Aortic valve regurgitation, also known as aortic valve insufficiency or aortic valve incompetence, is a valvulopathy that describes leaking of the aortic valve during diastole that causes blood to flow in the reverse direction from the aorta and into the left ventricle.
Aortic regurgitation occurs slightly more in males, and the incidence increases progressively after the age of 50 years 1.
Although chronic aortic regurgitation can be asymptomatic, even in reasonably severe disease, it eventually leads to left-predominant clinical features of heart failure such as dyspnea and angina 1-3. Clinical examination classically reveals a widened pulse pressure, pulsus bisferiens, a volume loaded (‘thrusting’) apex beat, and a decrescendo early diastolic murmur (the Key-Hodgkin murmur) that is heard on praecordial auscultation 1-4.
Occasionally the murmur heard may be holodiastolic, reflecting increased disease severity, and there may be an additional mid-diastolic Austin Flint murmur heard at the apex, attributed to the regurgitant jet striking the anterior mitral valve leaflet 1-3.
Aortic regurgitation is also infamously associated with a number of eponymous signs, all of which are now rare due to the decreased incidence of syphilitic aortitis 2,5,6. A detailed discussion of these rare signs is beyond the scope of this article.
Patients with chronic aortic regurgitation compensate for the leakage into the left ventricle by increasing total stroke volume (this is the forward ‘true’ stroke volume in addition to the volume leaking) ejected by the left ventricle through dilation and hypertrophy of the left ventricle 2,3. This results in systolic hypertension, accounting for the wide pulse pressure, and aortic and arterial pressures rapidly falling during late systole and diastole, accounting for the timing of the murmur and the various eponymous signs 2,3.
This adaptive mechanism is able to compensate for even severe aortic regurgitation, however, eventually fails and the end-diastolic volume becomes too large and the ejection fraction and forward (rather than ‘total’) stroke volume both fall 2,3. It is at this point where patients manifest clinical features of heart failure 2,3.
Predisposing factors or causes of chronic aortic regurgitation can broadly be divided into being due to root disease or due to intrinsic valvulopathy, although there is overlap 2,3:
- root disease: hypertension, congenital bicuspid aortic valve, connective tissue disorders (e.g. Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta, etc.), aortic dissection, Takayasu arteritis, syphilitic aortitis, etc.
- valvular: rheumatic heart disease, calcific aortic valve disease (i.e. calcific aortic stenosis), bacterial infective endocarditis, prolapse, quadricuspid aortic valve, ankylosing spondylitis, syphilitic aortitis, radiation-induced heart disease, etc.
Acute aortic regurgitation is less common, but also exists, with specific causes 2,3:
- bacterial infective endocarditis
- aortic dissection
- traumatic rupture
- iatrogenic (e.g. during transcatheter aortic valve implantation)
Variable appearance on chest radiographs depending on stage and severity of the disease 1. In chronic severe aortic regurgitation, the apex may be displaced to the left on posterior-anterior projections, and there may be signs of congestive heart failure 1. Furthermore, if the aortic regurgitation is due to aortic root disease, then aneurysmal dilation may be noted 1.
Echocardiography is useful for evaluating the cause of aortic regurgitation, either valvular or due to root disease, for assessing the regurgitant volume, and for assessing the left ventricle 3,7. Features which may be suggestive on 2D echocardiography include failure of valvular coaptation, flail or prolapsed leaflets, and, when chronic, progressive left ventricular dilation. Various parameters are used in order to determine severity, such as 3,7:
- the central jet has a width <25% of the left ventricular outflow tract (LVOT)
- vena contracta < 0.3 cm
- regurgitant volume < 30 mL/beat
- regurgitant fraction < 30%
- effective regurgitant orifice area < 0.10 cm2
- measurements are worse than mild aortic regurgitation but do not meet criteria for severe aortic regurgitation
- the central jet has a width ≥65% of the LVOT
- vena contracta > 0.6 cm
- regurgitant volume ≥ 60 mL/beat
- regurgitant fraction ≥ 50%
- effective regurgitant orifice area ≥ 0.30 cm2
Left ventricular structural derangements in chronic aortic regurgitation progress in proportion to the degree of regurgitant volume; a normal or hyperdynamic left ventricle in the presence of severe features suggest that the valvulopathy is acute 3,7.
Failure of coaptation of aortic valve leaflets in diastole can be a suggestive feature.
Cardiac MRI (CMR) is able to provide a more detailed assessment of the aortic valve and left ventricular function 9. It is able to highly accurately determine the size of the aortic root, assess regurgitant parameters, determine ejection fraction, measure left ventricular size, and detect underlying etiologies 9.
The following threshold for cardiac MRI was suggested as a risk for progression to aortic valve replacement 10,11:
- regurgitant volume > 42 mL/beat
- regurgitant fraction > 33%
Treatment and prognosis
The decision to treat aortic regurgitation is based on etiology and severity. Management involves a combination of lifestyle and pharmacotherapy measures (a similar armamentarium to that used in heart failure), aortic valve replacement, and aortic root reconstruction 2,3. Details of this management are beyond the scope of this article.
- congestive heart failure
- sudden cardiac death from arrhythmia
- aortic valve stenosis ('jet stenosis')
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