Aortic valve incompetence is the most common of the diastolic murmurs.

Clinical Features:

  • collapsing pulse (depending upon severity)
  • thrusting apex beat
  • displaced apex beat
  • wide pulse pressure (again depending upon severity)

There are a number of eponymous signs associated with aortic valve incompetence, which in reality, you will probably never see unless the patient has severe aortic valve incompetence and is somewhat decompensating. These include uvula pulsation (Muller’s sign), head-bobbing with each pulsation (De Mussett’s sign); capillary pulsation in the fingernails (Quincke’s sign); hepatic pulsation (Rosenbach’s sign) and the pistol shot sounds of both the systolic and diastolic femoral artery sounds (Duroziez’s sign).

The most well known is Corrigan’s sign which is the visualisation of the rise and fall of carotid pulsation.

ECG signs in aortic valve incompetence

  • sinus rhythm
  • left ventricular strain

Associations with aortic valve incompetence:

  • Argyll Robertson pupils (syphilis)
  • Marfan’s syndrome (high arched palate)
  • Ankylosing spondylitis

If the above are not present, then the aortic valve incompetence is most likely due to rheumatic heart disease. Another cause is primary aortic root dilatation, with aortic valve incompetence secondary.

Other causes of aortic valve incompetence include chronic hypertension (uncontrolled), rheumatoid arthritis and coarctation of the aorta. Infective causes include syphilitic aortitis and infective endocarditis. Another cause is the rare Hurler’s syndrome. [1]

The systolic element does not always mean co-existent stenosis, and could indicate just increased flow across the valve.

Management is primarily medical (ACE-Inhibitors and calcium channel blockers) and/or treatment of the underlying condition and surgical with valve replacement. The aim of surgery is to prevent significant left ventricular dysfunction from occurring.

  1. Hurler’s syndrome is a rare genetic metabolic disorder, also known as mucopolysaccharide type 1 (MPS1) where there is an enzymatic defect leading to accumulation of glycosaminoglycans.