AR itself may increase AR due to ascending aortic dilation- AR begets AR
    • Root dissection

Chronic AR


  • Preload is increased due to-
    • Increased EDV
    • (Note- Preload is the tension in the myocardium just before contraction- correlates with EDV)
    • (Note- Tension from Wikipedia-In physics, tension is the magnitude of the pulling force exerted by a string, cable, chain, or similar object on another object. It is the opposite of compression. As tension is the magnitude of a force, it is measured in newtons and is always measured parallel to the string on which it applies)
  • Afterload is increased due to-
    • Increased LV systolic pressure and
    • LV dilation
    • (Note- Afterload is the tension in the myocardium during contraction- it is proportional to PR/h where P is ventricular pressure, R is radius of ventricle and h is wall thickness)
  • Myocardial ischemia occurs due to-
    • Increased myocardial oxygen demand due to-
      • Increased afterload
      • Increased LV ejection time
      • Increased LV mass
    • Decreased myocardial oxygen supply due to-
      • Decreased aortic diastolic pressure
      • Decreased diastolic filling time due to increased LV ejection time
      • Decreased effective stroke volume
  • LV dysfunction occurs due to-
    • Increased afterload
    • Myocardial ischemia and
    • Increased LV mass
  • LV mass increase in AR-
    • Due to replication of sarcomeres in series and due to increased interstitial connective tissue
    • The increase is more than that in AS
  • Systolic wall stress in AR-
    • Initially, increased LV wall thickness (stress α tension/wall thickness) does not allow stress to increase in spite of increased afterload
    • Later, thickness cannot increase further to cope up with increased afterload. This is called afterload mismatch.
  • In AR, forward stroke volume does not fall due to-
    • Increased stroke volume to compensate for the leak (this occurs due to increased EDV)
  • In AR, LV is able to overcome the increased afterload due to-
    • Increased preload (Frank- Starling—increased preload increases contractility) and
    • LV hypertrophy (more muscle mass to contract)
  • LVEDP in AR-
    • Compensated phase- normal due to
      • Complete LV emptying (as LV function is compensatorily increased to deal with the increased afterload)
      • Increased LV compliance.
    • Decompensated phase- increased due to
      • Incomplete LV emptying (as LV function is not good enough for the increased afterload)
      • Decreased LV compliance due to interstial fibrosis
  • ESV in AR-
    • Compensated phase- normal due to complete LV emptying
    • Decompensated phase- increased due to incomplete LV emptying
  • Exercise in AR-
    • Compensated phase- Forward cardiac output usually increases efficiently without increase in LVEDP. The reasons are-
      • Decrease in SVR causes less AR
      • Diastole shortens (compared to systole) causing less AR
    • Decompensated phase- Failure to generate adequate cardiac output (fatigue on exertion). Increase in LVEDP (dyspnoea on exertion).


  • Palpitations
    • Occurs before LV dysfunction occurs unlike the other symptoms
    • Due to increased EDV
    • More on lying down
    • More after a VPC
  • Fatigue, dyspnoea and angina
    • Occurs after LV dysfunction occurs
    • Angina may be nocturnal due to lower heart rate at night (more AR)

