Aortic regurgitation

Aortic regurgitation, has many causes: degeneration of the cusps, endocarditis, bicuspid aortic valve, aortic root dilatation, trauma, connective tissue disorders such as Marfan syndrome or Ehlers-Danlos lead to imperfect closure of the valve during diastole, hence the blood is returning from the aorta towards the left ventricle of the heart.

Results in left ventricular volume overload which leads to left ventricle dilation and left ventricular function deterioration.

Acute regurgitation resulting from dissection of the ascending aorta requires immediate surgery to repair the dissection.

Severe aortic regurgitation is associated with a large forward stroke volume, which causes an increase in systolic blood pressure.

Severe aortic regurgitation is associated with the rapid loss of blood from the aorta backward into the left ventricle, which results in a relative decrease in diastolic pressure.

Large stroke volume and rapid runoff associated with severe aortic regurgitation can be manifested by pronounced arterial pulsation with the carotid pulse being described as bounding, often with visible pulsation or a collapsing Corrigan’s pulse.

Quincke’s sign  represents the visualization of capillary pulsations upon light compression applied to the tip of the fingernail bed. 

The major  finding for aortic insufficiency is an early diastolic, decrescendo murmur, which is best auscultated at the sternal border: It is a finding associated with chronic severe aortic insufficiency.

Quicke sign had alternating reddening and blanching of the nailbed with each pulsation.



The sign can be enhanced by illumination.



As with other signs of chronic severe aortic insufficiency, it is a result of a widened pulse pressure, with an increased systolic stroke volume and rapid decrease in arterial pressure.



The sign is most prominently demonstrable in patients with chronic severe aortic insufficiency.



Quincke’s sign can also occur in asymptomatic patients without any valvular heart disease. 



Its sensitivity and specificity for screening and establishing a diagnosis with this isolated sign are poor.

Other associated physical exam findings include Becker’s sign, Corrigan’s (water-hammer) pulse, de Musset’s sign, Duroziez’s sign, Hill’s sign, Müller’s sign, and Traube’s sign.


An observant clinician can quickly identify concerning signs of cardiac valvular disease on physical exam, which is confirmable with the use of transthoracic echocardiography.

These hemodynamic changes produce a wide pulse pressure defined is a diastolic pressure that is less than 50% of the systolic blood pressure.

When surgery is needed aortic valve replacement, rather than repair, is usually required.

Asymptomatic chronic aortic regurgitation with normal left ventricular systolic function the rate of progression to symptoms and/or left ventricular dysfunction is less than 6 percent per year.

Clinical course characterized by prolonged stability with left ventricle adaptation to volume overload with hypertrophy, increased end-diastolic pressure and increased compliance.

Use of vasodilators may prolong stable phase and delays left ventricle decompensation and postpones the need for surgery.

Asymptomatic chronic aortic regurgitation with left ventricular dysfunction the rate of progression to symptoms is higher than 25% per year.

Asymptomatic chronic aortic regurgitation with normal left ventricular systolic function the rate of sudden death is less than 0.2 percent per year.

In symptomatic patients the mortality rate is greater than 10 percent per year.

Volume determined by diastolic aortoventricular pressure gradient, regurgitant orifice area and diastolic filling time.

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