Aortic Regurgitation - History, Examination And Study Questions & Answers

Clinical History
· Patients may be asymptomatic (but may have normal or depressed left ventricular function).

· Dyspnoea and fatigue (due to left ventricular impairment and low cardiac output initially on exertion).
· Symptoms of left ventricular failure in later stages.
· Angina pectoris is less common than in aortic stenosis; it usually indicates coronary artery disease.

Examination

1. Pulse
· Collapsing pulse (large volume, rapid fall with low diastolic pressure).
· Visible carotid pulsation in neck (dancing carotids or Corrigan's sign).

· Capillary pulsation in fingernails (Quincke's sign).
· A booming sound heard over femorals ('pistol-shot' femorals or Traube's sign).
· To and fro systolic and diastolic murmur produced by compression of femorals by stethoscope
(Duroziez's sign or murmur).

2. Heart
· Heart sounds are usually normal.
· Apex beat is displaced outwards and is forceful.
· Third heart sound (in early systole with bicuspid aortic valve).
· Early diastolic, high-pitched murmur is heard at the left sternal edge with the diaphragm - if not
readily apparent, it is important to sit the patient forward and auscultate with the patient's breath held
at the end of expiration. When the ascending aorta is dilated and displaced to the right, the murmur
may be heard along the right sternal border as well.
· An ejection systolic murmur may be heard at the base of the heart in severe aortic regurgitation
(without aortic stenosis). This murmur may be as loud as grade 5 or 6, and underlying organic stenosis can be ruled out only by investigations.
· Ejection click suggests underlying bicuspid aortic valve.
· Mid-diastolic murmur of Austin Flint may be heard at the apex. It is typically low-pitched, similar to the murmur of mitral stenosis but without a preceding opening snap.
· Loud pulmonary component of second sound (suggests pulmonary hypertension).

3. General examination
· Head nodding in time with the heart beat (de Musset's sign) may be present.
· Visible carotid pulsation may be obvious in the neck - dancing carotids or Corrigan's sign.
· Check the blood pressure (wide pulse pressure).
· Look for systolic pulsations of the uvula (Muller's sign).
· Check pupils for Argyll Robertson pupil of syphilis.
· Look for stigmata of Marfan's syndrome - high arched palate, arm span greater than height.
· Check joints for ankylosing spondylitis and rheumatoid arthritis.

QUESTIONS

Mention a few causes of chronic aortic regurgitation.

· Rheumatic fever.

· Hypertension (accentuated tambour quality of second sound).

· Atherosclerosis.

· Bacterial endocarditis.

· Idiopathic dilatation of the aortic root and annulus.

· Syphilis.

· Marfan's syndrome.

· Rheumatoid arthritis.

· Cystic medial necrosis.

· Seronegative arthritis (ankylosing spondylitis, Reiter's syndrome).

· Bicuspid aortic valve.

How would you investigate a patient with aortic regurgitation?

· Chest radiograph is usually normal in mild aortic regurgitation; there may be valvular calcification or cardiomegaly.

· ECG typically shows features of left ventricular hypertrophy and strain (increased QRS amplitude

and ST/T wave changes in precordial leads) and left atrial hypertrophy (wide P wave in lead II and

biphasic P in lead V 1).

· Echocardiography is indicated to: confirm the diagnosis of AR; determine aetiology; assess valve

morphology; determine a semiquantitative estimate of severity of regurgitation; assess LV dimension,

mass and systolic function; assess aortic size; estimate the degree of pulmonary hypertension (when

TR is present); determine whether there is rapid equilibration of aortic and LV diastolic pressure.

Doppler is the best method for detecting aortic regurgitation

· Exercise testing: is useful to assess functional capacity, symptomatic responses and haemodynamic

effects of exercise in patients with severe AR with equivocal symptoms.

· Radionuclide angiography is useful in asymptomatic patients with poor quality echocardiographic

images.

· Cardiac catheterization is necessary when coronary artery disease is suspected (e.g. in patients >40

years) and when the severity of aortic regurgitation is doubted; injection of contrast into aortic root

gives information on degree of regurgitation and state of aortic root (presence of dilatation, dissection, root abscesses).

· MRI or spiral CT scan for assessment of aortic root size.

What are the clinical signs of severity?

· Wide pulse pressure.

· Soft second heart sound.

· Duration of the decrescendo diastolic murmur.

· Presence of the left ventricular third heart sound.

· Austin Flint murmur.

· Signs of left ventricular failure.

What do you know of Hill's sign?