Physical examination

    • Common-
      • de Musset sign- head nodding
      • Water-hammer pulse or Corrigan pulse or collapsing pulse- high volume pulse with quick ascent, ill sustained peak and quick collapse. Palpate in radial artery with arm elevated.
      • Bisferiens pulse- best palpated in brachial or femoral arteries.
      • Pistol shot sounds or Traube sign- femoral artery distal compression produces double sounds (systolic and diastolic)
      • Muller sign- systolic pulsation of uvula
      • Duroziez sign- femoral artery- systolic murmur with proximal compression and diastolic murmur with distal compression
      • Quincke sign- pressure on tip of fingernail, fingertip transillumination or glass slide on lip
      • Lighthouse sign- flushing and blanching of forehead
      • Landolfi’s sign- papillary constriction and dilation
      • Becker’s sign- retinal vessel pulsation
      • Rosenbach’s sign- liver pulsation
      • Gerhardt’s sign- splenic pulsation
      • Hill’s sign or popliteal-brachial gradient- Popliteal BP 20 mmHg more than brachial BP.
    • Uncommon-
      • Morton and Mahon sign- same as lighthouse sign
      • Ashrafian sign- pulsatile pseudoproptosis
      • Bozzolo sign- pulsatile nasal mucosa
      • Drummond sign- systolic expulsion of air from nose when mouth is closed
      • Mayen’s sign- when arm is raised, diastolic BP drops by more than 15 mmHg
      • Penny sign- flushing of wheals
      • Palmar click- pulsating palm
      • Dennison sign, Shelley sign- pulsatile cervix
      • Lincoln sign- popliteal pulsation
      • Sherman sign- dorsalis pedis prominent pulsation in age of 75 yrs or more
      • Other names for collapsing pulse-
        • Watson’s pulse
        • Cannon ball pulse
        • Pulsus celer
        • Rhazes pulse or Al Razi pulse
        • Cuming sign
        • Vieussens pulse
  • High volume pulse
  • High pulse pressure, high systolic pressure, low diastolic pressure. Beginning of phase IV should be taken as diastolic BP. Diastolic BP is higher in mild AR and in severe AR with heart failure (due to peripheral vasoconstriction).
  • Hyperdynamic diffuse apex displaced laterally and inferiorly.
  • Parasternal systolic retraction.
  • Palpable LVS3
  • Systolic thrill at aortic area and over carotids (carotid shudder)
    • (Note- Carotid shudder was initially described by Evans and Lewes in 1945 in AS + AR. Later, in 1976, it was shown by Alpert et al to be present in pure AS and pure AR also. In the same year, Chapman documented it in ascending aortic dissection also. Generally, the term is used in pure AS.)
  • S1 may be soft.
  • A2-
    • Soft or absent in valvular cause of AR
    • Normal or accentuated in AR due to root dilation (tambour sound)
  • S2 split-
    • Paradoxical split can occur (prolonged LVET)
    • Aortic ejection sound may occur due to aortic distension due to increased stroke volume
  • LVS3 can occur in pure AR and in AR with LV failure.
  • EDM-
    • High frequency
    • Begins with A2
    • Better heard with patient sitting and leaning forward, breath held in expiration.
    • Decrescendo.
    • High pitched in mild AR and rough in severe AR.
    • Early diastolic in mild AR and holodiastolic in severe AR.
    • Late diastolic component is abolished in LV failure due to high LVEDP.
    • Cooing dove murmur in cusp eversion or perforation.
    • Valvular cause of AR- radiation to left sternal border. Root dilation causing AR- radiation to right sternal border.
    • Increased with squatting and isometric exercise
    • Decreased with amyl nitrite and Valsalva
    • Cole-Cecil murmur- EDM radiating to apex and left axilla
  • MSM-
    • May be associated with a carotid thrill
    • Higher pitched than the murmur of AS
  • Austin Flint murmur-
    • Mid diastolic murmur with presystolic accentuation
    • Seen in severe AR only
    • Causes-
      • AR jet impinging on AML forcing it down thus decreasing mitral orifice
      • Turbulence when AR jet meets mitral inflow jet
      • AML fluttering due to AR jet
      • LV endocardial vibrations due to AR jet
    • With LV failure, due to elevated LVEDP, Austin Flint murmur begins and ends earlier
    • Increased with isometric exercise, reduced by amyl nitrite


  • Points to note-
    • Cause of AR
    • Severity of AR
    • LV function
  • High frequency diastolic fluttering of AML- seen in M mode- seen even in mild AR (unlike Austin Flint murmur)




    Jet width/LVOT diameter


    1/4 to 2/3


    Vena contracta (mm)


    3 to 6


    Pressure half-time (ms)

    > 700



    LV dilation




    Flow reversal in descending thoracic or abdominal aorta




    Regurgitant orifice area (cm2)


    0.1 to 0.3


    Regurgitant volume (ml)


    30 to 60


    Regurgitant fraction


    30 to 50



  • Continuity equation-
    • Regurgitant volume= LVOT flow- mitral flow
    • Regurgitant fraction= Regurgitant volume/ LVOT flow
    • Regurgitant area= Regurgitant volume/ AR TVI
  • PISA-
    • Regurgitant area= Flow through aliasing hemisphere surface/AR peak velocity
    • Regurgitant volume= Regurgitant area x AR TVI
    • Regurgitant fraction= Regurgitant volume/LVOT flow
  • (Note- In continuity equation, regurgitant volume is calculated first. In PISA, the calculations in order are regurgitant area, regurgitant volume and regurgitant fraction.)


