Aortic regurgitation results from an incompetent aortic valve causing a regurgitant flow of blood in diastole.
Aortic regurgitation tends to present between the fourth and sixth decades of life. It affects males three times more commonly than women. Severe disease is seen in < 1% of the population. The most common causes are degenerative disease and congenital bicuspid valve.
Causes of AR can be split into either primary disease of the aortic valve leaflets; or dilation of the aortic root.
An autoimmune condition which follows streptococcal (Group A) infection. Inflammation is a result of molecular mimicry. In effect, the immune system produces antibodies that confuse foreign- and self-antigens. Rheumatic heart disease results from cardiac inflammation with acute and chronic results.
Commonest cause in the developing world. Although an increasingly uncommon cause of valvular disease. Chronic disease leads to fibrosis and typically a stenotic valve though regurgitant valves may also develop.
Constitute the commonest causes of aortic regurgitation in the developed world.
Inflammation of the endocardium, typically as a result of infection. Results in acute disease. Vegetations may cause flailing of the valve leaflets.
Infective causes include Strep. viridans, Staph. aureus, Enterococci.
Aortic regurgitation may feature in a number of connective tissue disorders. Aortic root diameter should be monitored in these individuals.
Inflammation of the aortic root. May be associated with chronic inflammatory conditions such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Also, may occur in Takayasu arteritis, or may complicate Giant cell arteritis.
Occurs in Stanford A dissections, impairing leaflet coaptation or causing prolapse. Causes acute disease. A medical emergency.
Aortic regurgitation may develop acutely or chronically over a period of many years.
Acute aortic regurgitation is a medical emergency - an acute rise in left atrial pressure results in pulmonary oedema & cardiogenic shock.
Valvular incompetence occurs rapidly and the compensatory changes seen in chronic disease do not have time to develop. Regurgitation of blood during diastole causes an increase in the left ventricular end-diastolic volume (and pressure).
The effects of this are two-fold:
In chronic aortic regurgitation, patients may remain asymptomatic for many decades.
Valvular incompetence develops slowly. Regurgitation of blood during diastole causes an increase in the left ventricular end-diastolic volume (essentially the preload). This leads to systolic and diastolic dysfunction, left ventricular dilatation develops with eccentric hypertrophy.
The dilation allows for an increased stroke volume compensating for regurgitant flow supported by the ventricular hypertrophy. These changes maintain ejection fraction, with a greater preload leading to greater contractility (see notes ‘Heart failure’ subsection ‘Frank-Starling law’).
Eventually further increases in preload cannot be met by greater contractility and heart failure develops.
Acute disease has the features of acute heart failure, the peripheral symptoms that are seen in chronic disease may not be present.
Often asked about in examinations, the relevance of these signs in clinical practice today is questionable.
Surgical aortic valve replacement or repair is indicated in severe or symptomatic disease. Severity is indicated on echo by LVH, pressure gradient and valve area. Successful surgery leads to much-improved quality of life and improved mortality.
Acute AR is a surgical emergency. Aortic valve replacement or repair should be performed as soon as possible.
The decision of mechanical vs bioprosthetic valve should take into account patient-specific factors and wishes. Traditionally valve replacement has necessitated open surgery, novel techniques now allow percutaneous replacement: transcatheter aortic valve replacement (TAVR) - a minimally invasive technique that utilises an expandable valve, may be used in patients who are not candidates for open surgery.
Coronary angiogram may be used to demonstrate atherosclerotic disease that may be treated with CABG at the same time as the open surgery.
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