Hill's sign is the presence of higher systolic pressure in the leg than in the arm, and is said to be an

indicator of the severity of aortic regurgitation.

In mild aortic regurgitation the difference is less than 20 mmHg, in moderate regurgitation it is

between 20 and 40 mmHg and in severe regurgitation it is over 60 mmHg.

Do characteristics of the early diastolic murmur correlate with severity?

Yes. In mild aortic regurgitation the murmur is short but, as the severity of the regurgitation increases,

the murmur becomes longer and louder. In very severe regurgitation the murmur may extend throughout diastole.

What is an Austin Flint murmur?

It is an apical, low-pitched, diastolic murmur caused by vibration of the anterior mitral cusp in the

regurgitant jet, and is heard at the apex.

Mention a few causes of acute aortic regurgitation.

· Infective endocarditis.

· Aortic dissection.

· Trauma.

· Failure of prosthetic valve.

· Rupture of sinus of Valsalva.

What do you understand by the term cor bovinum?

In chronic aortic regurgitation there is slow and progressive left ventricular dilatation and hypertrophy in an attempt to normalize wall stress. The heart may thus become larger and heavier than in any other form of chronic heart disease - cor bovinum (bovine or ox heart).

What is the role of vasodilators in aortic regurgitation?

· Long-term vasodilator therapy with nifedipine reduces or delays the need for aortic valve replacement in asymptomatic patients with severe aortic regurgitation . 

Patients in whom left ventricular dysfunction developed when treated with nifedipine respond favorably to valve replacement in terms of both survival and normalization of ejection fraction.

· Long-term treatment of patients with severe AR who have symptoms and/or LV dysfunction who are considered poor candidates for surgery due to other factors.

· Long-term vasodilator therapy should not be recommended for patients with left ventricular

dysfunction.

· Patients with subnormal left ventricular ejection fractions should be considered candidates for aortic

valve replacement rather than vasodilator therapy, since valve replacement remains the more

definitive therapy to reduce volume overload.

· Vasodilator therapy is not recommended for asymptomatic patients with mild AR and normal LV

function in the absence of systemic hypertension, as these patients have an excellent outcome with

no therapy.

· The goal of vasodilator therapy is to reduce systolic blood pressure. However, it is rarely possible to

reduce systolic blood pressure to normal because of increased LV stroke volume, and hence drug

dosage should not be increased excessively in an altempt to achieve this goal. The benefit of

vasodilator therapy in patients with normal blood pressure and/or normal LV cavity size is not known

and hence is not recommended in these patients .

How is aortic regurgitation treated?

Aortic regurgitation is usually treated surgically. The timing of surgery is important and depends on

severity of symptoms and extent of left ventricular dysfunction . 

Valve replacement should be performed as soon as possible after the onset of ventricular dysfunction.

Indications for surgery include:

· Symptoms of heart failure and diminished left ventricular function (an ejection fraction of less than

50% but more than 20-30%).

· Concomitant angina and severe AR.

· A reduction in exercise ejection traction (as estimated with radionuclide ventriculography and

exercise testing) of 5% or more is considered by some to be an indication for surgery, even in the

absence of symptoms.

· Several investigators have suggested an end-systolic dimension of 55 mm to represent the limit of

surgically reversible dilatation of the left ventricle, so that aortic valve replacement is performed before this chamber size is exceeded. Others have challenged the validity of the 55 mm systolic limit, as postoperative reduction in chamber size remains variable.

· When aortic root dilatation reaches or exceeds 50 mm by echocardiography, AVR and aortic root

reconstruction are indicated in patients with disease of the proximal aorta and AR of any severity.

Note

1. In the young, mechanical prostheses are used as the valves are more durable.

2. Tissue valves are prone to calcification and degeneration. In the elderly and in those for whom

anticoagulants are contraindicated, tissue valves are preferred.

How would you follow up a patient with AR?

· Asymptomatic patients with mild AR, little or no LV dilatation, and normal systolic LV function may be followed on an annual basis with the advice to alert the physician if symptoms develop between appointments .

· Asymptomatic patients with normal systolic function but severe AR and significant LV dilatation

should be followed up at least every 6 months, preferably with an echocardiogram.

· Asymptomatic patients with normal systolic function but severe AR and with more severe LV

dilatation (end-diastolic dimension >70 mm or end-systolic dimension >50 mm) have a 10-20% risk of developing symptoms and hence should have serial echocardiograms every 4 months.

· Patients who have had valve replacement should also be seen regularly and monitored for signs of

failure of the aortic valve prosthesis (particularly in patients with biological valves) and endocarditis