  • High LV voltage
  • Q in lateral leads
  • Tall upright T waves in lateral leads initially; later strain pattern.


  • LV enlargement
  • LA enlargement if heart failure or mitral valve disease
  • Ascending aortic dilation- more than in AS
  • Look for ascending aortic aneurysm
  • Linear calcifications in ascending aorta- syphilitic aortitis


  • For assessing AR, contrast injection into aortic root must be at 25 to 35 ml/sec!

Radionuclide angiography

  • LV/RV stroke volume ratio > 2 indicates severe AR


  • Can accurately measure severity of AR by measuring regurgitant volume, regurgitant fraction and regurgitant area
  • Used when echo is suboptimal

Natural history

  • Main studies- Bonow et al, Borer et al
  • No symptoms, normal EF-
    • Annual chance of symptoms or LV dysfunction- 6%
    • Annual chance of sudden death- 0.5%
  • Angina-
    • Death in 4 years
  • Heart failure-
    • Death in 2 years
  • Survival and NYHA class in severe AR-
    • NYHA I- 10 yr survival of 75% (equal to general population)
    • NYHA III or IV- 4 yr survival 28%

Medical management

  • If diastolic BP is high, vasodilators like nifedipine or ACE inhibitors are to be given
  • Beta blockers should be avoided


  • Indications for surgery in chronic severe AR-
    • Class I-
      • Symptoms
      • Symptoms on TMT
      • EF less than 50% (echo, RVG or MRI)
    • Class IIa-
      • LVESD > 55 mm (50 to 55 is IIb)
      • LVEDD> 75 mm (70 to 75 is IIb)
  • Patients with severe LV dysfunction (EF < 25%) before AVR may not have an improvement in LV function after AVR.
  • Aortic valve repair-
    • Usually not possible, so AVR will be needed (unlike mitral repair which if often successful)
    • Cusp resuspension or cusp resection for cusp detachment from annulus due to trauma
    • Pericardial patch for cusp perforation in IE
    • Root dilation causing AR-
      • Encircling suture
      • Subcommissural annuloplasty
      • Aortic graft with prosthetic valve- coronaries need to be reimplanted
      • Aortic graft alone
  • AVR-
    • Large prosthesis can be implanted as annulus is dilated- so less chance of prosthetic gradient.
    • Operative mortality- 3 to 8%

Acute AR

  • Causes-
    • Infective endocarditis
    • Aortic dissection
    • Trauma
  • Pathophysiology
    • Normal LV size (not increased as compliance is not increased)
    • Increased LVEDP (dyspoesa) + decreased cardiac output (shock)
    • Increased LVEDP as LV cannot dilate rapid enough to accommodate the regurgitant volume
    • Decreased cardiac output due to-
      • Decreased forward stroke volume because-
        • EDV does not increase as LV compliance does not increase (In chronic AR, increased EDV increases total stoke volume so that forward stroke volume, which is total stroke volume – regurgitant volume, is maintained)
      • Decreased total stroke volume due to-
        • Premature mitral closure due to increased LVEDP
        • Tachycardia (less diastolic filling time). Tachycardia is a compensatory response to decreased cardiac output.
  • Physical examination-
    • Hypotension with tachycardia as a compensatory response
    • Dyspnoea due to increased LVEDP
    • Normal pulse pressure
    • No peripheral signs of AR
    • S1 is soft or absent due to premature closure
    • P2 may be loud
    • EDM-
      • Shorter than the murmur of chronic AR (due to rapidly rising LV diastolic pressure)
      • Lower pitched than the murmur of chronic AR (due to rapidly rising LV diastolic pressure)
    • Austin Flint murmur-
      • Shorter than in chronic AR, no presystolic accentuation (due to rapidly rising LV diastolic pressure)
  • Echocardiography-
    • AR jet- low end diastolic velocity
    • Mitral valve- late opening and premature closure
    • LV size- normal
    • EF- normal
    • Aortic valve- premature opening
  • ECG-
    • Non specific ST-T changes
  • Radiography-
    • PVH, pulmonary edema
    • Normal heart size
  • Management-
    • Early surgery
    • During preparation for surgery-
      • Dopamine/dobutamine + nitroprusside
      • Do not put on IABP (increased peripheral resistance during diastole increases AR)
      • Do not give beta blockers for tachycardia (increased diastolic interval increases AR)